Nutrition Therapy and Pathophysiology [4 ed.] 9780357041710, 2018965075

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NELMS SUCHER

Nutrition Therapy & Pathophysiology

Nutrition Therapy & Pathophysiology FO U RT H E D I T I O N

FOURTH EDITION

Marcia Nelms  Kathryn P. Sucher

9780357041710_cvr_hr.indd 1

SE/Nelms, Sucher: Nutrition Therapy and Pathophysiology 4e   ISBN-13: 978-0-357-04171-0  ©2020  Designer: Jeanne Schreiber Printer: Quad Graphics – Versailles   Binding: Casebound   Trim: 8.5” x 10.875”   CMYK

31/12/18 10:08 AM

Aids to Calculation

Conversion Factors

Percentages

A conversion factor is a fraction in which the numerator (top) and the denominator (bottom) express the same quantity in different units. For example, 2.2 pounds (lb) and 1 kilogram (kg) are equivalent; they express the same weight. The conversion factors used to change pounds to kilograms and vice versa are:

A percentage is a comparison between a number of items (perhaps the number of kcalories in your daily energy intake) and a standard number (perhaps the number of kcalories used for Daily Values on food labels). To find a percentage, first divide by the standard number and then multiply by 100 to state the answer as a percentage (percent means “per 100”).

1 kg 2.2 lb . and 2.2 lb 1 kg Because a conversion factor equals 1, measurements can be multiplied by the factor to change the unit of measure without changing the value of the measurement. To change one unit of measurement to another, use the factor with the unit you are seeking in the numerator (top) of the fraction.

Example 1 Convert the weight of 130 pounds to kilograms. • Choose the conversion factor in which the kilograms are on top and multiply by 130 pounds: 1 kg 2.2 lb

130 kg 2.2

130 lb

59 kg.

Example 2 Consider a 4-ounce (oz) hamburger that contains 7 grams (g) of saturated fat. How many grams of saturated fat are contained in a 3-ounce hamburger? • Because you are seeking grams of saturated fat, the conversion factor is: 7 g saturated fat. 4 oz hamburger • Multiply 3 ounces of hamburger by the conversion factor: 3 oz hamburger

7 g saturated fat 4 oz hamburger

3

7 4

21 4

Example 3 Suppose your energy intake for the day is 1500 kcalories (kcal): What percentage of the Daily Value (DV) for energy does your intake represent? (Use the Daily Value of 2000 kcalories as the standard.) • Divide your kcalorie intake by the Daily Value: 1500 kcal (your intake) 0.75

100

75% of the Daily Value.

Example 4 Sometimes the percentage is more than 100. Suppose your daily intake of vitamin C is 120 milligrams (mg) and your RDA (male) is 90 milligrams. What percentage of the RDA for vitamin C is your intake? 120 mg (your intake) 1.33

100

Milliequivalents to Milligrams Milligrams

39 mg

1 mEq Chloride (Cl−)

35.5 mg

1 mEq Sodium (Na2+)

23 mg

1 mEq Bicarbonate (HCO3−)

61 mg

1 mEq Calcium (Ca2+)

20 mg

1 mEq Potassium (PO43−)

31.67 mg

1 mEq Magnesium (Mg2+)

12.2 mg

4 kcal 1 g protein

9 kcal 1 g fat

Anions Milliequivalents

1 mEq Potassium (K+)

The equivalent weight of an electrolyte is its molecular weight divided by its valence. Therefore, because the molecular weight of K+ is 39 and its valance is one, 39/1 is 39 grams. Milliequivalents would be 1/1000 of the equivalents or 39 milligrams. One milliequivalent of Na+ is 23 milligrams [(23 grams/1) divided by 1000].

W

1.33.

Example 5 Sometimes the comparison is between a part of a whole (for example, your kcalories from protein) and the total amount (your total kcalories). In this case, the total is the number you divide by. If you consume 60 grams (g) protein, 80 grams fat, and 310 grams carbohydrate, what percentages of your total kcalories for the day come from protein, fat, and carbohydrate?

80 g fat

Milligrams

90 mg (RDA)

133% of the RDA.

60 g protein

Cations

0.75.

• Multiply the number of grams by the number of kcalories from 1 gram of each energy nutrient (conversion factors):

5 g saturated fat (rounded off).

Milliequivalents

2000 kcal (DV)

• Multiply your answer by 100 to state it as a percentage:

240 kcal.

720 kcal.

310 g carbohydrate

4 kcal 1 g carbohydrate

1240 kcal.

LENGTH 1 meter (m) 39 in. 1 centimeter (cm) 0.4 in. 1 inch (in) 2.5 cm. 1 foot (ft) 30 cm.

• Find the total kcalories: 240

720

1240

2200 kcal.

• Find the percentage of total kcalories from each energy nutrient (see Example 3): Protein: 240 2200 11% of kcal.

0.109

100

10.9

Fat: 720 2200 33% of kcal.

0.327

100

32.7

2200 Carbohydrate: 1240 56% of kcal. Total: 11%

33%

0.563 56%

100

56.3

100% of kcal.

In this case, the percentages total 100 percent, but sometimes they total 99 or 101 because of rounding—a reasonable estimate.

Ratios A ratio is a comparison of two (or three) values in which one of the values is reduced to 1. A ratio compares identical units and so is expressed without units.

Example 6

Suppose your daily intakes of potassium and sodium are 3000 milligrams (mg) and 2500 milligrams, respectively. What is the potassium-to-sodium ratio? • Divide the potassium milligrams by the sodium milligrams: 3000 mg potassium

Weights and Measures

2500 mg sodium

1.2.

The potassium-to-sodium ratio is 1.2:1 (read as “one point two to one” or simply “one point two”), which means there are 1.2 milligrams of potassium for every 1 milligram of sodium. A ratio greater than 1 means that the first value (in this case, potassium) is greater than the second (sodium). When the ratio is less than 1, the second value is larger.

TEMPERATURE Steam

100°C

212°F

Steam

Body temperature

37°C

98.6°F

Body temperature

Ice

0°C

32°F

Celsius*

Ice

Fahrenheit

• To find degrees Fahrenheit (°F) when you know degrees Celsius (°C), multiply by 9/5 and then add 32. • To find degrees Celsius (°C) when you know degrees Fahrenheit (°F), subtract 32 and then multiply by 5/9. VOLUME 1 liter (L) 1000 mL, 0.26 gal, 1.06 qt, or 2.1 pt. 1 milliliter (mL) 1/1000 L or 0.03 fluid oz. 1 gallon (gal) 128 oz, 8 c, or 3.8 L. 1 quart (qt) 32 oz, 4 c, or 0.95 L. 1 pint (pt) 16 oz, 2 c, or 0.47 L. 1 cup (c) 8 oz, 16 tbs, about 250 mL, or 0.25 L. 1 ounce (oz) 30 mL. 1 tablespoon (tbs) 3 tsp or 15 mL. 1 teaspoon (tsp) 5 mL. WEIGHT 1 kilogram (kg) 1000 g or 2.2 lb. 1 gram (g) 1/1000 kg, 1000 mg, or 0.035 oz. 1 milligram (mg) 1/1000 g or 1000 µg. 1 microgram (µg) 1/1000 mg. 1 pound (lb) 16 oz, 454 g, or 0.45 kg. 1 ounce (oz) about 28 g. ENERGY 1 kilojoule (kJ) 0.24 kcal. 1 millijoule (mJ) 240 kcal. 1 kcalorie (kcal) 4.2 kJ. 1 g carbohydrate 4 kcal 17 kJ. 1 g fat 9 kcal 37 kJ. 1 g protein 4 kcal 17 kJ. 1 g alcohol 7 kcal 29 kJ.

*Also known as centigrade.

X

Nutrition Therapy and Pathophysiology

FOURTH EDITION

Marcia Nahikian Nelms The Ohio State University

Kathryn Sucher

San Jose State University

Kristen Roberts

The Ohio State University

Holly Estes Doetsch The Ohio State University

Sarah Rusnak

The Ohio State University

Georgianna Sergakis The Ohio State University

Melissa Hansen-Petrik

The University of Tennessee–Knoxville

Roschelle A. Heuberger

Source: XiXinXing/Shutterstock.com, Andrey_Popov/Shutterstock.com

Central Michigan University

Australia • Brazil • Mexico • Singapore • United Kingdom • United States

Nutrition Therapy and Pathophysiology, Fourth Edition Marcia Nahikian Nelms, Kathryn P. Sucher Product Director: Thais Alencar Product Manager: Courtney Heilman Product Assistant: Lauren Monz Marketing Manager: Julie Nusser Learning Designer: Miriam Myers Content Manager: Oden Connolly Art Director: Helen Bruno Text Designer: Jeanne Schreiber Cover Designer: Jeanne Schreiber Cover Image: Super food mix slices – iStock.com/lindavostrovska; scale & measuring tape – docent/ ShutterStock.com; red stethoscope – iStock.com/Rinelle; blackberries, cranberries, raspberries, blueberries – iStock.com/Azure-Dragon; prescription pad – iStock.com/studiocasper Production Service: Lumina Datamatics

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Dedication For my husband Jerry, my children: Taylor, Eva, Emory, Marialejandra, my grandchildren: Campbell and Andrea—you are the light of my life. Marcia Nahikian-Nelms

For my supportive and loving husband Peter, and my son Alexander Kathryn Sucher

Brief Table of Contents PART 1

The Role of Nutrition Therapy in Health Care 1 Role of the Registered Dietitian Nutritionist in the Health Care System  2 PART 2

The Nutrition Care Process 2 Overview: The Nutrition Care Process  18 3 Nutrition Assessment: Foundation of the Nutrition Care Process  38

4 Nutrition Intervention, Nutrition ­Monitoring and Evaluation  76

5 Enteral and Parenteral Nutrition Support  92

6 Nutrition Informatics and ­Documentation of the Nutrition Care Process  123

PART 4

Nutrition Therapy 12 Diseases and Disorders of Energy Imbalance  254

13 Diseases of the Cardiovascular System  296 14 Diseases of the Upper ­Gastrointestinal Tract  342

15 Diseases of the Lower ­Gastrointestinal Tract  379

16 Diseases of the Liver, Gallbladder, and Exocrine Pancreas  435

17 Diseases of the Endocrine System  477 18 Diseases of the Renal System  529 19 Diseases of the Hematological System  568 20 Diseases and Disorders of the ­Neurological System  603

21 Diseases of the Respiratory System  641 PART 3

Introduction to Pathophysiology 7 Fluid and Electrolyte Balance  138 8 Acid–Base Balance  159 9 Cellular and Physiological Response to Injury: The Role of the Immune System  171

10 Nutritional Genomics  208 11 Pharmacology  234

iv    Brief Table of Contents

22 Metabolic Stress and the Critically Ill  674 23 Neoplastic Disease  701 24 Diseases of the Musculoskeletal System  727 25 Metabolic Disorders  751 APPENDICES  A-1 GLOSSARY  G-1 INDEX  I-1

Table of Contents PART 1

The Role of Nutrition Therapy in Health Care   1  Role of the Registered Dietitian

Nutritionist in the Health Care System  2

1.1 Introduction 3 1.2 The Registered Dietitian ­Nutritionist in Clinical Practice  3 The Role of the Registered Dietitian Nutritionist  3 Scope of Practice  3 The Clinical Nutrition Team  5

Health Status  19 Nutritional Status  19

2.2  Purpose of Providing Nutrition Care  20 2.3  The AND’s Standardized NCP  21 Standardized Nutrition Language  21 Use of the NCP to Improve Quality of Care  21 Critical Thinking  22

2.4  Big Picture of Nutrition Care: The Model  22 Central Core  22 Two Outer Rings  23 Supportive Systems: Screening and Referral System and Outcomes Management System  23

2.5  Steps of the NCP  25 Step 1: Nutrition Assessment  25

1.3 Other Health Professionals—Interdisciplinary Teams  8

Obtain and Verify Appropriate Data  25

1.4 Health Care Services and Reimbursement for Medical Nutrition Therapy (MNT)  10

Evaluate the Data Using Reliable Standards  26

1.5 Developing Clinical Skills and Professional Performance  11 Specific Knowledge Base  11 Experience 12 Medical Problem Solving  12 Evidence-Based Dietetics Practice (EBP)  12 Problem Solving  12 Decision Making  13 Diagnostic Reasoning  13 Attitudes 13

Standards 13 Levels of Clinical Practice  14

1.6 Conclusion 14 PART 2

The Nutrition Care Process   2  Overview: The Nutrition Care

Process  18

2.1 Improving Health and Nutritional Status through Nutrition Care  19

Cluster and Organize Assessment Data  26

Step 2: Nutrition Diagnosis  27 PES Statements  28 Criteria for Evaluating PES Statements  29 Relationship of Nutrition Diagnosis to the Other Steps of the NCP  29

Step 3: Nutrition Intervention  31 Prioritize the Nutrition Diagnoses  31 Write the Nutrition Prescription  31 Set Goals  31 Select the Nutrition Intervention  31 Implement the Nutrition Intervention  32

Step 4: Nutrition Monitoring and Evaluation  32 Monitor Progress  32 Measure Outcomes  32 Evaluate Outcomes  33

2.6 Documentation 33 2.7 Conclusion 33

  3  Nutrition Assessment: Foundation

of the Nutrition Care Process  38

3.1 Introduction 39 3.2  Nutritional Status  39 Table of Contents   v

3.3 An Overview: Nutrition ­Assessment and Screening  40 Subjective and Objective Data  40 Subjective Data Collection  41 Client History  41 Information Regarding Education, Learning, and Motivation 43

Tools for Data Collection  44

3.4  Food- and Nutrition-Related History  45 Nutrition Care Indicator: Twenty-Four-Hour Recall  45 Nutrition Care Indicator: Food Record/Food Diary  46 Nutrition Care Indicator: Food Frequency  46 Nutrition Care Indicator: Observation of Food lntake/“Calorie Count”  49

3.5 Evaluation and I­nterpretation of Dietary Analysis Information  49 Nutrition Care Criteria: Evaluation and ­Interpretation Using the U.S. Dietary Guidelines  49 Nutrition Care Criteria: Evaluation and Interpretation Using the USDA MyPlate Tools  49 Nutrition Care Criteria: Evaluation and Interpretation Using Choose Your Foods: Food Lists for Diabetes/ Weight Management  49 Nutrition Care Criteria: Evaluation and Interpretation Using Individual Nutrient Analysis  49 Web-based Dietary Analysis  50

Nutrition Care Criteria: Evaluation and ­Interpretation Using Dietary Reference Intakes and Daily Values  50

Nutrition Care Criteria: Interpretation and Evaluation of BIA Measurements  58 Nutrition Care Indicator: Hydrostatic (Underwater) Weighing 58 Nutrition Care Indicator: Dual Energy X-Ray Absorptiometry 59 Nutrition Care Indicator: Ultrasound  59 Nutrition Care Indicator: Air Displacement Plethysmography 59

3.7 Biochemical Assessment and Medical Tests and Procedures  60 Protein Assessment  60 Somatic Protein Assessment  60 Visceral Protein Assessment  61

Immunocompetence Assessment  63 Nutrition Care Indicator: Total Lymphocyte Count (TLC)  63

Nutrition Care Indicators for Hematological Assessment  63 Hemoglobin (Hgb)  63 Hematocrit (Hct)  63 Mean Corpuscular Volume (MCV)  64 Mean Corpuscular Hemoglobin (MCH)  64 Mean Corpuscular Hemoglobin Concentration (MCHC)  64 Ferritin 64 Transferrin Saturation  64 Protoporphyrin 64 Serum Folate  64 Serum B12 64

3.6 Anthropometric/Body ­Composition Measurements  51

Vitamin and Mineral Assessment  64 Other Labs with Clinical Significance  64

Anthropometrics 51

3.8 Nutrition Care Criteria: Nutrition-Focused Physical Findings  65

Nutrition Care Indicator: Height/Stature/Length  51 Nutrition Care Indicator: Weight  53

Nutrition Care Criteria: Evaluation and ­Interpretation of Height and Weight in Infants and Children  53 Growth Charts  53 Body Mass Index  53

Nutrition Care Criteria: Evaluation and Interpretation of Height and Weight in Adults  53 Usual Body Weight  53 Percent Usual Body Weight and Percent Weight Change 55 Reference Weights  55 Body Mass Index  55 Waist Circumference  55

Body Composition  55 Nutrition Care Indicator: Skinfold Measurements  56 Nutrition Care Criteria: Interpretation and Evaluation of Skinfold Measurements  57 Nutrition Care Indicator: Bioelectrical Impedance Analysis (BIA)  58 vi    Table of Contents

3.9 Nutrition Care Criteria: ­Functional Assessment  65 3.10 Nutrition Care Criteria: Energy and Protein Requirements  67 Measurement of Energy Requirements  67 Estimation of Energy Requirements  68 Energy Requirements Based on DRI  69 Activity Factor  69 Stress Factors  70

Measurement of Protein Requirements  70 Estimation of Protein Requirements  70 RDA for Protein  70 Protein Requirements in Metabolic Stress, Trauma, and Disease 70

3.11 Interpretation of Assessment Data: Nutrition Diagnosis  71 3.12 Conclusion 71

  4  Nutrition Intervention, Nutrition

­Monitoring and Evaluation  76

4.1 Introduction 77

Aspiration 107 Dehydration 107 Electrolyte Imbalances  107 Underfeeding or Overfeeding  107

4.2  Nutrition Prescriptions  78

Hyperglycemia 108

4.3  Food and/or Nutrient D ­ elivery (Oral Diets)  79

Refeeding Syndrome  108

Modification of Meals and Snacks  79 Supplements 81 Medical Food Supplements  81

5.3  Parenteral Nutrition  108 Indications 110 Venous Access Devices  110

Modified Beverages and Foods  82

Short-Term VADs  111

Vitamin and Mineral Supplements  82

Long-Term VAD  111

Bioactive Substance Management  83

Feeding Assistance and Feeding Environment  83 Nutrition-Related Medication Management  83

4.4  Nutrition Education  84 4.5  Nutrition Counseling  85 Counseling Skills  85 Theoretical Basis/Approach for Nutrition Counseling  87 Counseling Strategies  87

4.6  Coordination of Nutrition Care  89 4.7  Nutrition Monitoring and Evaluation  89 4.8 Conclusion 90

  5  Enteral and Parenteral

Nutrition Support  92

5.1 Introduction: Planning and Implementation of Nutrition Interventions with Enteral and Parenteral Nutrition Support  93 5.2  Enteral Nutrition  94 Indications 94 GI Access  95 Formulas 98 Protein 99 Carbohydrate 99

Solutions 112 PN Substrates  112 Protein 112 Carbohydrate 113 Lipid 113 Electrolytes 113 Vitamins and Minerals  114 Medications 114

Nutrition Assessment and Intervention: ­Determination of the PN Prescription  115 Administration 115 Monitoring and Evaluation: Complications  115

5.4  Special Considerations  118 Transitional Feedings  118 Home PN  118

5.5  Initiation of Home PN  118 Monitoring Home PN  118 PN Product Shortages  119 Clinical Ethics  119

5.6 Conclusion 119

  6  Nutrition Informatics and

­ ocumentation of the Nutrition D Care Process  123

Lipid 100

6.1 Introduction 124

Vitamins/Minerals 100

Brief History of Nutrition Informatics  124 ANDHII 124 Electronic Clinical Quality Measure—Electronic Clinical Quality Measure  125 Standardized Terminology  125

Fluid and Nutrient Density  101 Regulation of Enteral Formula Manufacture  102 Cost 102

Feeding Initiation and Advancement  102 Feeding Delivery Methods  102 Equipment 102 Nutrition Assessment and Intervention: ­Determination of the EN Prescription  103 Monitoring and Evaluation: Complications  104 Tube-Related Complications  105 GI Complications  105

6.2  Charting: Documentation of the NCP  126 Standardized Language and Medical Abbreviations  127 Problem-Oriented Medical Records  127 Organization of Nutrition Documentation  128 SOAP 128 Problem, Etiology, Signs/Symptoms Statements (PES) 129 Table of Contents   vii

Assessment, Diagnosis, Intervention, and M ­ onitoring and Evaluation (ADIME)  129 IER Notes  129 FOCUS Notes  129 PIE Notes  129 Charting by Exception (CBE)  130

Keeping a Personal Medical Notebook  130 Guidelines for All Charting  131 Confidentiality 132

6.3 Beyond Charting: An Overview of Writing in the Profession  132 The Functions, Contexts, Parts, and Processes of Writing  132 Rhetorical Norms  132 Levels of Discourse  132 Steps in the Writing Process  133

Reporting Your Own Research  133

6.4 Conclusion: Your Ethos—Establishing Expertise  133 PART 3

Introduction to Pathophysiology   7  Fluid and Electrolyte Balance  138 7.1 Introduction 139 7.2 Normal Anatomy and Physiology of Fluids and Electrolytes  139 Total Body Water  139 Fluid Compartments  140 Movement of Fluid between Blood and Interstitial Spaces 140 Movement between Extracellular Fluid and Intracellular Fluid 140

Total Body Water Balance  141 Fluid Intake  141 Fluid Output  142 Fluid Requirements  142

7.3  Body Solutes  143 Types of Solutes  143 Distribution of Electrolytes  143 Movement of Solutes  143 Electrolyte Requirements  143

7.4 Physiological Regulation of Fluid and Electrolytes  144 Thirst Mechanism  144 Renal Function  144 Hormonal Influence: Renin–Angiotensin–­Aldosterone System and Arginine Vasopressin  144 viii    Table of Contents

Electrolyte Regulation  144 Sodium 144 Potassium 144 Calcium and Phosphorus  145

7.5  Disorders of Fluid Balance  145 Alterations in Volume  146 Hypovolemia 146 Hypervolemia 147

Alterations in Osmolality  147 Sodium Imbalances  148 Hyponatremia 148 Hypernatremia 150

Potassium Imbalances  151 Hypokalemia 151 Hyperkalemia 152

Chloride and Acetate  153 Calcium Imbalances  153 Hypocalcemia 153 Hypercalcemia 154

Phosphorus Imbalances  154 Hypophosphatemia 154 Hyperphosphatemia 154

Magnesium Imbalances  154 Hypomagnesemia 155 Hypermagnesemia 155

7.6 Conclusion 155

  8  Acid–Base Balance  159 8.1 Introduction 160 8.2  Basic Concepts: Acids, Bases, and Buffers  160 Acids 160 Bases 160 Buffers 160 pH 161 Terms Describing pH  161

8.3  Regulation of Acid–Base Balance  161 Chemical Buffering  161 The Bicarbonate–Carbonic Acid Buffer System  161 Other Chemical Buffer Systems  161

Respiratory Regulatory Control  162 Renal Regulatory Control  163 Control of Hydrogen and Bicarbonate lons  163 Other Renal Regulatory Controls  164

Effect of Acid and Base Shifts on Electrolyte Balance  164 Assessment of Acid–Base Balance  165 Acid–Base Disorders  165 Respiratory Acidosis  165

Etiology 166

Communication between Immune Cells  183

Pathophysiology 166

Complement 183

Clinical Manifestations  166

Cytokines 183

Treatment 166

Respiratory Alkalosis  166 Etiology 166 Pathophysiology 166 Clinical Manifestations  167 Treatment 167

Metabolic Acidosis  167 Etiology 167 Pathophysiology 168 Clinical Manifestations  168 Treatment 168

Metabolic Alkalosis  168

9.6  The Immune Response  184 Innate and Adaptive Immunity  184 Innate Immune Response  184 Inflammation and Healing  184 Nutrition and Wound Healing  188 Adaptive Immune Response  191

9.7 Autoimmunity 194 9.8 Attacking Altered and Foreign Cells: Tumors and Transplants  196 Tumor Immunology  196 Transplantation Immunology  196

Etiology 168

Transplant Rejection  196

Pathophysiology 168

Matching 196

Clinical Manifestations  169

Immunosuppression 197

Treatment 169

Transplantation of Specific Organs and Tissues  197

Mixed Acid–Base Disorders  169 Assessment of Acid–Base Disorders  169

8.4 Conclusion 169

  9  Cellular and Physiological Response

to Injury: The Role of the Immune System  171

9.9 Immunization 197 Passive Immunity  197 Active Immunization  198 Types of Vaccines  198

9.10 Immunodeficiency 198

9.1 Introduction 174

Malnutrition and Immunodeficiency  198 Inherited Immunodeficiencies  199 Acquired Immunodeficiencies  199

9.2  The Disease Process  174

9.11  Hypersensitivity (Allergy)  199

9.3  Cellular Injury  175

Overview of Hypersensitivity  199

Mechanisms of Cellular Injury  175 Cellular Response to Injury  176 Cellular Accumulations  176 Cellular Alterations in Size and Number  176 Cellular Injury from Infection  177 Types of Microorganisms  178 Course of Infection  178 Cellular Death  178

Definition Hypersensitivity  199 Epidemiology 199 Etiology: Classifications of Allergic Reactions  199 Pathophysiology 200 Medical Diagnosis and Treatment  200 Additional Medical Interventions  200 Delayed Hypersensitivity  200

Adverse Reactions to Food  200

Host Resistance to Infectious Cellular Injury  178

Definition 200

9.4  Preventing Transmission of Infection  179

Etiology 201

9.5  Foundations of the Immune System  180 Organs of the Immune System  180 Cells of the Immune System  181

Epidemiology 201 Pathophysiology 201 Medical Diagnosis  202

Nutrition Therapy for Food Allergy  203

Monocytes and Macrophages  181

Nutrition Implications  203

Leukocytes 182

Nutrition Assessment  203

Other Cells Derived from the Myeloid Stem Cell  182

Nutrition Diagnosis  203

Lymphocytes 182

Nutrition Intervention  203

Major Histocompatibility Complex/Human ­Leukocyte Antigens  182

9.12 Conclusion 206 Table of Contents   ix

 10  Nutritional Genomics  208 10.1 Introduction 210 10.2 Nutritional Genomics: Nutrigenetics, Nutrigenomics, and Nutritional Epigenomics  211 10.3 An Overview of the Structure and Function of Genetic Material  213 Deoxyribonucleic Acid and Genome Structure  213 Translating the Message from DNA to Protein  215 Transcription and Translation  216

Distribution of Drugs  240 Metabolism of Drugs  240 Excretion of Drugs  240 Alterations in Drug Pharmacokinetics  241 Altered GI Absorption  241 Altered Distribution  241 Altered Metabolism  241 Altered Urinary Excretion  242

How Foods and Drugs Interact  242 Effect of Nutrition on Drug Action  242 Effect of Nutrition on Drug Dissolution  242

Genetic Variation  216

Effect of Nutrition on Drug Absorption  242

Inheritance 216

Effect of Nutrition on Drug Metabolism  242

Single-Nucleotide Polymorphisms  218 Other Polymorphisms  218

Epigenetic Regulation  219 DNA Methylation  219 Histone Modification  219 The Epigenotype  220 Developmental Origins of Adult Disease  220

10.4  Genomics and Technology  221 10.5  Nutritional Genomics in Disease  222 Cancer 222 From Single-Gene Inherited Cancers to Gene–Nutrient Interactions 222

Variations in Xenobiotic Metabolism Influence Risk  222 MTHFR and ADH Polymorphisms Interact with Dietary Folate and Alcohol  223 Fruits and Vegetables  224

Obesity 224 Diabetes 226 Cardiovascular Disease  227

10.6 Nutritional Genomics and the Practice of Nutrition and Dietetics  228 Individual Genomic Testing in Practice  228 Evolving Knowledge and Practice Requirements for Dietitians  229

10.7 Conclusion 229

 11  Pharmacology  234 11.1  Introduction to Pharmacology  235 11.2 Role of Nutrition Therapy in Pharmacotherapy  237 11.3  Drug Mechanisms  238 11.4  Administration of Drugs  239 11.5 Pharmacokinetics 239 Absorption of Drugs  239 x    Table of Contents

Effect of Nutrition on Drug Excretion  243

Nutritional Complications Secondary to Pharmacotherapy  244 Drug Consequence: Effect on Nutrient Ingestion  244

Drug Consequence: Effect on Nutrient Absorption  244 Drug Consequence: Effect on Nutrient Metabolism  246 Drug Consequence: Effect on Nutrient Excretion  246 At-Risk Populations  246 Drug–Nutrient Interactions in the Older Adult  246 Drug–Nutrient Interactions in Nutrition Support  247

11.6  Nutrition Therapy  249 Nutritional Implications  249 Nutrition Assessment  249

11.7 Conclusion 251 PART 4

Nutrition Therapy  12  Diseases and Disorders of Energy

Imbalance  254

12.1 Introduction 255 12.2  Energy Balance  256 Energy Intake  256 Energy Expenditure  256 Resting Energy Expenditure  256 Thermic Effect of Food  256 PA Energy Expenditure  257

Estimating and Measuring Energy Requirements  257 Equations 257 Indirect Calorimetry  258

Regulation of Energy Balance and Body Weight  258 Neurochemicals That Regulate Appetite and Food Intake  259 Metabolic Activity of the Adipocyte and ­Adipose Tissue  259

12.3  Overweight and Obesity  260 Assessment and Identification of Overweight and Obesity  260 Body Composition  260 Body Mass Index  260 Body Fat Distribution  261 Waist Circumference  263

Waist-to-Hip Ratio and Waist-to-Height Ratio  263 Epidemiology 263 Socioeconomic Status: Race, Gender, and Education  263

Adverse Health Consequences of Overweight and Obesity  263 Psychosocial and Emotional Consequences  263

Physiological Consequences  263 Type 2 Diabetes  263 Hypertension 264 Dyslipidemia 264 Hepatobiliary Disorders  264 Cancers 264 Reproductive Disorders  264

Etiology of Obesity  264 Additional Etiology  264

Genetic Effects on Body Weight  264 Obesogenic Factors  266 Physical, Social, Cultural, and Economic Environment 267 Dietary Patterns, Food Choices, and Eating Behaviors 267 Changes in PA  268 Sleep Patterns  270

Treatment of Overweight and Obesity  270 Evidence-Based Guidelines  270 Pharmacologic Treatment  270 Bariatric/Metabolic Surgical Interventions  272

Patient Selection  272 Preoperative care  274

Postoperative care  274 Nutrition Therapy for Overweight and Obesity  274 Nutrition Assessment  274 Client History  274 Anthropometric Measurements  274 Biochemical Indices and Laboratory Measurements  275 Food-/Nutrition-Related History  276

Nutrition Diagnosis  278 Nutrition Prescription  278

12.4  Nutrition Intervention  278 Weight-Loss Goals  278 Dietary Interventions  279 Physical Activity  281 Nutrition Counseling Strategies for Behavior Change  282

Underweight 283 Possible Nutrition Diagnoses  284

Underweight in Infants and Children  284 Nutrition Intervention  284 Monitoring/Evaluation 284

12.5  Eating Disorders  284 Diagnosis and Behavioral Manifestations  284 Anorexia Nervosa  285 Bulimia Nervosa  285 Binge Eating Disorder  285 Common Features  286

Epidemiology of Eating Disorders  287 Etiology of Eating Disorders  287 Complications of Eating Disorders  288 Health Complications of AN  288 Health Complications of BN  289 Health Complications of BEDs  289

Treatment of Eating Disorders  289 Medical Treatment  290 Behavioral/Psychotherapy Treatment  290 Nutrition Therapy  290

12.6 Conclusion 291

 13  Diseases of the Cardiovascular

System  296

13.1 Introduction 297 13.2  Anatomy and Physiology of the Cardiovascular System  298 The Heart  298 Electrical Activity of the Heart  298 Cardiac Cycle  298

Cardiac Function  299 Regulation of Blood Pressure  299

13.3 Hypertension 300 Epidemiology 301 Pathophysiology 301 Treatment 302

13.4  Nutrition Therapy for Hypertension  305 Nutrition Assessment  305 Nutrition Diagnosis  305 Nutrition Intervention  305 DASH—Dietary Approaches to Stop Hypertension  307 Weight Loss  307 Sodium 307 Alcohol 309 Potassium, Calcium, and Magnesium  309 Physical Activity  311 Smoking Cessation  312 Table of Contents   xi

13.5 Atherosclerosis 312 Definition 312 Epidemiology 312 Pathophysiology 313 Risk Factors  313 Family History  314 Age and Sex  314 Obesity 314 Dyslipidemia 314 Hypertension 315 Physical Inactivity  315 Diabetes Mellitus  315 Impaired Fasting Glucose and Metabolic Syndrome  315 Cigarette Smoke  315

Clinical Manifestations and Diagnosis  316 Medical Treatment  316

13.6  Nutrition Therapy for Atherosclerosis  316 Nutrition Assessment  316 Nutrition Diagnosis  318 Nutrition Intervention  319 Physical Activity  320 Saturated Fat  320

Clinical Manifestations, Medical Diagnosis, and Treatment  326

13.10  Heart Failure  326 Definition 326 Epidemiology 326 Etiology 326 Pathophysiology 326 Clinical Manifestations  328 Treatment 328

13.11  Nutrition Therapy for Heart Failure  328 Nutrition Assessment and Diagnosis  330 Nutrition Intervention  330 Sodium 330 Energy and Protein  330 Fluid 330 Drug–Nutrient Interactions  331

Nutrition Support Recommendations in Heart Failure  332

13.12 Medical Procedures for Heart Failure  332 CRT, Ventricular Restoration, and VAD  333 Heart Transplant  333

Trans Fatty Acids  320

Selection Criteria and the Donor List  333

Monounsaturated Fat  320

Transplant Surgery  333

Ω-3 (Omega-3) Fatty Acids: Linolenic Acid ­320 Other Polyunsaturated Fatty Acids  321 Cholesterol 322 Fiber 322 Nuts 322 Plant/Sterols (Phytosterols)  322 Nutrition Education and/or Nutrition Counseling  322

Monitoring and Evaluation  322

13.13  Nutrition Therapy for Heart Transplant  333 Nutrition Assessment  333 Nutrition Diagnosis  333 Nutrition Intervention, Monitoring, and Evaluation  335 Nutrition Support Route  335 Energy 335 Carbohydrate 335

13.7  Ischemic Heart Disease and Myocardial Infarction  323

Lipid 335

Definition 323 Epidemiology 323 Pathophysiology 323 Clinical Manifestations  324 Medical Diagnosis  324 Treatment 325

Fluid 335

13.14  Atrial Fibrillation  335

13.8  Nutrition Therapy for ­Myocardial Infarction  325

13.15 Conclusion 335

Nutrition Intervention  325

13.9  Peripheral Arterial Disease  326 Definition 326 Epidemiology 326 Etiology 326 Pathophysiology 326 xii    Table of Contents

Protein 335 Micronutrients 335

Epidemiology 335 Treatment 335 Nutritional Implications and Nutrition Intervention  335

 14  Diseases of the Upper

­Gastrointestinal Tract  342

14.1 Introduction 344 Normal Anatomy and Physiology of the Upper Gastrointestinal Tract  344 Motility, Secretion, Digestion, and Absorption  344

Anatomy and Physiology of the Oral Cavity  345 Oral Cavity Motility  345 Oral Cavity Secretions  345 Physical Assessment of the Oral Cavity: An Important Component of Nutrition Assessment  345

Normal Anatomy and Physiology of the Esophagus  345 Normal Anatomy and Physiology of the Stomach  347

Clinical Manifestations  362 Treatment 362

Dysphagia 362 Definition 362 Clinical Manifestations  362 Diagnosis 362

Nutrition Therapy for Dysphagia  363

Gastric Motility  348

Nutritional Implications and Assessment  363

Gastric Secretions  348

Nutrition Diagnosis  363

Control of Gastric Secretions  348

Nutrition Intervention  363

Release of Gastric Secretions  349

Monitoring and Evaluation  364

Gastric Digestion  349 Gastric Absorption  349

Introduction to Pathophysiology of the Upper Gastrointestinal Tract  349 Pathophysiology of the Oral Cavity  349 Dental Caries  350 Individuals at Risk for Dental Disease  351 Prevention of Dental Disease  351

Inflammatory Conditions of the Oral Cavity  351 Conditions Resulting in Altered Salivary Gland Function  352 Surgical Procedures for the Oral Cavity  353 Nutrition Assessment and Diagnosis  353 Nutrition Intervention  354

Impaired Taste: Dysgeusia/Ageusia  355 Nutrition Therapy for Pathophysiology of the Oral Cavity  355 Nutritional Implications  355 Nutrition Diagnosis  355 Nutrition Intervention  355 Monitoring and Evaluation  356

Pathophysiology of the Esophagus  356 Gastroesophageal Reflux Disease  356

Hiatal Hernia  365 Definition 365 Clinical Manifestations  365

Achalasia 365 Definition 365 Etiology 365 Pathophysiology 365

Clinical Manifestations  365 Treatment 365

Nutrition Therapy for Achalasia  365 Esophageal Surgery  366 Definition 366 Nutrition Therapy after Esophagectomy  366 Pathophysiology of the Stomach  366 Indigestion 366 Nausea and Vomiting  366 Nutrition Therapy for Nausea and Vomiting  367 Nutritional Implications  367 Nutrition Diagnosis  367

Nutrition Intervention  367

Gastritis 367 Definition 367

Definition 356

Etiology 367

Epidemiology 356

Pathophysiology 367

Pathophysiology 356

Peptic Ulcer Disease  367

Clinical Manifestations  356

Definition 367

Medical Diagnosis  356

Epidemiology 367

Treatment 356

Etiology 368

Nutrition Therapy for GERD  359 Nutrition Diagnosis  359 Nutrition Assessment  360 Nutrition Intervention  360 Monitoring and Evaluation  360

Barrett’s Esophagus—A Complication of GERD  360 Eosinophilic Esophagitis  360 Definition 360 Epidemiology 360 Etiology 362

Clinical Manifestations  368 Diagnosis 368 Treatment 368

Nutrition Therapy for Peptic Ulcer Disease  368 Nutritional Implications and Assessment  368 Nutrition Diagnosis  369

Nutrition Intervention  369

Monitoring and Evaluation  370

Gastric Surgery  370 Vagotomy 370

Diagnosis 362 Table of Contents   xiii

Gastroduodenostomy (Billroth I), Gastrojejunostomy (Billroth II), and Roux-en-Y Procedure  370

Nutrition Therapy for Gastric Surgery  370

Nutrition Diagnosis  395 Nutrition Interventions  395

Constipation 396

Nutritional Implications  370

Definition 396

Nutrition Diagnosis  371

Epidemiology 398

Dumping Syndrome  371

Etiology 399

Nutrition Intervention  371

Clinical Manifestations  399

Monitoring and Evaluation  372

Medical Diagnosis  399

Bariatric Surgery  372

Treatment 399

Gastroparesis 374

Nutrition Therapy for Constipation  399

Definition 374

Nutrition Assessment  399

Etiology 374

Nutrition Diagnosis  399

Diagnosis 374

Nutrition Interventions  399

Clinical Manifestations  374 Treatment 374

Nutrition Therapy for Gastroparesis  374

Malabsorption 399 Definition 399 Etiology 401

Nutritional Implications  374

Pathophysiology 401

Nutrition Diagnosis  374

Fat Malabsorption  401

Nutrition Intervention  374

Stress Ulcers  376 Zollinger–Ellison Syndrome  376

14.2 Conclusion 376

 15  Diseases of the Lower

­Gastrointestinal Tract  379

15.1 Introduction 381 15.2  Normal Anatomy and Physiology of the Lower Gastrointestinal Tract  381 Small Intestine Anatomy  381

Carbohydrate Malabsorption  402 Protein Malabsorption  402 Treatment 402

Nutrition Therapy for Malabsorption  402 Nutrition Assessment  402 Nutrition Diagnosis  402 Nutrition Intervention  402 Nutrition Therapy for Fat Malabsorption  402 Nutrition Therapy for Lactose Malabsorption  403

Celiac Disease  404 Definition 404 Epidemiology 405

15.3  Small Intestine Motility  382

Etiology 405

Small Intestine Secretions  382 Small Intestine Digestion  382 Small Intestine Absorption  386 Large Intestine Anatomy  386 Large Intestine Motility  386 Large Intestine Secretions  386 Large Intestine Digestion and Absorption  386 Nutrition Assessment for Lower Gastrointestinal Tract Conditions  389 Pathophysiology of the Lower Gastrointestinal Tract  389 Diarrhea 389

Pathophysiology 405 Clinical Manifestations  405 Medical Diagnosis  405 Prognosis and Treatment  405

Nutrition Therapy for Celiac Disease  406 Nutrition Assessment  406 Nutrition Diagnosis  406 Nutrition Intervention  406

Irritable Bowel Syndrome  406 Definition 406 Epidemiology 414

Definition 389

Etiology 414

Epidemiology 389

Pathophysiology 414

Etiology 390

Clinical Manifestations  415

Clinical Manifestations  391 Medical Diagnosis  391 Treatment 393

Nutrition Therapy for Diarrhea  395 Nutrition Assessment  395 xiv    Table of Contents

Medical Treatment  415

Nutrition Therapy for Irritable Bowel Syndrome  415 Nutrition Assessment  415 Nutrition Diagnosis  415 Nutrition Intervention  416

Inflammatory Bowel Disease  418 Definition 418 Epidemiology 418 Etiology 418 Pathophysiology 418 Clinical Manifestations  418 Treatment 419

Nutrition Therapy for Inflammatory Bowel Disease  420

 16  Diseases of the Liver, Gallbladder,

and Exocrine Pancreas  435

16.1 Introduction 436 16.2 Anatomy and Physiology of the Hepatobiliary System  436 Anatomy of the Liver  436 Functions of the Liver  438

Nutrition Assessment  421

Bile Synthesis Secretion  438

Nutrition Diagnosis  421

Enterohepatic Circulation of Bile  440

Nutrition Intervention  421 Nutrition Therapy during Exacerbation of Disease  421 Nutrition Therapy for Rehabilitation during Periods of Remission 423

Diverticulosis/Diverticulitis 423 Definition 423 Epidemiology 423 Etiology 423 Pathophysiology 423 Clinical Manifestations  424 Treatment 424

Nutrition Therapy for Diverticulosis/Diverticulitis  424 Nutrition Assessment  424 Nutrition Diagnosis  424 Nutrition Intervention  424

Common Surgical Interventions for the Lower Gl Tract  424 Jejunostomy, Ileostomy, and Colostomy  425

Nutrition Therapy for Jejunostomy, Ileostomy, and Colostomy  425 Nutrition Intervention  425

Short Bowel Syndrome  426 Definition 426 Epidemiology 427 Etiology  427 Pathophysiology 427 Treatment 427

Nutrition Therapy for Short Bowel Syndrome  428 Nutrition Assessment  428 Nutrition Diagnosis  428 Nutrition Intervention  428

Small Intestinal Bacterial Overgrowth (SIBO)  429 Definition 429 Pathophysiology 429 Clinical Manifestations  429 Treatment 429

Nutrition Therapy for SIBO  429 Intestinal Transplantation  429 Nutrition Therapy for Intestinal Transplantation  429

15.4 Conclusion 429

Anatomy and Physiology of the Gallbladder  440 Anatomy and Physiology of the Pancreas  440 Diagnostic Procedures  441

16.3 Pathophysiology Common to the Hepatobiliary Tract  443 Jaundice 443 Portal Hypertension/Ascites  443 Encephalopathy 445

16.4  Pathophysiology of the Liver  447 Hepatitis 447 Hepatitis A Virus  447 Serum Hepatitis or Hepatitis B Virus  447 Hepatitis C Virus  447 Hepatitis D and E Virus  448

Nutrition Therapy for Viral Hepatitis  448 Nutritional Implications  448 Nutrition Assessment  448 Nutrition Diagnosis  450 Nutrition Intervention  450 Monitoring and Evaluation  451

Alcoholic Liver Disease  451

16.5  Nutritional Implications of ALD  452 Nutrition Assessment  452 Nutrition Diagnosis  453 Nutrition Intervention  453 Monitoring and Evaluation  456 Fatty Liver  456 Nutrition Implications for NAFLD  457 Nutrition Therapy for NAFLD  457

Cirrhosis 459 Clinical Manifestations  459 Treatment 460

Nutrition Therapy for Cirrhosis  460 Nutritional Implications  460 Nutrition Assessment  460 Nutrition Diagnosis  461

Nutrition Intervention  461 Energy 461

Table of Contents   xv

Vitamins and Minerals  461 Other Considerations  461 Monitoring and Evaluation  461

Liver Transplant  461 Nutrition Therapy for Liver Transplant  461 Nutritional Implications  461 Nutrition Assessment  461 Nutrition Diagnosis  461

 17  Diseases of the Endocrine

System  477

17.1 Introduction 479 17.2 Normal Anatomy and ­Physiology of the Endocrine System  481 Classification of Hormones  481 Endocrine Function  482

Nutrition Intervention  462

Pituitary Gland  482

Monitoring and Evaluation  462

Thyroid Gland  482

Pathophysiology of the Biliary System  462 Cholelithiasis (Gallstones)  462 Biliary Obstruction  463

Adrenal Glands  482 Endocrine Pancreas  484

Endocrine Control of Energy Metabolism  484

Cholecystitis 463

Insulin 485

Cholangitis 463

Glucagon 487

Nutrition Therapy for Cholelithiasis  463 Nutritional Implications  463 Nutrition Assessment  464 Nutrition Diagnosis  464 Nutrition Intervention  464 Monitoring and Evaluation  464

16.6 Pathophysiology of the ­Exocrine Pancreas  464 Acute Pancreatitis  464 Etiology 464

Pathophysiology 465 Medical Diagnosis  465 Signs/Symptoms 465 Medical Treatment  465 Nutrition Implications  465 Assessment 465 Diagnosis 465

Intervention 465 Monitoring and Evaluation  467 Chronic Pancreatitis  467 Etiology 467 Pathophysiology 467 Medical Treatment  468 Nutrition Implications  469 Nutrition Assessment  469 Nutrition Diagnosis  469

Nutrition Intervention  469 Monitoring and Evaluation  469

Pancreatic Surgery  469 Nutrition Implications  470 Nutrition Intervention  470 Monitoring and Evaluation  472

16.7 Conclusion 472

17.3 Pathophysiology of the Endocrine System  487 17.4 Diabetes 488 Type 1 Diabetes  489 Epidemiology 489 Etiology 489 Pathophysiology and Clinical Manifestations  491

Type 2 Diabetes  491 Epidemiology 491 Etiology 492 Pathophysiology 492 Metabolic Syndrome  492 Clinical Manifestations  492 Prediabetes (Increased Risk for Diabetes)  493 Diagnosis of Diabetes  494 A1C (Glycosylated Hemoglobin)  494 Oral Glucose Tolerance Test  494 Islet Cell Autoantibodies  496 Glutamic Acid Decarboxylase Autoantibodies  496 Islet Cell Autoantibodies  496 Insulin Autoantibodies  496 C-Peptide 496

Medical Treatment of Diabetes  496 Insulin 499 Types of Insulin  499 Determining Insulin Doses  500 Insulin Regimens  500 Syringes and Pens  502 Insulin Pumps  502 Medications for T2DM  503

Bariatric Surgery  504 Pancreas and Islet Cell Transplantation  504 Nutrition Therapy for Diabetes  504 Nutritional Implications  504

xvi    Table of Contents

Nutrition Assessment  505

17.5  Reactive Hypoglycemia  519

Nutrition Diagnosis  505

Definition 519 Etiology 519 Pathophysiology 520

Nutrition Intervention  506 Goals of Nutrition Therapy  506 Nutrition Prescriptions  506

Fasting Hypoglycemia  520

Meal Patterns and Planning  507

Postprandial (Reactive) Hypoglycemia  520

Carbohydrate Counting  509 Food Lists  510 Monitoring and Evaluation  511

Clinical Manifestations  520 Medical Treatment  520 Nutrition Therapy for Reactive Hypoglycemia  520

Glycated Hemoglobin Assays (A1C)  512

Nutritional Implications  520

Self-Monitoring of Blood Glucose  512

Nutrition Diagnosis  520

Continuous Glucose Monitoring Devices  512

Nutrition Intervention  520

Testing for Ketones  512 Other Testing  513

Physical Activity  513 Nutritional Implications  513 Nutrition Assessment  513 Nutrition Intervention  513

Acute Complications  513 Side Effects and Complications of Insulin Therapy  513 Dawn Phenomenon  514 Diabetic Ketoacidosis  514 Pathophysiology  514 Medical Treatment  514 Hyperglycemic Hyperosmolar Syndrome  514 Short-Term Illness  514 Nutrition Assessment  514 Nutrition Diagnosis  516 Nutrition Intervention  516

Long-Term Complications of Hyperglycemia  516 Macrovascular Complications: Cardiovascular Disease  516 Nephropathy  516 Retinopathy 517 Nervous System Diseases  517 Nutrition Therapy for Long-Term Complications of Hyperglycemia 517

Gestational Diabetes Mellitus  517 Definition 517 Epidemiology 517 Etiology 517 Pathophysiology 517

17.6  Other Endocrine Disorders  520 Hypothyroidism 520 Definition 520 Epidemiology 520 Etiology 520 Pathophysiology 521 Clinical Manifestations  521 Medical Treatment  522

Nutrition Therapy for Hypothyroidism  522 Hyperthyroidism 522 Definition 522 Epidemiology and Etiology  522 Pathophysiology 522 Clinical Manifestations  522 Medical Treatment  523

Nutrition Therapy for Hyperthyroidism  523 Pituitary Disorders  523 Pituitary Tumors  523 Hyperpituitarism 523 Acromegaly 523 Cushing’s Syndrome  523 Hypopituitarism 524 Diabetes Insipidus  524

Adrenal Cortex Disorders  525 Excess Secretion of Glucocorticoids  525 Insufficient Secretion of Adrenal Cortex ­Steroids  525

17.7 Conclusion 525

Clinical Manifestations  518

 18  Diseases of the Renal System  529

Diagnosis 518

18.1 Introduction 531

Medical Treatment  518 Monitoring 518

Nutrition Therapy for GDM  519 Nutritional Implications  519 Nutrition Diagnosis  519 Nutrition Intervention  519

18.2  The Kidneys  531 Anatomy 531 Physiological Functions  532 Laboratory Evaluation of Kidney Function  533 Pathophysiology 534

Monitoring and Evaluation  519 Table of Contents   xvii

18.3  Chronic Kidney Disease  535 Definition and Medical Diagnosis  535 Epidemiology 535 Etiology 535 Treatment 536 Dialysis 536 Hemodialysis 537 Peritoneal Dialysis  539 Renal Transplantation  539

18.4 Nutrition Therapy for Chronic Kidney Disease  540 Nutrition Assessment  540 Nutrition Diagnosis  541 Nutrition Intervention  541 CKD Stages 1–4 (Predialysis)  541 CKD Stage 5  546 Protein 548 Energy 548 Adjusted Edema-Free Body Weight (aBWef) for Obese and Underweight Patients  548 Fat 549 Potassium 549 Fluid and Sodium  551 Phosphorus 552 Calcium 552 Vitamin Supplementation  555 Mineral Supplementation  555

Nutrition Therapy for Comorbid Conditions and Complications  555 Cardiovascular Disease  555 Secondary Hyperparathyroidism  556 Anemia 556

Medicare Coverage for ­Medical Nutrition Therapy  557 Nutrition Therapy for Kidney Transplant  557 Protein and Energy Needs  557 Carbohydrate 557 Fat 558 Sodium 558 Potassium 558 Immunosuppressants 558 Cardiovascular Disease  558 Hypomagnesemia 559 Obesity 560 Chronic kidney disease bone mineral disorder (CKD-BMD) 560 Rejection 560

Monitoring and Evaluation  560

18.5  Acute Kidney Injury  560 Definition 560 Epidemiology 560 xviii    Table of Contents

Etiology 560 Clinical Manifestations  561 Electrolytes 561 Blood Urea Nitrogen and Creatinine  561

Treatment 561

18.6 Nutrition Therapy for Acute Kidney Injury  561 Nutrition Intervention  561

18.7 Nephrolithiasis 562 Definition 562 Epidemiology 562 Pathophysiology 562 Diagnosis and Treatment  562

18.8  Nutrition Therapy for Nephrolithiasis  562 Nutrition Assessment  562 Nutrition Diagnosis  562 Nutrition Intervention  562

18.9 Conclusion 564

 19  Diseases of the Hematological

System  568

19.1  Overview of the Hematological System  570 Blood Composition  570

19.2 Anatomy and Physiology of the Hematological System  571 The Cells of the Hematological System  571 The Development of the Hematological Cells  571 Hemoglobin 572

19.3 Homeostatic Control of the Hematological System  574 Blood Clotting  574 Factors Affecting Hemostasis  574 Summary 575

19.4  Nutritional Anemias  575 Microcytic Anemias: Iron-Deficiency and ­Functional Anemia  576 Definition 576 Epidemiology 576 Etiology 577 Blood Loss  577 Inadequate Intake and/or Absorption  577 Mineral Excesses  578 Contaminants 578

Associated Health Conditions  578 Pica 578 Obesity 578 Anemia of Chronic Disease  579

Helicobacter pylori Infection 579 Alcoholic Liver Disease  579 Gastrointestinal Disease  579 Impaired Thyroid Function  579 Anorexia Nervosa  580 Phenylketonuria 580 Physical Activity  580 Restless Leg Syndrome   580 Clinical Manifestations  581 Treatment 581

Nutrition Therapy for Microcytic Anemias  581 Nutritional Implications  581 Nutrition Diagnosis  581 Nutrition Intervention  581 Monitoring and Evaluation  584 Sample Nutrition Diagnostic Terminology for ­Microcytic Anemia 584 Sample PES Statements for Microcytic Anemia  586

Megaloblastic Anemias  586 Definition 586 Epidemiology 586 Etiology 586

Pathophysiology 586 Cyanocobalamin 586 Folate 587 Clinical Manifestations  587 Treatment 587

Hemoglobinopathies: Non-nutritional Anemias  591 Sickle Cell Anemia  591 Nutrition Therapy  591

Thalassemia 591 Nutrition Therapy  591

Polycythemia 594 Nutrition Therapy  594

Hemolytic Anemia  594 Nutrition Therapy  594

Anemia of Prematurity  594 Nutrition Therapy  594

Aplastic Anemia  594 Nutrition Therapy  594

19.6  Clotting and Bleeding Disorders  594 Hemophilia 594 Nutrition Therapy  594

Hemorrhagic Disease of the Newborn  596 Nutrition Therapy  596

19.7 Conclusion 596

 20  Diseases and Disorders of the

­Neurological System  603

20.1 Introduction 605 20.2 Normal Anatomy and ­Physiology of the Nervous System  605

Nutritional Implications  588

20.3 Communication within the Nervous System  605

Nutrition Diagnosis  588

20.4  The Central Nervous System (CNS)  606

Nutrition Therapy for Megaloblastic Anemias  587

Nutrition Intervention  588 Sample Nutrition Diagnostic Terminology for Megaloblastic Anemia  588 Sample PES Statement for Megaloblastic A ­ nemia  588 Monitoring and Evaluation  588

19.5 Hemochromatosis 589 Definition   589 Epidemiology 589 Etiology 589 Pathophysiology 590 Clinical Manifestations  590 Treatment 590 Nutrition Therapy for Hemochromatosis  591

20.5  Epilepsy and Seizure Disorders  607 Definition 607 Epidemiology 607 Etiology 607 Pathophysiology 607 Clinical Manifestations  607 Medical Diagnosis  608 Treatment 608 Antiepileptic Drugs  608 Other Medical Treatments  609

20.6 Nutrition Therapy for ­Epilepsy and Seizure Disorders  609

Sample PES Statement for Iron Overload  591

Nutritional Implications  610 Nutrition Assessment  612 Nutrition Diagnosis  612 Nutrition Intervention  612 Monitoring and Evaluation  613

Nutrition Intervention  591

20.7  Stroke and Aneurysm  614

Nutritional Implications  591 Nutrition Diagnosis  591 Sample Nutrition Diagnostic Terminology for Iron Overload  591

Monitoring and Evaluation  591

Definition 614 Table of Contents   xix

Epidemiology 614 Etiology 614 Pathophysiology 615 Clinical Manifestations  615 Medical Diagnosis  616 Treatment 616

20.8  Nutrition Therapy for Stroke  617 Nutritional Implications  617 Nutrition Diagnosis  617 Nutrition Intervention  617 Monitoring and Evaluation  618 Nutrition and Stroke Prevention  618 Progressive Neurological Disorders  618 Parkinson’s Disease  618 Definition 618 Epidemiology 618 Etiology 618

Clinical Manifestations  624 Medical Diagnosis  624 Treatment 624

Multiple Sclerosis  624 Definition 624 Epidemiology 625 Etiology 625 Pathophysiology 625 Clinical Manifestations  625 Treatment 625

20.10 Nutrition Therapy for Multiple Sclerosis  626 Nutritional Implications  626 Nutrition Diagnosis  626 Nutrition Intervention  626 Monitoring and Evaluation  627

Dementia 627

Pathophysiology 618

Definition 627

Clinical Manifestations  618

Epidemiology 627

Medical Diagnosis  618

Etiology 627

Treatment 621

Pathophysiology 627

20.9 Nutrition Therapy for Parkinson’s Disease  621 Nutritional Implications  621

Clinical Manifestations  627 Medical Diagnosis  628 Treatment 628

Nutrition Diagnosis  622

20.11  Nutrition Therapy for Dementia  628

Sample PES Statement  622

Nutritional Implications  628

Nutrition Intervention  622

Nutrition Diagnosis  629

Monitoring and Evaluation  623

Nutrition Intervention  629

Amyotrophic Lateral Sclerosis  623 Definition 623 Epidemiology 623 Etiology 623 Pathophysiology 623 Clinical Manifestations  623 Medical Diagnosis  623 Treatment 623

Guillain–Barré Syndrome  623 Definition 623 Epidemiology 623 Etiology 623 Pathophysiology 624 Clinical Manifestations  624 Medical Diagnosis  624 Treatment 624

Myasthenia Gravis  624 Definition 624 Epidemiology 624 Etiology 624 Pathophysiology 624 xx    Table of Contents

Monitoring and Evaluation  630

20.12  Neurotrauma and Spinal Cord Injury  630 Traumatic Brain Injury  630 Definition 630 Epidemiology 631 Etiology 631 Pathophysiology 631 Clinical Manifestations  631 Medical Diagnosis  631 Treatment 631

20.13 Nutrition Therapy for Traumatic Brain Injury  632 Nutritional Implications  632 Nutrition Diagnosis  632 Nutrition Intervention  632 Monitoring and Evaluation  632

Spinal Cord Injury  633 Definition 633 Epidemiology 633

Pathophysiology 633

21.7 Nutrition Therapy for Chronic Obstructive Pulmonary Disease  657

Treatment 633

Nutrition Assessment and Diagnosis  657

Etiology 633

20.14 Nutrition Therapy for Spinal Cord Injury  633 Nutritional Implications  633 Nutrition Diagnosis  633 Nutrition Intervention  633 Monitoring and Evaluation  634

20.15 Conclusion 634

 21  Diseases of the Respiratory

System  641

21.1 Introduction 643 21.2 Normal Anatomy and Physiology of the Respiratory System  643 Measures of Pulmonary Function  645 Nutrition and Pulmonary Health  646

21.3 Asthma 647

Anthropometric Measurements  658 Medication Use  658 Physical Activity and Function   658

Nutrition Intervention  658 Energy and Nutrient Needs  658 Pulmonary Rehabilitation  659

21.8  Cystic Fibrosis  659 Definition 659 Epidemiology 659 Etiology 660 Pathophysiology 660 Medical Diagnosis  660

21.9  Nutrition Therapy for Cystic Fibrosis  660 Nutritional Implications  661 Nutrition Assessment  661 Anthropometric Measurements  661 Biochemical Data and Medical Tests  661

Definition 647 Epidemiology 647 Etiology 647 Pathophysiology 648 Clinical Manifestations  648 Treatment 648 Nutrition Therapy for Asthma  648

Nutrition Diagnosis  662 Nutrition Intervention  662

21.4 Bronchopulmonary Dysplasia 649

21.10 Conclusion 664

Definition 649 Etiology 649 Treatment 649

21.11 Pneumonia 664

21.5 Nutrition Therapy for ­Bronchopulmonary Dysplasia  651 Nutrition Assessment and Diagnosis  651 Energy and Protein Requirements  651 Nutrition Intervention  652 Monitoring and Evaluation  653

21.6 Chronic Obstructive Pulmonary Disease  654 Definition 654 Epidemiology 654 Etiology 655 Pathophysiology: Chronic Bronchitis  655 Clinical Manifestations: Chronic Bronchitis  655 Pathophysiology: Emphysema  655 Clinical Manifestations: Emphysema  655 Treatment 655

Nutrition-Related Medication Management: Pancreatic Enzyme Therapy  662 Energy and Macronutrients  662 Vitamin and Mineral Supplements  663 Recommended Infant Feeding  663

Definition 664 Epidemiology 664 Etiology 665 Aspiration Pneumonia  665 Patients with Tracheostomies  665 Nutritional Implications  666 Respiratory Failure  666

21.12 Nutrition Therapy for Mechanically Ventilated Individuals  667 Nutritional Implications  667 Nutrition Assessment and Intervention  667 Nutrient Requirements  667

21.13 Transplantation 668 Definition and Epidemiology  668 Pathophysiology 668

21.14  Nutrition Therapy for Transplantation  668 Nutritional Implications  668 Table of Contents   xxi

Nutrition Assessment  668 Nutrient Requirements  668

Nutrition Intervention  668

21.15 Conclusion 668

 22  Metabolic Stress and the

Critically Ill  674

22.1 Introduction 675 22.2  Physiological Response to Starvation  675 22.3  Physiological Response to Stress  676 Definition 676 Epidemiology 677 Etiology 677 Clinical Manifestations  677 Pathophysiology 677 Medical Diagnosis and Treatment  680

22.4  Nutrition Therapy for ­Metabolic Stress  680 Nutrition Assessment  680 Nutrition Diagnosis  682 Nutrition Intervention  682

22.5 Sepsis 686 Definition 686 Epidemiology 686 Etiology 686 Clinical Manifestations  686 Pathophysiology 686 Treatment 686

22.6  Nutrition Therapy for Sepsis  686

22.10 Peri-/Postoperative Nutrition Therapy: Enhanced Recovery after Surgery Protocols (ERAS)  691 Postoperative Nutrition Therapy  692

22.11  HIV and AIDS  693 Epidemiology 693 Pathophysiology 693 Clinical Manifestations  693 Medical Diagnosis  695 Treatment 695 Nutrition Assessment  696 Nutrition Intervention  696

22.12 Conclusion 696

 23  Neoplastic Disease  701 23.1 Introduction 702 23.2 Definition 702 23.3 Epidemiology 702 23.4  Etiology of Cancer  703 23.5  Cancer Genetics  703 23.6  Cancer and Nutrition  705 Pathophysiology 706 Medical Diagnosis  706 Treatment 706 Surgery 708 Cancer Diagnoses Requiring Surgery  708 Cancers of the Head and Neck  709 Esophageal Cancer  709 Gastric Cancer  710

22.7 Burns 687

Intestinal Cancers  710

Definition 687 Epidemiology 687 Etiology 688 Clinical Manifestations  688 Pathophysiology 688 Treatment 688

Pancreatic Cancer  710

22.8  Nutrition Therapy for Burns  689 Nutrition Assessment  689 Nutrition Diagnosis  689 Nutrition Intervention  690

22.9 Surgery 690 Definition 690 Epidemiology 690 Etiology 690 Clinical Manifestations  691 Nutrition Assessment  691 xxii    Table of Contents

Chemotherapy 710 Radiation 711 Biological and Targeted Therapy  712 Immunotherapy 712 Hematopoietic Stem Cell Transplantation  714

23.7 Nutrition Therapy for ­Individuals with Cancer  714 Nutritional Implications  715 Nutrition Assessment  715 Determining Nutrient Requirements  715

Nutrition Diagnosis  716 Nutrition Intervention  716 Interventions for Common Side Effects of Cancer and Treatment  716 Early Satiety  717 Mucositis 717

Diarrhea 718

24.5  Rickets and Osteomalacia  742

Dysgeusia 719

Rickets 743

Xerostomia 719

Epidemiology, Etiology, and Clinical Manifestations  743

Anorexia 720

Prevention 743

Immunosuppression 720 Nutrition Interventions during Chemotherapy and Radiation Treatment  720 Interventions before and after Surgery  721

Nutrition ­Interventions for Hematopoietic Cell Transplantation  722 Monitoring and Evaluation  722 Nutrition for Cancer Survivors  722

23.8 Conclusion 722

 24  Diseases of the Musculoskeletal

System  727

24.1 Introduction 728 24.2 Normal Anatomy and ­Physiology of the Skeletal System  729 24.3 Cartilage 729 Bone 730 The Cells of Osseous Tissue  730 Skeletal Growth and Development  731 Cortical and Trabecular Bone  731

Hormonal Control of Bone Metabolism  732 Osteoporosis 734 Epidemiology 734 Etiology 734 Nutritional Risk Factors for Osteoporosis  735 Calcium 735

Treatment 743

Osteomalacia 743 Etiology and Clinical Manifestations  743 Treatment 743

24.6  Arthritic Conditions  744 Definition and Epidemiology  744

24.7 Osteoarthritis 745 Epidemiology, Etiology, and Clinical Manifestations  745 Treatment 746 Nutrition Implications  747 Nutrition Assessment  747 Nutrition Interventions  747

Gout 747 Epidemiology and Etiology  747 Pathophysiology and Clinical Manifestations  747 Treatment 747

24.8 Conclusion 748

 25  Metabolic Disorders  751 25.1 Introduction 752 25.2  Epidemiology and Inheritance  753 25.3 Pathophysiology of Impaired Metabolism  753 25.4  Medical Diagnosis/Newborn Screening  754

Other Nutrients and Food Components  736

25.5 Clinical Manifestations of Inborn Errors of Metabolism  755

Physical Activity  737

25.6  Medical Approaches to Treatment  756

Cigarette Smoking  737

Acute Medical Therapy  756 Use of Scavenger Drugs to Remove Toxic By-Products  756

Vitamin D  735

Alcohol 737

Pathophysiology 737 Medical Diagnosis  738 Treatment 739 Adequate Calcium and Vitamin D  739 Physical Activity and Fall Prevention  740 Pharmaceutical Treatment  740

24.4  Nutrition Therapy for Osteoporosis  740 Nutrition Assessment  740 Nutrition Diagnosis  742 Nutrition Intervention  742 Monitoring and Evaluation  742

25.7 Medical Nutrition Therapy for Inborn Errors of Metabolism: General Guidelines  757 Acute Medical Nutrition Therapy  757 The Nutrition Care Process for Inborn Errors of Metabolism  757 Chronic Medical Nutrition Therapy  757 Restriction of Precursors  757 Supplementation of the End Products  757 Providing Alternate Substrates for M ­ etabolism  759 Supplementation of Vitamins or Other Cofactor Nutrients 759

Table of Contents   xxiii

25.8  Amino Acidopathies  759 Epidemiology, Etiology, and Clinical Manifestations  759 Phenylketonuria 760 Medical Nutrition Therapy for Amino Acid Disorders  761 Nutrition Intervention  761 Monitoring and Evaluation  763 Management during Pregnancy  765

Organic Acidemias  765 Epidemiology, Etiology, and Clinical ­Manifestations of Propionic Acidemia  766 Medical Nutrition Therapy for Propionic Acidemia  766 Nutrition Intervention  766 Monitoring and Evaluation  767

Adjunct Medical and Nutritional Therapies  767

25.9  Urea Cycle Disorders  767 Epidemiology, Etiology, and Clinical Manifestations  767 Acute Medical Treatment  769 Chronic Medical Treatment  769 Medical Nutrition Therapy for Urea Cycle Disorders  769 Acute Nutrition Intervention  769

Fructose-1,6-Diphosphatase Deficiency  777 Medical Nutrition Therapy for FDP Deficiency  777 Nutrition Intervention  777 Monitoring and Evaluation  777

Glycogen Storage Diseases  777 Glycogen Storage Disease Type I  778

Medical Nutrition Therapy for Glycogen ­Storage Diseases  778 Nutrition Intervention  778 Monitoring and Evaluation   779

25.12  Disorders of Fat Metabolism  781 Etiology and Clinical Manifestations  781 Medical Nutrition Therapy for Disorders of Fat Metabolism  782 Acute Nutrition Intervention  782 Chronic Nutrition Intervention  783 Monitoring and Evaluation  783

Adjunct Medical Therapies  784

25.13 Conclusion 784

Chronic Nutrition Intervention  770

APPENDICES

Monitoring and Evaluation  770

Appendix A—Answers to Chapter Review Questions  A-1 Appendix B—Answers to Application of the Nutrition Care Process Questions  A-44 Appendix C1—Healthy U.S.- Style Eating Pattern  A-59 Appendix C2—Healthy Mediterranean-Style Eating Pattern  A-61 Appendix C3—Healthy Vegetarian Eating Pattern  A-62 Appendix D1—Triceps Skinfold Thickness, Arm Muscle Area (AMA), and Mid-Upper Arm Fat Area (AFA): Procedures, Computations, Interpretations, and Percentiles  A-63 Appendix D2—Nomogram for Calculations of Arm Muscle Circumference and Area  A-72 Appendix E—Routine Laboratory Tests with Nutritional Implications  A-74 Appendix F—Normal Values for Physical Examination  A-76 Appendix G—Nutritional Deficiencies Revealed by Physical Examination  A-77 Appendix H—Choose Your Foods: Exchange Lists for Diabetes  A-79 Appendix I—Common Medical Abbreviations  A-94

25.10  Mitochondrial Disorders  771 Etiology and Clinical Manifestations  771 Medical Diagnosis  771 Respiratory Chain Defects  771 Medical Nutrition Therapy for Mitochondrial Disorders  772 Nutrition Intervention  772 Monitoring and Evaluation  773

25.11 Disorders Related to ­Vitamin Metabolism and Vitamin-­Responsive Metabolic Disorders  773 Etiology 773 Medical Nutrition Therapy for Vitamin-­Responsive ­Metabolic Disorders  774 Nutrition Intervention  774 Monitoring and Evaluation  775

Disorders of Carbohydrate Metabolism  775 Galactosemia 775 Medical Nutrition Therapy for Galactosemia  775 Nutrition Intervention  775 Monitoring and Evaluation  776

Hereditary Fructose Intolerance  776 Medical Nutrition Therapy for Hereditary Fructose Intolerance  777 Nutrition Intervention  777 Monitoring and Evaluation  777

xxiv    Table of Contents

Glossary  G-1 Index  I-1

Preface The authors of this text are educators, clinicians, and researchers. Therefore, our purpose in the fourth edition of this text is to continue our original goals to provide the most up-to-date research and application of evidence-based nutritional care for students, clinicians, and researchers as they seek to understand and treat nutrition-related disease. Most of us look to primary reference texts as the cornerstone of our practice. Many names come to mind—Modern Nutrition in Health and Disease, the ASPEN Nutrition Support Core Curriculum, and Harrison’s Book of Internal Medicine. We continue to strive for this text to be one of those reference texts not only to provide the information necessary to understand nutrition practice but also provide it in such a way that the learning environment will support students’ development of critical thinking, clinical reasoning, and decision-making skills. This edition places additional emphasis on the interprofessional team where we explicitly emphasize that optimal patient care will require all members of the health care team to work together to provide the most efficient and accurate care for the public. What continues to make this text different from other clinical nutrition therapy texts? The clinical environment evolves as a result of the impacting forces of research, health care funding, evidence-based nutrition practice, and development of the nutrition care process, standardized language, and standardized nutrition diagnoses. To meet the demands of these evolving forces, this text includes not only the most current research and integration of evidence-based practice within the context of the nutrition care process but also an overview of health care systems and the dietitian’s role within these systems as a member of the health care team; guidelines for documentation and other professional writings; and coverage of emerging fields such as nutrigenomics. Furthermore, as the framework for the nutrition care process has progressed over the previous seven years, the structure for our text has organized its pedagogy to be consistent with each step of the nutrition care process. This text incorporates standardized language, the Evidence Analysis Library, the Academy of Nutrition and Dietetics Nutrition Care ­Manual, the Standards of Practice for the Registered Dietitian Nutritionist, and the professional Code of Ethics. The text begins with a discussion of the dietitian’s role as a nutrition expert, and then proceeds through the nutrition care process, introducing the basics of assessment, diagnosis, intervention, and monitoring/evaluation. Next, a comprehensive review of physiological concepts required to integrate nutrition therapy as a component of medical care is presented. These foundational chapters cover physiological response to injury, the immune system, fluid and electrolyte balance, pharmacology, and genetics—focusing specifically

on the application of each of these topics to clinical nutrition practice. The final section of this text is organized using a systems approach consistent with other medical texts. Each nutrition therapy chapter discusses normal structure and function of a body system, explains how the disease process interrupts normal functioning, and then describes appropriate medical and nutrition interventions. This edition has retained the pedagogical features students and educators found especially helpful—Clinical Applications boxes, nutrition assessment summary tables, sample documentation, PES statements, case studies, overviews of common medical care and drug–nutrient interactions, and interviews with current clinical practitioners. New features for this edition include many additional Life Cycle Perspectives boxes for applications of nutritional care for pediatrics and older adults. This approach allows any health care professional to benefit from this text. Though every effort has been made to address the most recent research and the most common clinical and medical practices, this text has the same limitation any medical textbook will have: new diagnoses, new drugs, new treatments, and a new understanding of the relationship between nutrition and disease will inevitably continue to be cultivated after publication. Thus, this book strives to educate students about not only facts and theories that comprise current medical knowledge but also the process of skill development that empowers students to grow in expertise within their field. As practitioners of the future utilize the nutrition care process, it will be refined even as their knowledge of disease and its treatment evolves. As clinical practitioners and current dietetic educators, we have experienced a need for not only this different approach to a clinical nutrition text but also a reference for clinical practitioners. We believe that this fourth edition continues to serve this purpose.

NEW TO THIS EDITION The fourth edition of Nutrition Therapy and Pathophysiology has built upon the strengths of prior editions to include a comprehensive focus on pathophysiology and medical treatment with a thorough review of the most current research. Throughout this fourth edition, the need for the interprofessional health care team is emphasized. Specific diets and food recommendations are covered within each chapter, and new research and life-cycle perspectives are integrated throughout. This book’s chapter organization will allow the student and practitioner to follow the steps of the nutrition care process. Nutrition therapy within each systems chapter Preface  xxv

emphasizes real-life application of the standards in patient care and has been updated with the latest evidence-based practice. Figures and tables have been modified to provide visual explanations of concepts within the text. New photos of wholesome foods and real clinical settings have been added to both enhance chapters pedagogically and add visual appeal. Specific changes for the fourth edition include the following:

PART 1

The Role of Nutrition Therapy in Health Care • Chapter 1 Role of the Dietitian in the Health Care System provides updated information on the nutrition care process, evidence-based practice, Code of Ethics and 2017 Standards of Professional Practice, updates for dietetic education, as well as new information on the Academy of Nutrition and Dietetics Scope of Practice. There is a specific emphasis on the interprofessional core competencies and need for interprofessional care. This chapter continues to have a significant discussion on evidence-based practice and its role as the foundation of dietetic’s practice.

PART 2

The Nutrition Care Process • Chapter 2 The Nutrition Care Process has been updated to include the most current terminology for all steps of the NCP. The 2017 updated model more clearly depicts the interrelationships of the steps of the NCP.

• Chapter 3 Nutrition Assessment: Foundation of the Nutrition Care Process integrates the adult and pediatric malnutrition guidelines within the tools for nutrition assessment as well as the use of the nutrition-focused physical examination. This chapter includes newer screening tools including NRS 2002 and NUTRIC score as well as the use of screening for food insecurity within the overall nutrition assessment process. There is a thorough coverage of anthropometric measurements including the use of pediatric growth charts, pediatric midarm muscle circumference, and z-scores. Newer research regarding sarcopenia and use of portable ultrasound and DXA is additionally reviewed. There is a thorough review of protein assessment with a clear discussion of the impact of inflammation on acute-phase protein synthesis and its’ impact on assessment interpretation. Up-to-date reference standards are used throughout this chapter and the text with an emphasis on the use of dietary patterns and the 2015–2020 U.S. Dietary Guidelines. • Chapter 4 Nutrition Intervention and Nutrition Monitoring and Evaluation builds on the updated intervention terminology from Chapter 2 to explain the process of developing interventions, beginning with oral diets as examples of interventions within the acute care setting.

xxvi    Preface

This chapter includes a new section discussing the monitoring and evaluation step of the nutrition care process.

• Chapter 5 Enteral and Parenteral Nutrition Support has been extensively revised to incorporate the most recent ASPEN and evidence-based guidelines for prescribing nutrition support. All calculation examples have been revised for simplification of student use. • Chapter 6 Nutrition Informatics and Documentation of the Nutrition Care Process has a new emphasis on the importance of informatics and its application to the dietetics profession.

PART 3

Introduction to Pathophysiology • Chapter 7 Fluid and Electrolyte Balance and Chapter 8 Acid-Base Balance have been updated with the latest research to provide a thorough review for the student and comprehensive reference for the practitioner.

• Chapter 9 Cellular and Physiological Response to Injury: The Role of the Immune System features additional information on both the acute and chronic inflammatory response and its application to the disease process. This edition has increased references to food allergies, diagnostics, and treatment. • Chapter 10 Nutritional Genomics presents new research on the genetics of nutrition-related diseases and a snapshot of the nutritional genetics marketplace. Nutritional genomics in disease is emphasized within the topics of cancer, obesity, diabetes, cardiovascular disease incorporating the latest nutrition related research in this fast-growing field. The chapter additionally covers the role of nutritional genomics and the practice of nutrition and dietetics. • Chapter 11 Pharmacology provides the framework for the dietetic student to learn to evaluate the role of pharmacology within the nutrition care process. This explicit framework in the chapter provides the foundation to meet the latest update for dietetic education performance indicators within this competency area.

PART 4

Nutrition Therapy Each chapter in Part 4 provides updated coverage of common diagnostic procedures and medications—with improved information on nutrition assessment and nutrition therapies. • Chapter 12 Diseases and Disorders of Energy Imbalance explains the application of the most recent evidence-based guidelines for assessment, treatment, and prevention of overweight and obesity for both pediatric and adult populations. Nutrition therapies for weight loss and for postbariatric surgeries are covered within this updated chapter. Behavioral assessment, physical activity readiness, and nutrition counseling strategies for behavior change are also addressed within the chapter. Malnutrition is additionally emphasized in this chapter

with discussion of both adult and pediatric malnutrition guidelines.

• Chapter 13 Diseases of the Cardiovascular System has been reorganized and includes updated information on epidemiology, pathophysiology, and risk factors, along with the most recent treatment guidelines and medications. The chapter includes a new section on heart transplantation and three new boxes discussing aging and heart disease, congenital heart defects, and food safety for immune-compromised patients. • Chapter 14 Diseases of the Upper Gastrointestinal Tract has been updated with the latest research with discussion for eosinophilic esophagitis (EoE), a comparison between the National Dysphagia Diet and the International Dysphagia Diet Standardization Initiative. The updated chapter also includes steps for physical assessment of the oral cavity and its’ role within the nutrition-focused physical exam. Additionally this new chapter incorporates discussion of the microbiome, ERAS protocols, and the most recent nutrition therapies for gastroparesis and EoE.

• Chapter 15 Diseases of the Lower Gastrointestinal Tract has been revised to incorporate more in-depth ­coverage of the microbiome, use of probiotics, and the role of nutrition therapies for diarrhea, constipation, malabsorption, inflammatory bowel disease, short bowel syndrome, irritable bowel syndrome (IBS), small intestinal bacterial overgrowth (SIBO), and celiac disease. A new section covering intestinal rehabilitation and transplant has been added. The use of nutrition support is integrated throughout the nutrition therapy sections and supported with the most recent evidence-based guidelines including ERAS protocols.

• Chapter 16 Diseases of the Liver, Gallbladder, and Exocrine Pancreas has been extensively revised and reorganized with more in-depth coverage of nonalcoholic fatty liver disease, acute and chronic pancreatitis, and the appropriate nutrition assessment and interventions. Protocols for use of micronutrient supplementation and pancreatic enzymes are additionally covered within this chapter. Pancreatic surgical procedures, ERAS protocols, and postoperative nutrition therapy are included. A new practitioner interview discusses the role of the dietitian on the transplant team. • Chapter 17 Diseases of the Endocrine System has been revised to reflect the American Diabetes Association’s 2018 standards of medical care in diabetes with updates for diagnosis, medication protocols, medical nutrition therapy, and lifestyle interventions. Practical examples incorporating carbohydrate counting, insulin dosing, and

correction factors are provided. New to this addition is the discussion of bariatric surgery and pancreatic and islet cell transplantation as treatments for diabetes.

• Chapter 18 Diseases of the Renal System continues to update medical care and nutrition therapies for both acute kidney injury and chronic kidney disease with the latest research and evidence-based guidelines. • Chapter 19 Diseases of the Hematological System has been thoroughly updated and can continue to be used as an important reference to support all of the nutrition therapies within this text.

• Chapter 20 Diseases and Disorders of the Neurological System incorporates the most recent research through enhanced discussions of the ketogenic diet and interventions for prominent nutrition problems such as dysphagia and drug–nutrient interactions.

• Chapter 21 Diseases of the Respiratory System update brings a new author who is a professor of respiratory therapy. Her knowledge of pulmonary anatomy and mechanical ventilation brings a significant update to this chapter. There are additionally important and significant updates to the sections for bronchopulmonary dysplasia, cystic fibrosis, and nutrition support in respiratory failure. A new practitioner interview from a dietitian with 30 years of experience in cystic fibrosis adds a historical value to the changes in the care for individuals with CF.

• Chapter 22 Metabolic Stress and the Critically Ill incorporates the ASPEN critical care guidelines, ERAS protocols, and a thorough integration of new research and its application to surgery, trauma, sepsis, traumatic brain injury, burns. HIV and AIDS. Updated figures and protocols for prescribing nutrition support are provided. • Chapter 23 Neoplastic Disease has been significantly reorganized. The discussions of cancer-related genetics, nutrigenomics, cancer risk, and cancer prevention have been expanded. The information on epidemiology, pathophysiology, medical treatments, medications, and nutrition care guidelines has been updated.

• Chapter 24 Diseases of the Musculoskeletal System has been updated with a focus on osteoporosis, o ­ steoarthritis, and gout, and features new boxes covering pediatric ­muscular dystrophy and the use of alternative treatments for arthritis among older adults.

• Chapter 25 Metabolic Disorders’ new author brings an excellent organization and writing style to a difficult topic. The chapter has been thoroughly updated with the latest treatment guidelines, and case discussion examples for the most common inborn errors of metabolism are provided.

Preface  xxvii

Acknowledgments We are grateful to our contributing authors for their expertise and dedication in their contributions to this text: Kristen Roberts, PhD, RD, LD, CNSC The Ohio State University Holly Estes Doetsch, MS, RDN, CNSC The Ohio State University Colette LaSalle, PhD, RDN San Jose State University Sarah Rusnak, MS, RDN, LD The Ohio State University Georgianna Sergakis, PhD, RRT, RCP, FAARC The Ohio State University Melissa Hansen-Petrik, PhD, RDN, LD The University of Tennessee–Knoxville Roschelle A. Heuberger, PhD, RDN, LD Central Michigan University Jennifer Smith, MS, RD Nationwide Children’s Hospital Columbus Ohio Colleen Spees, PhD, RDN, LD The Ohio State University We believe the practitioner interviews will assist students in understanding the role of the dietitian within the many facets of the dietetic profession and serve as significant role models. We would like to thank the following individuals for their gracious consent for interviews within this text: Ashley Burgess, MS, RDN DaVita Kidney Care Dena Champion, MS, RD, LD, CNSC Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Wexner Medical Center at the Ohio State University Susan Gemma, MS, RD, LD Nationwide Children’s Hospital, Columbus, Ohio Marianne Hutton, RD, CDE Novo Nordisk Jeanette M. Hasse, PhD, RD, LD, FADA, CNSC Baylor University Medical Center, Dallas, Texas Neha Parekh, MS, RDN, LD, CNSC Cleveland Clinic, Cleveland, Ohio Lynne Schonder, MS, RD, CNSC Valley Care Medical Center, Pleasonton, CA La Paula Sakai, MS, RD, CNSD (retired) Grace Shea, RD, CSP, LDN Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Jill Weisenberger, MS, RD, CDE Private practice nutritionist, author, and consultant xxviii    Acknowledgments

Jennifer A. Wooley, MS, RD, CNSC GE Healthcare: Anesthesia and Respiratory Care Mara Weber, MS, RD Ross Heart Hospital—Ohio State University Wexner Medical Center, Columbus, Ohio Beth Zupec-Kania, RD, CD Children’s Hospital of Wisconsin We would like to thank the many reviewers whose insights and suggestions proved invaluable during the writing process: Laura Acosta, MS, RDN, CSSD, LDN University of Florida Jennifer D Bean, MS, RDN, LD University of Missouri Columbia Mallory Boylan, PhD, RDN Texas Tech University Wendy Buchan, PhD, RDN CSU Sacramento Chimene Castor, EdD, RDN, LDN, CHES Howard University Lora N. Day, MA, RD, LD UT Southwestern Medical Center Kathleen M. Hill Gallant, PhD, RD Purdue University Karen Gibson, DCN, RDN Viterbo University Emily Wilcox Gier, MBA, RD Cornell University Erin Gonzalez, RD, LD Minnesota State University, Mankato Susan N. Hawk, PhD, RD Central Washington University Norman G. Hord, PhD, MPH, RD Oregon State University Deanne K. Kelleher, MS, RD Michigan State University Yeonsoo Kim, PhD, RD Central Michigan University Julie Larsen, PhD, RDN, ACSM CEP Washington State University Spokane Michelle Lee, PhD, RD East Tennessee State University Mary-Jon Ludy, PhD, RDN, FAND Bowling Green State University Mary Marian, DCN, RDN, CSO, FAND University of Arizona

Dorothy Chen-Maynard, PhD, RD CSU San Bernardino

Jane Burrell Uzcategui, MS RD Syracuse University

Kimberli Pike, MS, RD, CSSD Ball State University

Long Wang, PhD, MD, RD California State University, Long Beach

Lisa Ritchie, EdD, RDN, LD Harding University

Allisha Weeden, PhD, RD, LD Idaho State University

Karen J Schmitz, PhD, RD Madonna University

Stanley R. Wilfong, MS, RD, LD, FAND Baylor University

Padmini Shankar, PhD, RD Georgia Southern University

Shahla Wunderlich, PhD, RD Montclair State University

Kelly Secosky, MFN, RDN, LDN Meredith College

Jean A. Zancanella, MS, RD, CD University of Utah

LuAnn Soliah, PhD, RD Oklahoma State University Serah Theuri, PhD, RD University of Southern Indiana Jennifer Tomesko, DCN, RD, CNSC Montclair State University

The authors would like to acknowledge Peter Madril, MS, RDN, LD and McKel Hill, MS, RD, LD for their beautiful photography that has been used within this edition. The authors would like to acknowledge the assistance of Ashley Kennedy, graduate student at Ohio State University, for her assistance in research and preparation of Appendices A and B.

Acknowledgments  xxix

Part 1 The Role of Nutrition Therapy in Health Care IN THIS PART Chapter 1 ROLE OF THE REGISTERED

Source: Andrey_Popov/Shutterstock.com

DIETITIAN NUTRITIONIST IN THE HEALTH CARE SYSTEM

1

CHAPTER 1

Source: Courtesy of Marcia Nelms.

Role of the Registered Dietitian Nutritionist in the Health Care System Kathryn Sucher, ScD, RDN San Jose State University

LEA RNING O B JECTIV ES LO 1.1  Describe the three categories of the Scope of Practice developed by the Academy of Nutrition and Dietetics. LO 1.2  Differentiate between the four clinical nutrition team members.

2

LO 1.3  Identify other health professionals that are part of the Interprofessional team.

LO 1.5  Describe the five components of critical thinking and their applications in providing nutrition care.

LO 1.4  Explain why nutrition services are expected to expand under the Affordable Care Act (ACA).

LO 1.6  Define evidence-based practice and its relevance.

G LOSSARY Affordable Care Act (ACA)—federal legislation meant to ensure that all Americans have access to affordable health care while containing U.S. health care costs critical thinking—the act of thinking using the mind to organize and integrate information, identify relationships, make inferences, form conclusions, and make decisions evidence-based dietetics practice—dietetics practice in which systematically reviewed scientific evidence is used to make food and nutrition practice decisions health insurance—financial protection against health care costs associated with treatment of disease or accidental injury nurse—a health care professional who has earned at least an associate’s degree in nursing, has been licensed by the state, and assists patients in activities related to maintaining or recovering health. Examples of advanced practice nursing include nurse practitioner, clinical nurse specialist, nurse midwife, and nurse anesthetist occupational therapist—A health professional who has obtained a master’s or doctoral degree from an accredited OT educational program and passed a national registration exam. OTs evaluate and provide intervention in collaboration with the client, family, caregiver; develop, improve, sustain, or restore skills in activities of daily living (ADL), work or productive activities, and play or

leisure; identify and facilitate engagement in meaningful and healthy occupations; develop, remediate, or restore sensorimotor, cognitive, or psychosocial components of performance; educate the client, family, caregiver, or others in carrying out appropriate nonskilled interventions; and consult with groups, programs, organizations, or communities to provide population-based services outcomes research—evaluation of care that focuses on the status of participants after receiving care pharmacist—a licensed health professional with a doctorate of pharmacy who compounds and dispenses medications, provides direct patient care by assessing tolerance to medications, and provides education on health and wellness physical therapists—health care professionals who can help patients reduce pain and improve or restore mobility; teach patients how to prevent or manage their condition so that they will achieve long-term health benefits; work with individuals to prevent the loss of mobility before it occurs by developing fitness- and wellness-oriented programs for healthier and more active lifestyles. Physical therapists can further specialize in these areas: cardiovascular and pulmonary, clinical electrophysiology, geriatric, neurology, orthopedic, pediatric, and sports physician—health care professional who practices medicine, which is concerned with

1.1 INTRODUCTION The connection between diet and health has long been recognized. The profession of dietetics was first defined in 1899 by the American Home Economics Association as “individuals with knowledge of food who provide diet therapy for the medical profession.” After 1917, dietitians were affiliated with the Academy of Nutrition and Dietetics (AND),1 formerly known as the American Dietetic Association (ADA). Dietitians who were employed in hospitals became known as clinical dietitians. Over time, the clinical dietitian’s role became the provision of specialized care and modification of diets to treat various medical conditions. In the early 1970s, after high levels of malnutrition in hospitalized patients were reported2 and new and improved procedures for delivering enteral and parenteral nutrition were developed, clinical dietitians began to take a leadership role in screening patients and monitoring their needs for adequate nutrition support. In addition, as research pointed to the role of diet in the development of chronic disease, clinical dietitians began to provide primary and secondary disease prevention for such diseases as atherosclerosis, cancer, and type 2 diabetes mellitus.3 The information provided in this chapter is meant to help you understand where you might find potential sources of employment, your contribution to the nutrition care of a patient as part of the heath care team, reimbursement issues that you might encounter, and your

promoting, maintaining, or restoring health through the study, diagnosis, and treatment of disease, injury, and other physical and mental impairments physician assistant—health care professionals who diagnose illness, develop and manage treatment plans, prescribe medications, and often serve as a patient’s principal health care provider respiratory therapist—health care professionals who have earned a minimum of an associate’s degree in respiratory therapy from an accredited educational program. These individuals provide testing, treatment, and care to patients who have difficulty breathing caused by cardiopulmonary disorders such as heart failure or pulmonary hypertension; chronic respiratory issues like asthma, COPD, or cystic fibrosis; and medical emergencies social worker—a professional with at least a master’s degree in social work who provides persons, families, or vulnerable populations with psychosocial support, advises family caregivers, counsels patients, and helps plan for patients’ needs after discharge speech-language pathologist—a health professional who has earned a master’s degree and passed a national examination, who assesses, diagnoses, treats, and helps to prevent speech, language, cognitive, communication, voice, swallowing, fluency, and other related disorders

professional responsibilities, and to help you develop skills that are necessary for the nutrition care process (NCP).

1.2  THE REGISTERED DIETITIAN

­NUTRITIONIST1 IN CLINICAL PRACTICE The Role of the Registered Dietitian Nutritionist The practice of clinical nutrition is called nutrition therapy. Registered Dietitian Nutritionists are the educated and trained professionals who can best deliver nutrition therapy by using the NCP. The NCP consists of four major components: (1) nutrition assessment, (2) nutrition diagnosis, (3) nutrition intervention, and (4) nutrition monitoring and evaluation.4,5

Scope of Practice The Scope of Practice (Figure 1.1) was developed by the AND and “focuses on food, nutrition and dietetics as well as related services.” The Scope of Practice is divided into three categories, and all three are supported by the education and credentials you are now in the process of obtaining. The first area is Foundational that defines the roles, functions, responsibilities, and activities that dietetics practitioners are educated and authorized/proficient to perform within the boundaries of federal, state, and facility regulations. Practice Standards are used to evaluate a dietitian’s job performance. The next area, Management and Advancement, provides tools, guides,

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    3

Figure 1.1 AND revised 2017 Scope of Practice for the Registered Dietitian Nutritionist

SCOPE OF PRACTICE: Encompasses the range of roles, activities, and regulations within which nutrition and dietetics practitioners perform.

Resources • • • • • • • • • • • •

Academy Definition of Terms List Academy of Nutrition and Dietetics Health Informatics Infrastructure Dietetics Practice Based Research Network Evidence Analysis Library Evidence-Based Nutrition Practice Guidelines/Toolkits Journal of the Academy of Nutrition and Dietetics National Guideline Clearinghouse Nutrition Care Manuals Nutrition Care Process and Terminology Reference Position Papers and Practice Papers Practice Tips and Case Studies Quality Resource Collection

Foundational • Accreditation Standards • Codes of Ethics (eg, Academy/CDR, national organizations, and employer code of ethics) • Federal and State Regulations • National Organization Practice Standards and Guidelines • Organizational Policies and Procedures • Scope of Practice for the RDN and for the NDTR • Standards of Practice in Nutrition Care and Standards of Professional Performance for RDNs and for NDTRs • Standards of Practice and Standards of Professional Performance for RDNs in Focus Areas of Nutrition and Dietetics Practice

Management and Advancement • Advanced Degrees and Certifications (eg, CDR AdvancedPractice Certification in Clinical Nutrition) • Board Certified Specialist Credentials • CDR Professional Development Portfolio • Certificate Programs (eg, Certificates of Training) • Medical Nutrition Therapy Tools • Nutrition and Dietetics Career Development Guide • Nutrition Focused Physical Exam Workshop • Nutrition Services Payment Webinars • Scope of Practice Decision Tool • Standards of Excellence Metric Tool • Quality Improvement Tools and Electronic Clinical Quality Measures

Credentials Achieve and maintain the Commission on Dietetic Registration’s (CDR: www.cdrnet.org) Registered Dietitian Nutritionist (RDN) credential or the Nutrition and Dietetics Technician, Registered (NDTR) credential.

Education Complete academic requirements and supervised practice experience specified by the Accreditation Council for Education in Nutrition and Dietetics (ACEND: www.eatrightpro.org/acend).

Source: Journal of the Academy of Nutrition and Dietetics, 2018: 18(141–65). 201810.1016/j.jand

4  Part 1  The Role of Nutrition Therapy in Health Care

BOX 1.1

CLINICAL APPLICATIONS

AND Scope of Practice for the Profession of Nutrition and Dietetics: A Roadmap and Resource for Your Current Education and Training and Future Career When you look at the Scope of Practice diagram (Figure 1.1), the first thing you notice is probably the education block since you are likely taking a course to complete the academic requirements for becoming a credentialed registered dietitian nutritionist (RDN) or dietetic technician, registered (NDTR). You are probably less familiar with the three sections of the circle—Foundational, Management, and Resources, but they provide the roadmap and resources for your education, training, and future career. 1. Foundational includes the Scope of Practice for the RDN and NDTR, Standards, and Standards of Professional Practice, along with other documents. The Practice standards is used by licensing or certifying boards to define the procedures, actions, and processes that are permitted for practice. The AND Scope of Practice is the guide for dietetics education requirements at your college or university and demonstrated competency for supervised practice sites (e.g., dietetic internships). Your dietetics education and supervised practice are accredited by the Accreditation Council for Education in Nutrition and Dietetics (ACEND), whose mission is to ensure educational quality that “­prepares

­ raduates with the foundation g knowledge, skills and/or competencies for current dietetics practice and lifelong learning.” The Standards of Professional Practice are developed by the AND to ensure that RDNs or NDTRs are competent to provide safe, ethical, and high-quality nutrition care; plus, they provide criteria for evaluating care. The standards may be used to develop job descriptions or evaluate your performance. Practice Standards also require continued education for RDNs and NDTRs for maintenance of their credentials and nutrition care competencies. 2. After you become an RDN or NDTR, Management and Advancement will provide tools to assist you in determining whether (1) a new work activity is within your scope of practice, and (2) this activity will require you to obtain additional training or education. These tools are meant to help you expand your practice as food and nutrition opportunities, roles, and services evolve. In addition, any education and training you complete, which you will document in the online Commission on Dietetic Registration (CDR) Professional Development

and information to help an RDN determine whether she or he has the necessary knowledge and skills to take on a new job responsibility within her or his scope of practice. Career advancement may require obtaining additional credentials, certifications, and/or advanced degrees. The last area, Practice Resources, includes materials available to help the practitioner provide current, safe, ethical, and high-quality food/ nutrition services. The Scope of Practice is meant to be flexible so that, as the profession changes or as an individual specializes or advances in her or his practice, evaluation resources and decision aids will also be modified. See Box 1.1 for more details.

The Clinical Nutrition Team Health care is defined as the prevention, treatment, and/or management of illness. Registered Dietitian Nutritionists are employed in a number of acute and chronic health care facilities, as listed in Table 1.1. Depending on the institution, nutrition therapy services may be organized along different lines.

Portfolio, will help you maintain your credential. 3. Resources provide materials to support quality nutrition care. You may already be familiar with some of the resources, such as the AND Evidence Analysis Library (www​ .adaevidencelibrary.com), from your dietetics coursework. The AND’s “Definition of Terms List” can be found at www.eatright.org/ WorkArea/linkit.aspx?LinkIdentifier=id&ItemID=6442451086&libID=6442451082 In your medical nutrition therapy course, you will learn the nutrition care process and use of the eNutrition Care Process and Terminology (eNCPT) (Chicago, IL: Academy of Nutrition and Dietetics; 2018) so you can appropriately document medical nutrition therapy in the medical record. You may also use the AND Nutrition Care Manual to increase your understanding of medical conditions that require nutrition support or dietary modification. Source: Academy of Nutrition and Dietetics Quality Management Committee and Scope of Practice Subcommittee of the Quality Management Committee. Academy of Nutrition and Dietetics: Scope of Practice in Nutrition and Dietetics. J Acad Nutr Diet. 2018; 118(1).

The manager of the services may have the title of chief clinical manager or clinical nutrition manager. This person often reports to the director of nutrition services, who commonly supervises the clinical nutrition manager and food service manager/directors. In turn, inpatient and outpatient clinical dietitians usually report to the clinical manager. Other important personnel in nutrition therapy services are registered nutrition dietetic technicians (NDTRs), who assist dietitians in the nutritional screening of patients and provision of nutrition education in addition to other duties, and dietary assistants/ diet clerks, who are often responsible for the documentation and processing of diet orders and assuring accuracy of the meals that are provided for patients. Table 1.2 provides common job specifications for clinical nutrition team members. RDNs’ services may be provided to general patient care units, such as those on a general medical or surgical floor, or may be based on a medical specialization, such as treatment of patients in intensive care units (e.g., burn/trauma unit or pediatric/neonatal intensive care units). Boxes 1.2 and 1.3

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    5

Table 1.1 Types of Acute and Chronic Health Care Facilities in the United States Acute Care Facilities Hospitals Public not for profit

Often owned and managed by the county or state government

Private not for profit

Owned or managed by the community, a religious organization, district health councils, or their own hospital board

Private for profit

Investor-owned (for-profit) health care organizations

Veterans and military

Government-run health care facilities for veterans of the U.S. military service and active-duty enlisted men and women

Clinics Outpatient

For preventative, primary health care (e.g., treatment for ear infection) and secondary health care (e.g., treatment of type 2 diabetes)

Urgent care

Provide primary care

Post Acute-Care Facilities Skilled nursing facilities

Provide 24/7 nursing care for complex medical needs

Long-term acute care hospital

Provide care for those with complex medical needs who have a longer than average hospital admission

Residential/assisted living

Provide for activities of daily living (e.g., bathing)

Continuing care retirement community

Provides continuum of care from independent living, assisted living, and skilled nursing on one geographical site

Rehabilitation/restorative

Provide integrated, multidisciplinary assistance for recovery from acute or chronic illness and/or surgical procedures (e.g., stroke)

Adult day care

Facilities offer supervision, social and recreational activities, meals/snacks. Provides daily respite for family members

Hospice

Focus on relieving symptoms and supporting those with a life expectancy of 6 months or less

Source: © Cengage Learning; Adapted from: Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: individualized nutrition approaches for older adults: long-term care, post-acute care, and other settings. J Acad Nutr Diet. 2018; 118:724–35

Table 1.2 Responsibilities and Tasks of Clinical Nutrition Team Members Nutrition Team Member

Responsibilities

Major Tasks

Clinical nutrition manager

Directs the activities of RDN, NDTR, and dietetic assistants

Hiring, evaluating, and training employees; reviewing productivity reports, writing job descriptions, scheduling employees, developing policies and procedures, designing performance standards, and developing and implementing goals and objectives of the department*

Registered dietitian (RDN)

Provides nutritional care for patients

Nutritional screening/assessment of patients to determine the presence or risks of developing a nutrition-related problem, development of nutritional diagnosis, nutrition intervention, and monitoring and evaluation of the nutrition care plan

Dietetic technician (NDTR)

Assists the clinical dietitian

Gathering data for nutritional screening; assigning a level of risk for malnutrition according to predetermined criteria; administering nourishment and dietary supplements for patients and monitoring tolerance; and providing information to help patients select menus and giving simple diet instructions

Dietetic assistant/diet clerk

Assists the clinical dietitian and/or dietetic technician in some routine aspects of nutritional care

Processing diet orders, checking menus against standards, setting up standard nourishment, tallying special food requests; distributing and collecting patient menus and trays; may be involved in evaluating patient food satisfaction and helping to gather food records used to evaluate nutrient intake

*

Howells A, Sauer K, Shanklin C. Evaluating clinical nutrition managers’ involvement in key management functions. J Acad Nutr Diet. 2017; 117(9): 1339–48. http://dx.doi.org/10.1016/j.jand.2016.08.010, accessed August 1, 2017.

6  Part 1  The Role of Nutrition Therapy in Health Care

BOX 1.2

LIFE CYCLE PERSPECTIVES

The Role of the RDN in Post-Acute Care Colette LaSalle, PhD, RDN  San Jose State University The aging population has resulted in an increased need for registered dietitian nutritionists in post-acute care. There are a variety of settings that include skilled nursing facilities, inpatient rehabilitation facilities, long-term care hospitals, intermediate care facilities for individuals with intellectual disabilities, assisted living facilties, senior housing, adult day care, hospice and care provided through home health care. The working environment for post-acute care has a few advantages over other settings because typically there is only one RDN on site and she or he has greater autonomy and can set flexible schedules. Though the residents tend to have multiple chronic and acute medical problems, which increases the complexity of care required, the RDN has time to get to know them and their families and can follow up regularly to monitor the outcomes of each nutrition intervention. The RDN is an integral part of the interdisciplinary health care team and works closely with other health professionals to optimize the nutritional status of the residents. The RDN has several important roles in post-acute care the first of which is related directly to patient care. Many residents have physical and cognitive limitations secondary to chronic disease that can impact intake; thus, the prevalence of malnutrition (both under- and overnutrition) in this population is high. The RDN is responsible for conducting a thorough nutrition assessment of the resident, evaluating the potential for functional problems during eating, such as impaired chewing ability, dental status, or swallow function, and disabilities such as the presence of contractures or postural impairments. RDNs also assess dietary intake by investigating dislikes and allergies, typical meal patterns at home, beverage preferences, diet knowledge, weight history, and previous diet restrictions. RDNs work to correct or attenuate nutrition-related problems by recommending diet changes and educating staff, families, and residents regarding the risks and benefits associated with therapeutic diet orders including restrictive diets, altered diet textures, and thickened fluid viscosities. RDNs also play a role in discussing end-of-life care, honoring advance directives, coordinating hospice care, and initiating and monitoring adequacy of enteral feeding orders. While it is of primary importance to honor the wishes of the residents, complicating factors arise related to issues of

BOX 1.3

mental competency, conservatorship, and family dynamics, with family members sometimes desiring different levels of care for the resident. The length of stay and required level of care vary widely; some residents are admitted for short-term injury rehabilitation or caregiver respite, whereas others are admitted long term with no expected discharge date. This means that the RDN is usually able to follow up with residents and evaluate the outcome of nutrition-related interventions by monitoring oral food and beverage intake, acceptance of snacks and supplements, wound status, laboratory values, and weekly or monthly weights. Also, because this population is often at risk for weight loss and decline, RDNs look not only for significant changes in weight but also for gradual, “insidious” weight loss. In addition to providing direct clinical care, the RDN may also be responsible for overseeing all aspects of food service and food safety. The RDN conducts in-services for nurses, diet clerks, and all food service staff regarding safe food-handling practices (including HACCP) and preparing texture-modified and other therapeutic diets. Additionally, the RDN performs extensive food service inspections and monitors the tray line, the dish room, emergency menu, emergency food and water supplies, and cleaning, sanitizer, and temperature logs in order to ensure compliance with extensive federal, state, and city regulations. References 1. Academy Quality Management Committee. Academy of Nutrition and Dietetics: Revised 2017 Standards of Practice for Registered Dietitian Nutritionists. J Acad Nutr Diet. 2018; 118:141–65. 2. Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: individualized nutrition approaches for older adults: long-term care, post-acute care, and other settings. J Acad Nutr Diet. 2018; 118:724–35. 3. O’Sullivan Maillet J, Baird Schwartz D, Posthauer ME, Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: ethical and legal issues in feeding and hydration. J Acad Nutr Diet. 2013 Jun; 113(6): 828–33. Erratum in: J Acad Nutr Diet. 2013 Jul; 113(7): 985. 4. Schwartz DB, Posthauer ME, O’Sullivan Maillet J. Practice paper of the Academy of Nutrition and Dietetics abstract: ethical and legal issues of feeding and hydration. J Acad Nutr Diet. 2013 Jul; 113(7): 981. 5. Touger-Decker R, Mobley C, Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: oral health and ­nutrition. J Acad Nutr Diet. 2013 May; 113(5): 693–701.

LIFE CYCLE PERSPECTIVES

The Role of the RDN in Pediatric Care Colette LaSalle, PhD, RDN  San Jose State University The role of the registered dietitian nutritionist (RDN) in ­pediatric care encompasses distinct challenges related to meeting the specialized needs of children. The primary role of the pediatric RDN is to optimize nutrient intake to promote growth and development in the presence of ­complicating factors such as acute or chronic illness or

­ evelopmental delays. The RDN conducts a comprehensive d nutrition assessment to obtain i­nformation related to m ­ edical and nutritional history, food preferences, typical eating patterns, and allergies while using pediatric guidelines to estimate nutritional requirements, analyze intake, and assess weight as compared to standards for age and length. One

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    7

The Role of the RDN in Pediatric Care  (continued) unique feature of pediatric practice is that, depending on the age of the child, some if not all of this information will be obtained from the caregivers. Pediatric RDNs design nutrition interventions to address feeding problems, behavior at mealtimes, and altered energy and nutrient needs. While these interventions focus on optimizing intake for the child, this cannot be accomplished unless the family or caregiver understands the recommendations and is willing and able to adhere. Thus, pediatric RDNs also educate family members and provide referrals to other health care providers such as speech-language pathologists, occupational therapists, and community food programs. RDNs may work in intensive care units (ICUs) that are specialized to either neonates (NICU) or pediatrics (PICU). In each of these ICUs, the RDN plays a specialized role due to the increased level of nutritional risk associated with preterm birth, congenital defects, trauma, sepsis, and critical care. RDNs working in these settings screen patients for level of risk and develop early nutrition interventions for high-risk cases such as children who require enteral and parenteral feedings. Additionally, in the neonate unit, RDNs may educate mothers on how to breastfeed premature infants or, if necessary, supplement infant feeding with high-calorie breast milk fortifiers. Pediatric dietitians work with diverse disorders in several specialized areas of practice encompassing a large variety of

discuss dietetics practice in a few common settings. In addition, clinical dietitians may be certified in a medical specialty and become, for example, diabetes educators, lactation consultants, or nutrition support specialists. Nutrition therapy practice certifications and their requirements are listed in Table 1.3.

1.3  OTHER HEALTH PROFESSIONALS— INTERDISCIPLINARY TEAMS In the health care setting, individuals from different disciplines communicate with each other regularly in order to best care for their patients. Dietitians are integral members of the patient’s health care team and collaborate with physicians, pharmacists, nurses, respiratory therapists, speech pathologists, occupational therapists, social workers, and many others when providing nutritional treatment see Figure 1.2. Dietitians must know the roles of the other team members in order to be effective and to ensure optimal patient care. Table 1.4 covers the education and training requirements for health professionals and the job roles with which a dietetics student should be familiar when first starting to practice dietetics. The practice of medicine by physicians includes the diagnosis, treatment, correction, advisement, or prescription for any human disease, ailment, injury, infirmity, deformity, pain, or other condition, physical or mental. All physicians in the United States have advanced training and certification in a specialized area of medicine or surgery.6 Table 1.5 lists the recognized board specialties and subspecialties. Nutritionally, physicians are responsible for prescribing nutrition support 8  Part 1  The Role of Nutrition Therapy in Health Care

conditions that may impact nutritional needs or status, including the following: • Metabolic disorders such as phenylketonuria, homocystinuria, tyrosinemia, disorders of the urea cycle pathways, methylmalonic and propionic acidemia, fatty acid oxidation disorders, mitochondrial disorders, disorders of carbohydrate metabolism • Genetic disorders such as cystic fibrosis and fragile X syndrome • Gastrointestinal diseases such as inflammatory bowel disease, Crohn’s disease, and ulcerative colitis • Chronic organ disease (kidney disease, heart disease) • Respiratory diseases such as bronchodysplasia • Feeding difficulties related to developmental delay or functional impairments such as cleft palate and eating disorders • Infectious diseases such as HIV • Cancers • Endocrine disorders such as type 1 or type 2 diabetes mellitus References 1. Academy Quality Management Committee. Academy of Nutrition and Dietetics: Revised 2017 Standards of Practice for Registered Dietitian Nutritionists. J Acad Nutr Diet. 2018; 118:141–65. 2. Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: nutrition services for individuals with intellectual and developmental disabilities and special health care needs. J Acad Nutr Diet. 2015; 115:593–608. 3. Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: nutrition guidance for healthy children ages 2 to 11 years. J Acad Nutr Diet. 2014; 114:1257–76.

and nutrition prescriptions for their patients but typically work in collaboration with the RDN. The largest group of health care workers in the United States is nurses. Registered nurses (RNs) assist in the treatment of patients, administer medications and intravenous

Figure 1.2 Collaboration Nutritional care requires collaboration among members of the entire health care team. Interprofessional teams work together to provide optimal patient care.

Source: Courtesy of Marcia Nelms.

Table 1.3 Dietetics Practice Certifications Requirements Specialty

Certifying Organization (webpage)

Requirements

Board Certified Specialist in Pediatric Nutrition (CSP)

Academy of Nutrition and Dietetics/ Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD, 2 years minimum length of RDN status, 2000 hours of pediatric practice within the past 5 years, and successful completion of the Board Certification as a Specialist in Dietetics examination

Board Certified Specialist in Renal Nutrition (CSR)

Academy of Nutrition and Dietetics/ Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD, 2 years minimum length of RDN or RD status, 2000 hours of renal practice within the past 5 years, and successful completion of the Board Certification as a Specialist in Dietetics examination

Board Certified Specialist in Gerontological Nutrition (CSG)

Academy of Nutrition and Dietetics/ Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD, 2 years minimum length of RDN or RD, 2000 hours of gerontological practice within the past 5 years, and successful completion of the Board Certification as a Specialist in Dietetics examination

Board Certified Specialist in Sports Dietetics (CSSD)

Academy of Nutrition and Dietetics/ Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD, 2 years minimum length of RD status, 1500 hours of sports dietetics practice within the past 5 years, and successful completion of the Board Certification as a Specialist in Dietetics examination

Board Certified Specialist in Oncology Nutrition (CSO)

Academy of Nutrition and Dietetics/ Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD, 2 years minimum length of RD status, 2000 hours of oncology dietetics practice within the past 5 years, and successful completion of the Board Certification as a Specialist in Dietetics examination

Advanced Practice Certification Academy of Nutrition and Dietetics/ in Clinical Nutrition Commission on Dietetic Registration (http://cdrnet.org)

Current RDN or RD for 4 calendar years, graduate degree from a US-regionally accredited college or university, document 8000 hours post RDN or RD of clinical nutrition practice no older than the past 15 years (800 of the required hours must be within the past 2 years), and CDR Advanced Practice Certification in Clinical Nutrition Examination

Certified Diabetes Educator (CDE)

National Certification Board for Diabetes Education (www.ncbde.org)

Minimum of 2 years’ experience working as a registered dietitian, minimum of 1000 hours of professional practice experience in diabetes self-management education with a minimum of 40% (400 hours) accrued in the most recent year preceding application, minimum of 15 clock hours of continuing education activities applicable to diabetes within the 2 years prior to applying for certification, and successful completion of the Certified Diabetes Educator examination

Certified Nutrition Support Clinician® (CNSC)

National Board of Nutrition Support Certification (www.nutritioncare.org/ nbnsc)

Current RD, RDN, or Canadian equivalent, at least 2 years’ experience in specialized nutrition support (parenteral and enteral nutrition) recommended for candidates, and successful completion of the Certification Examination for Nutrition Support Clinician

Lactation Consultant (IBCLC)

International Board of Lactation Consultant Examiners (http://iblce.org)

Minimum of 90 hours of continuing education in lactation, 1000 hours of lactation-specific clinical practice within 5 years, and successful completion of the certification examination

Table 1.4 Education and Certification Requirements of Selected Members of the Health Care Team Health Profession

Education

Degree Initials

Credentialing

Physician

Doctoral or professional degree

MD; DO

State licensure exam

Nurse

Two-year degree

AA

State licensure exam

Four-year degree

BSN

Graduate degree

Advanced Practice RN (Nurse Practitioner, Nurse Midwife, Nurse Anesthetist)

Four years graduate education

PharmD

Pharmacist

State licensure exam and National exam (NAPLEX)

Occupational therapist

Clinical doctorate degree

OTD

National exam for registration (NBCOT)

Physical therapist

Clinical doctorate degree

DPT

National exam for registration (NPTE)

Speech-language pathologist

Master’s degree plus a clinical fellowship

MS or MA

National exam for Certificate of Clinical Competence (CCC)

Social worker

Bachelor’s degree or master’s degree

BSW or MSW

State licensing, certification, or registration

Source: Occupational Outlook Handbook (OOH), April 13, 2018. Washington, DC: U.S. Bureau of Labor Statistics. http://www.bls.gov/ooh/

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    9

Table 1.5 American Boards of Medical Specialties • Allergy and Immunology

• Orthopedic Surgery

• Anesthesiology

• Otolaryngology

• Colon and Rectal Surgery

• Pathology

• Dermatology

• Pediatrics

• Emergency Medicine

• Physical Medicine and Rehabilitation

• Family Practice

• Plastic Surgery

• Internal Medicine*

• Preventive Medicine

• Medical Genetics and Genomics Neurological Surgery

• Psychiatry and Neurology

• Nuclear Medicine • Obstetrics and Gynecology • Ophthalmology

• Radiology • Surgery • Thoracic Surgery • Urology

*Subspecialties of Internal Medicine include Adolescent Medicine, Cardiovascular Disease, Critical Care Medicine, Endocrinology, Diabetes and Metabolism, Gastroenterology, Geriatric Medicine, Hematology, Hospice and Palliative Medicine, Infectious Disease, Medical Oncology, Nephrology, Pulmonary Disease, Rheumatology, Sleep Medicine, Sports Medicine. (This partial list was effective August 2017, American Board of Medical Specialties®, www.abms.org.) The subspecialties are only noted for Internal Medicine.

solutions, educate patients on various medical conditions, and provide advice, follow-up care, and emotional support to patients’ family members.6 Since they provide care 24 hours a day, 7 days a week, nurses are commonly responsible for the initial nutrition screening of patients and then documenting a patient’s food intake during hospitalization as well as notifying the dietitian if a patient’s intake is inadequate. Advanced practice nurses such as a nurse practitioner have specialized training that allow for a higher level of patient care such as prescribing medications. A licensed pharmacist dispenses medications and advises the medical staff on the selection and effects of drugs. In addition, pharmacists monitor laboratory results for therapeutic drug levels as well as electrolyte levels for patients receiving parenteral nutrition and review risks for drug–drug and drug–nutrient interactions. Pharmacists are commonly responsible for compounding sterile solutions including parenteral nutrition support solutions.6 Physical therapists help patients reduce pain and improve or restore mobility; teach patients how to prevent or manage their condition so that they will achieve long-term health benefits; work with individuals to prevent the loss of mobility before it occurs by developing fitness- and wellness-oriented programs for healthier and more active lifestyles. Physical therapists can further specialize in these areas: cardiovascular and pulmonary, clinical electrophysiology, geriatric, neurology, orthopedic, pediatric, and sports.6 Physician assistants diagnose illness, develop and manage treatment plans, prescribe medications, and often serve as a patient’s principal health care provider Physician assistants have to be supervised by a physician.6 Occupational therapists evaluate and provide intervention in collaboration with the client, family, care giver; develop, improve, sustain, or restore skills in activities of daily living (ADL), work or productive activities, and play or leisure; identify and facilitate engagement in meaningful and healthy occupations; develop, remediate, or restore sensorimotor, cognitive, or psychosocial components of performance; 10  Part 1  The Role of Nutrition Therapy in Health Care

educate the ­client, family, caregiver, or others in carrying out appropriate nonskilled interventions; and consult with groups, programs, organizations, or communities to provide population-based services.6 They often work with patients with swallowing disorders and clients with physical disabilities to provide special instructions on eating and use of adaptive feeding devices. Respiratory therapists provide testing, treatment and care to patients who have difficulty breathing caused by cardiopulmonary disorders such as heart failure or pulmonary hypertension, chronic respiratory issues like asthma, COPD or cystic fibrosis, and medical emergencies.6 Speech-language pathologists—sometimes called speech therapists—assess, diagnose, treat, and help to prevent speech, language, cognitive, communication, voice, swallowing, fluency, and other related disorders. Speech-language pathologists working in a health center provide clinical services to individuals with swallowing disorders, and they work closely with physicians, nurses, and dietitians to help assess the need for and to provide nutrition support.6 Medical social workers work with individuals and families to provide the psychosocial support needed to cope with chronic, acute, or terminal illnesses. They also educate family caregivers, counsel patients, and help plan for patients’ needs after discharge by arranging community and financial resources to cover medical needs, food-related services, and costs.6

1.4  HEALTH CARE SERVICES AND REIMBURSEMENT FOR MEDICAL NUTRITION THERAPY (MNT) Where do nutrition services fit within our current health care picture? Nutrition therapy remains an essential component of medical treatments, and research indicates its importance will continue to be recognized. The provision of nutrition therapy and its reimbursement are affected by health care financing. The pluralistic system of health care in the United States includes many components: private insurance, group insurance, Medicare, Medicaid, workers’ compensation, the Veterans Health Administration medical care system, Department of Defense hospitals and clinics, the Public Health Service’s Indian Health Service, state and local public health programs, and the Department of Justice’s Federal Bureau of Prisons. Currently, the system is structured around the provision of health insurance. In 2012, 84.6% of the U.S. population was insured, and 15.4% was not.7 Many Americans were forced to live without health insurance because they could not afford it. In the United States currently, there are two general categories of health insurance: private and public. Of the insured population, approximately 64% under age 65 has private insurance and 33% is covered by public health insurance provided by the government. Table 1.6 lists the types of private and public health insurance and typical reimbursements for medical nutrition therapy. The Affordable Care Act (ACA), enacted under President Barack Obama, extended the availability of health insurance to all Americans, began in 2014. By 2015, the uninsured rate was 9.1%. The ACA allows individuals and

Table 1.6 Reimbursements for Nutrition Therapy Services Private Insurance Private health insurancea

Alliance Healthcare Initiative: Children 3–18 years old and their families will be able to see an RDN for nutrition counseling (a minimum of four visits).b

Group contract (e.g., managed care organization)

RDNs can obtain provider numbers that allow for reimbursement of services.

Public Insurance Medicare

Medicare pays RDNs who enroll in the Medicare program as providers. Providers are able to bill Medicare for MNT services provided to Medicare beneficiaries for type 1 diabetes, type 2 diabetes, gestational diabetes education, nondialysis kidney disease, and post–kidney transplant status and more recently Intensive Behavioral Therapy for Obesity.c

Medicaid

Some states include benefits for nutrition services, but there is significant variability among states.

a

Note: Differences in coverage for nutrition services vary by region and insurance.

b http://www.eatrightpro.org/resources/about-us/alliances-and-collaborations/healthier-generation-benefit, accessed August 4, 2017. c

CMS Program Memorandum, MNT Services for Beneficiaries with Diabetes or Renal Disease. Baltimore, MD: Center for Medicare and Medicaid Services. http://www.cms.gov/Regulations-and-Guidance/Guidance/ Transmittals/downloads/B0148.pdf, published August 7, 2001; accessed February 1, 2014. January 1, 2015, the Centers for Medicare & Medicaid Services (CMS) will now pay for Intensive Behavioral Therapy for Obesity for Medicare Part B beneficiaries as a group service, in addition to the existing coverage for individual services. AND. Practice: Getting Paid. http://www.eatrightpro.org/resources/practice/getting-paid, accessed May 12, 2017.

small businesses to compare and purchase health plans similar to those traditionally provided by larger companies. For middle- and low-income families, a significant portion of the cost of health care programs is covered by tax credits. In addition, individual state Medicaid programs are expanding to serve more lower-income Americans. Nutrition services expanded since ACA requires preventative services such as counseling regarding obesity, weight loss, healthy diet, and exercise and behavioral counseling for adults with hyperlipidemia and other known risk factors for cardiovascular and other chronic, diet-related diseases.8

1.5  DEVELOPING CLINICAL SKILLS AND PROFESSIONAL PERFORMANCE The 2017 National Cancer Institute defined medical nutrition therapy as “treatment based on nutrition. It includes assessment of a person’s nutrition status, and giving the appropriate foods or nutrients to treat conditions such as those caused by diabetes, heart disease, and cancer. It may involve simple changes in a person’s diet, or enteral/parenteral nutrition support. Medical nutrition therapy may help patients recover more quickly and spend less time in the hospital.”9 As mentioned previously, RDNs are educated and trained professionals and are the members of the health care team best able to deliver accurate and appropriate clinical judgments in order to provide appropriate nutritional care. Completing the didactic program in dietetics with a bachelor’s degree is your first step to becoming an RDN. The next step, supervised practice, provides the opportunity for a dietetics intern to apply her or his education in the clinical setting. See Box 1.4 for current updates in dietetic education. As a dietetics student, you will acquire a great deal of knowledge during your didactic education. However, students usually do not have the opportunity to apply their knowledge other than through hypothetical disease case assignments or stimulations. When a student enters the clinical environment, usually as a dietetic intern, she or he quickly finds that providing nutrition care requires more than mastery of a textbook. This textbook provides you with information on the NCP, or a medical condition, its diagnosis, and medical and dietary treatment, but it does not integrate the diagnosis or treatment with the patient’s own experiences, symptoms, behaviors, values, social perspectives, and other medical problems. To provide optimal nutritional care, many aspects of a patient’s life must be considered. To do this, the practitioner must be able to think critically in order to solve problems and develop the best solution for a client’s needs. Dietetics educators know that the dietitians’ problem-solving skills, along with their critical thinking skills, evolve with experience and practice. Thus, the path to becoming an RDN requires both education and practice. The act of thinking involves using the mind to organize and integrate information, identify relationships, make inferences, form conclusions, and make decisions.10

Specific Knowledge Base  Nutrition and its role in health and disease is the primary foundational knowledge required to practice as a RDN. RDNs will all have at least a minimum

BOX 1.4

Change to Dietetic Education in 2024. The Commission of Dietetic Registration (CDR) moved to change the entry-level registration eligibility education requirements for dietitians, beginning in 2024, from a baccalaureate degree to a minimum

of a graduate degree. A graduate degree includes a master’s degree, practice doctorate, and/or a doctoral degree. Commission on Dietetic Registration Graduate Degree Registration Eligibility

Requirement. Frequently Asked Questions (FAQ), July 2013. https://www​ .cdrnet.org/vault/2459/web/files/GraduateDegreeFAQJan2017.pdf, accessed August 3, 2017.

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    11

level of knowledge based on the Accreditation Standards for Didactic Programs in Nutrition set by the Accreditation Council for Education in Nutrition and Dietetics (ACEND).10,11,12 Most dietitians exceed the m ­ inimum standards, depending on the programs from which they have graduated, the continuing education choices they make, and the advanced degrees they pursue. The dietitian’s knowledge base includes information and theories related to communications, physical and biological sciences, social sciences, integration of information, research, food science, nutrition, counseling, management, health care systems, informatics, and governance of dietetics practice. The dietitian’s knowledge base is also continually changing and expanding. Learning is a lifelong process, and dietitians engage in continuing education throughout their careers. Nutrition is a developing science, and as new information becomes available, dietitians must apply the new developments to practice. The AND’s Standards of Practice in Nutrition Care and Professional Performance for Registered Dietitian Nutritionists require the dietitian to reflect on her or his practice in order to anticipate and react appropriately to change and thus to remain effective as practitioners.10

Experience  Dietetic students in nutrition therapy courses

often feel overwhelmed by all the information they are expected to know. Though they can effectively apply the information to “mock patients” in case studies or simulations, students do not think themselves capable of applying what they have learned to patients in the “real” clinical setting. This occurs in part because dietitians do not learn from textbooks alone; they also learn by observing, listening to patients, interacting with other health care professionals, reading patients’ medical charts, and reflecting on the situations that arise. Dietitians are required to complete a supervised practice experience (dietetics internship, coordinated program, or individualized supervised practice pathway [ISPP]) before they are eligible to write the exam for registration. This period of supervised practice allows the student to gain experience in all areas of dietetics practice. Real patients with real problems provide the most effective learning experiences by stimulating the dietetics intern’s intellectual curiosity and promoting retention of the information. As an illustration, consider a skill that you developed in the past and now may take for granted: the skill of driving a car. Sometime around the age of 15 to 18, you had the opportunity to drive a car after years of observing others drive. You most likely had to complete a driver’s education course that included learning about all the legal aspects of driving. Then you probably got behind the wheel with the driver training instructor or one of your parents. No doubt that first ride was a little frightening, and you may have made some decisions that could be improved upon. Now compare your performance that first time behind the wheel with the way you drive today. The difference is that now you have had experience driving and making related decisions.

Medical Problem Solving  In addition to having knowledge and skills related to nutritional care, you must also have the ability to identify nutrition-related problems and make decisions regarding the most appropriate nutrition-related solutions.13

12  Part 1  The Role of Nutrition Therapy in Health Care

Consider the following example for you to identify the nutrition-related problem in a clinical setting. The dietitian is alerted that an older patient is not eating most of the food on his trays at mealtime. The dietitian checks the medical record and sees that the patient lost his wife 6 months ago and has no family to visit him. The dietitian visits the patient, and she or he learns that the patient wears dentures. By observing and asking questions, the dietitian determines that the patient is experiencing a great deal of discomfort with them. The dietitian suspects that the cause of the patient’s poor intake might be that he cannot chew the foods due to pain; hence, the dietitian using the NCP recommends that soft, easy-to-chew foods be served to the patient (test of the hypothesis through experimentation). The next day, the nurse reports that the patient’s intake has been 100% for the past three meals.

Evidence-Based Dietetics Practice (EBP)  As defined by the AND, “EBP is the incorporation of systematically reviewed scientific evidence into food and nutrition practice decisions. It integrates professional expertise and judgment with client, customer and community values and evaluates outcomes.”14 Changes in nutrition therapy recommendations are inevitable because of new developments in science and medicine, including ongoing research in nutrition therapy. Some of what you learn in your professional training will be outdated by the time you finish your internship and become an RDN. As a dietitian, you must be able to critically review research findings by utilizing the research methodology skills you learned during your dietetics education. Dietetics practice should not be based on tradition but on evidenced-based research. For example, imagine you are an RDN working in a facility where the standard of practice is that the initial diet order for all postoperative patients is clear liquids. However, you have just attended the local dietetic meeting, and the speaker mentioned that most abdominal postoperative patients can tolerate a regular house diet and do not necessarily need to be on clear liquids. What do you do? A search of the medical literature reveals several research articles that support the use of regular diets postoperatively.15–19 You should critically analyze each article and summarize the evidence. If the evidence supports use of regular diets postoperatively, this information should be presented to the appropriate staff members at your facility for discussion. The AND has been instrumental in the development of the Evidence Analysis Library and Evidence-Based Guidelines, which are posted online for its members. As defined by AND, a guideline is a “systematically developed statement based on scientific evidence to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances.”14 Guidelines are tied to the evidence-based library, which is updated as new research is published. This process is not unique to dietetics, and it is rapidly becoming the standard for all health care professions. RDNs use EBP guidelines from all other health care professions to provide the optimal level of health care for their clients. Problem Solving  The process of problem solving involves obtaining information about the problem and then using the information to effectively solve the problem. For instance, suppose you walk into a room and flip the light switch, but the

light does not go on. To determine the source of the problem, you would probably check the light bulb first. If the light bulb is not burned out, then other possible sources of the problem need to be checked. A similar process is used to determine a patient’s nutritional problem. The practitioner can assume that there is a problem when the patient’s nutritional status is not optimal; the patient’s nutrition-related information is then collected in order to find “clues” that point to the nutrition diagnosis and solution. Consider the client who presents with abdominal cramps, diarrhea, and flatulence throughout the day. Assessment information includes: 50-year-old Asian-American female, postmenopausal; family medical history includes a 75-year-old mother who developed osteoporosis resulting in a broken hip; and her 24-hour diet recall indicates she recently started drinking an 8-oz glass of 1% fat milk at every meal and sometimes before going to bed, because her doctor had told her to consume more calcium in her diet. Although additional information remains to be collected to rule out other possible problems, one plausible explanation for the client’s abdominal symptoms could be her inability to digest lactose (altered GI function) related to her recent increase in milk consumption.

Decision Making Making a decision involves making a

choice. The activities involved in decision making include the following: • • • • •

Identify and define a problem or situation. Assess all options for solving the problem. Weigh each option against a set of criteria. Test possible options. Consider the consequences of the decision (examine the positive and negative aspects of each option). • Make a final decision. The activities do not necessarily take place in a particular sequence. The clinician is usually moving back and forth and considering things simultaneously. The outcome of this process is a decision that is informed and supported by evidence and reasoning. Continuing the previous example, if it is determined that a patient has lactose intolerance, options for solving this problem could include the following: discontinue the use of milk but take a calcium supplement; drink smaller quantities of milk more frequently; or continue to consume milk with every meal but use products containing lactase.

Diagnostic Reasoning  Diagnostic reasoning is defined as

a series of clinical judgments that result in an informal judgment or a formal diagnosis.20 Physicians are responsible for making a patient’s medical diagnosis. However, dietitians continually use the process of diagnostic reasoning to determine the nutrition diagnosis and monitor a patient’s progress and/ or response to nutrition therapy. For example, a patient with protein-energy malnutrition (PEM) will manifest specific signs and symptoms associated with this condition. Once nutrition interventions have begun, the dietitian continues to observe anthropometric and laboratory values and compare them with those common to PEM. This diagnostic reasoning process allows the dietitian to monitor the patient’s progress.

Figure 1.3 Creative Menu Planning This salad with mixed greens, vegetables, and protein can accommodate many nutrition therapies.

Source: Courtesy of Peter Madril, MS, RDN, LD.

Attitudes  Attitudes reflect the dietitian’s values and should ensure that clinical judgment is made fairly and responsibly. Dietitian’s attitude includes integrity, thinking independently, and risk taking. Her or his questioning of a standard not based on the latest scientific evidence may change a traditional practice of postoperative feeding (thinking independently); it takes courage to take action even when change is based on solid research that improves client care (risk taking). A creative attitude toward menu planning (see Figure 1.3) facilitates problem solving with clients who are finding necessary dietary changes difficult.

Standards Professional standards include ethical standards, c­ riteriabased evaluation of outcomes, and Standards for Professional Performance. The AND’s Code of Ethics and Standards of Professional Performance both require measurable, evidence-based evaluation of outcomes. For example, one principle in the Code of Ethics is “The dietetic practitioner practices dietetics based on evidence-based principles and current information.”21 While the Standards of Professional Performance 10 are broader statements to help guide the practice of dietetics, they do require that dietitians continuously improve their knowledge and skills and that they regularly evaluate the quality of their practice, revising it if necessary. An important link among the NCP, the Standards of Professional Performance, and the Code of Ethics is that outcomes research may be a consequence of regular evaluation of practice quality. If abdominal postoperative diets are changed from clear liquid diets to regular house diets, data should be collected on patient outcomes. Did this impact surgical outcomes in any way? Published research on the outcomes would be added to the evidencedbased research library, possibly resulting in the release of updated clinical nutrition care intervention guidelines for postoperative feeding. In the classroom, critical thinking

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    13

typically is used for exams and assignments, but for the practitioner, critical thinking leads to higher levels of clinical reasoning that could influence the practice of dietetics.

Levels of Clinical Practice When a dietetics student completes the required supervised practice and then passes the Registration Examination for Dietitians, she or he is considered to have entry-level competence. As the new dietitian develops professionally and moves beyond entry level, she or he becomes more proficient and develops expertise in her or his area of practice. For an entry-level dietitian, skills may be at a basic level. The dietitian has only limited experience and may rely on the facts and sets of rules or principles to make decisions. These facts and principles are perceived as appropriate because they are established by the accreditation and educational authorities. There may be little adaptation of the principles to the patient’s own unique needs. As the dietitian becomes more experienced, she or he begins to examine alternatives independently and systematically, disconnecting from the authorities. The dietitian is better prepared to anticipate possible outcomes and identify a broader range of options. It is evident that there is more than

one solution to a problem and that the patient’s own unique needs will influence which solutions are viable. The highest level of clinical practice involves an analysis of the entire situation: the person, the illness, the meaning of the illness to that person, the person’s lifestyle, the family’s needs, the social influences, and the physical environment in which the person lives.21 At this level, the dietitian is acting in support of the patient, the principles of the NCP, and the professional standards that underlie the discipline of dietetics.

1.6 CONCLUSION During the medical nutrition therapy course, you will be required to complete assignments that will help you apply much of the information presented in this text. You may find some assignments so overwhelming that you do not know where to start. Do not despair; after you have completed the first such assignment, the subsequent ones will become easier, and you will gain confidence just as the inexperienced driver does with daily practice driving a car. As with driving, after you start your supervised practice, your fears will decrease and your competence will grow with each new patient.

CHAPTER REVIEW QUESTIONS 1. Identify members of the clinical nutrition care team. What are the major tasks performed by the clinical dietitian and the chief clinical manager? 2. Why is continuing education ­necessary for the practice of dietetics?

3. A new friend finds out you are a nutrition major and asks your advice about overeating late in the day. She tells you that she has no time to eat lunch and wants to save money, but then she eats too much when she gets home. Suggest three possible solutions. What are the possible

consequences (both positive and negative) of each solution? How could your attitude affect each solution? 4. Why is outcomes research necessary for the advancement of dietetics practice?

ENDNOTE 1. The Commission on Dietetic Registration allows registered dietitian nutritionist (RDN) or registered dietitian (RD) credential to be used.

REFERENCES 1. Cassell JA. Carry the Flame: The History of ADA. Chicago, IL: American Dietetic Association; 1990. 2. Butterworth E. The skeleton in the hospital closet. Nutrition Today. 1974; 9:4–8. 3. Winterfeldt E, Bogle M, Ebro L. Dietetics: Practice and Future Trends. 2nd ed. Sudbury, MA: Jones & Bartlett; 2005. 4. Lacey K, Pritchett E. Nutrition care process and model: ADA adopts road map to quality care and outcomes management. J Amer Diet Assoc. 2003; 103:1061–72.

5. Academy of Nutrition and Dietetics. eNutrition Care Process and Terminology (eNCPT) Academy of Nutrition and Dietetics, https://www. ncpro.org/, accessed September 9, 2017. 6. Occupational Outlook Handbook (OOH), 2012–13 ed. Washington, DC: U.S. Bureau of Labor Statistics. http://www.bls.gov/ooh/, accessed May 15, 2017. 7. DeNavas-Walt C, Proctor BD, Smith JC. Income, poverty, and health insurance coverage in the United States: 2012. Washington, DC: U.S. Department of Commerce, Economics and

14  Part 1  The Role of Nutrition Therapy in Health Care

Statistics Administration, U.S. Census Bureau. http://www.census.gov/prod/2013pubs/p60-245.pdf 8. Affordable Care Act. U.S. Department of Health & Human Services, 200 Independence Avenue, S.W. Washington, D.C. 20201. https:// www.healthcare.gov/, accessed May 19, 2017. 9. New RD-Provided Nutrition Counseling Coverage for Obese/Overweight Children. Chicago, IL: American Dietetic Association. http://www.eatright.org/alliance 10. Delphi Report. Critical thinking: a statement of expert consensus for purposes of educational

assessment and instruction (ERIC Reproduction Service No. 315–423). Millbrae, CA: California Academic Press; 1990. 11. Academy Quality Management Committee. Academy of Nutrition and Dietetics: Revised 2017 Standards of Practice for Registered Dietitian Nutritionists. J Acad Nutr Diet. 2018; 118:141–65. 12. Kataoka-Yahiro M, Saylor A. Critical thinking model for nursing judgment. J Nurs Educ. 1994; 33:351. 13. ACEND Accreditation Standards for Didactic Programs and Standards for Internship Programs in Nutrition & Dietetics Leading to the RD Credential. Updated June 1, 2017. http://www​ .eatrightpro.org/acend/, accessed August 4, 2017. 14. ACEND Accreditation Standards for Nutrition and Dietetics Didactic Programs.

Updated January 26, 2018. https://www .eatrightpro.org/-/media/eatrightpro-files/acend/ about-program-accreditation/accreditationstandards/2017standardsfordpdprograms.pdf?la= en&hash=B981CA74C919679C37830041802FF4E711C9E9CF, / accessed July 31, 2018. 15. Elstein AS, Shulman LS, Sprafka SA. Medical Problem Solving: An Analysis of Clinical Reasoning. Cambridge, MA: Harvard University Press; 1978. 16. Evidence Analysis Library. Chicago, IL: Academy of Nutrition and Dietetics. http://www​ .adaevidencelibrary.com 17. Jeffery KM, Harkins B, Cresci GA, Martindale RG. The clear liquid diet is no longer a necessity in the routine postoperative management of surgical patients. American Surgery. 1996; 63:167–70.

trial of a regular diet as the first meal in gynecologic oncology patients undergoing intraabdominal surgery. Obstet Gynecol. 2002; 100(Suppl):230–34. 19. Lewis SJ, Andersen HK, Thomas S. Early enteral nutrition within 24 h of intestinal surgery versus later commencement of feeding: a systematic review and meta-analysis. J Gastrointest Surg. 2009; 13(3):569–75. 20. Carnevali D, Thomas MD. Diagnostic Reasoning and Treatment Decision Making in Nursing. Philadelphia, PA: Lippincott; 1993. 21. Academy of Nutrition and Dietetics. American Dietetic Association/Commission on Dietetic Registration Code of Ethics for the Profession of Dietetics and Process for Consideration of Ethics Issues. J Am Diet Assoc. 2009; 109:1461–67.

18. Pearl ML, Frandina M, Mahler L, Valea FA, DiSilvestro PA, Chalas EA. Randomized controlled

Chapter 1  Role of the Registered Dietitian Nutritionist in the Health Care System    15

Part 2 The Nutrition Care Process IN THIS PART Chapter 2  OVERVIEW: THE NUTRITION CARE PROCESS

Chapter 3  NUTRITION ASSESSMENT: ­ OUNDATION OF THE NUTRITION F CARE PROCESS

Chapter 4  NUTRITION INTERVENTION, NUTRITION MONITORING AND EVALUATION

Chapter 5  ENTERAL AND PARENTERAL ­NUTRITION SUPPORT

Chapter 6  NUTRITION INFORMATICS AND

Source: XiXinXing/Shutterstock.com

17

Source: Courtesy of Marcia Nelms.

DOCUMENTATION OF THE NUTRITION CARE PROCESS

17

CHAPTER 2

Source: iStock.com/Fertnig

Overview: The Nutrition Care Process Kathryn Sucher, ScD, RDN Faculty Emerita, San Jose State University

LEA RNING O B JECTIV ES LO 2.1  Describe at least three factors that impact nutritional status. LO 2.2  Explain why it is important to know the factors that influence a ­nutrition problem.

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LO 2.3  Define the nutrition care process (NCP) and its purpose. LO 2.4  Describe the purpose of the screening and referral system and who might be responsible for completing the tasks.

LO 2.5  Describe the four steps involved in the nutrition care process and each of their components. LO 2.6  List the different types of charting formats for documentation.

G LOSSARY AND’s evidence-based guides for ­practice—specific nutrition practice guidelines available from the AND’s Evidence Analysis Library environmental factors—social and economic factors (wages, transportation, etc.) that impact both lifestyle choices and the consumption of food and nutrients; other external factors such as food safety and sanitation determine the quality of food that is consumed, and food availability/access contributes to the amount and type of food consumed evidence-based practice guides—a series of guiding statements and treatment algorithms that are developed using a systematic review process of identifying, analyzing, and synthesizing scientific evidence food and nutrient factors—the amount and type of foods and nutrients that are consumed and therefore made available to the body human biological factors—conditions that determine a person’s nutrient requirements; one’s age, gender, and stage of growth and development are used to estimate kcal and nutrient needs; illnesses that alter organ function or metabolism influence not only the amount of nutrients required but also the form of nutrients that the body needs and can tolerate ideal goals—science-based values intended to control or improve specific health conditions lifestyle factors—a person’s knowledge, attitudes/beliefs, and behavior patterns that directly impact the choices that are made

regarding food and physical activity; assessment of these factors provides information about a person’s ability and/or readiness to make behavior changes nutrition assessment—a systematic process of obtaining, verifying, and interpreting data in order to make decisions about the nature and cause of nutrition-related problems nutrition care process (NCP)—a systematic problem-solving method developed by the AND that dietetics practitioners use to think critically, make decisions addressing nutrition-related problems, and provide safe, effective, high-quality nutrition care nutrition care process and terminology (eNCPT)—dietetic language for nutrition care nutrition diagnosis—the identification and descriptive labeling of an actual occurrence of a nutrition problem that dietetics practitioners are responsible for treating independently nutrition intervention—a specific set of activities and associated materials used to address a (nutrition-related) problem nutrition monitoring and evaluation— active measurement and documentation of the appropriate outcome indicators relevant to a nutrition diagnosis in order to determine the degree to which progress is being made and whether or not the client’s goals are being met outcomes—the desired changes to be achieved over time as a result of nutrition intervention

2.1  IMPROVING HEALTH AND NUTRITIONAL STATUS THROUGH NUTRITION CARE Health Status A person’s state of health is a continuum that can change from (1) being healthy and resistant to disease, to (2) having an acute illness, to (3) living with a chronic disease or condition that significantly alters one’s capacity to function well, and finally to (4) having a terminal illness. Regardless of the state of health, nutrition is very important. Registered dietitian nutritionists (RDN) are uniquely qualified to provide nutrition care to persons in different states of health to improve their nutritional status. The focus of nutrition care is different for various states of health. For example, a primary prevention strategy for a healthy adult may be to promote appropriate caloric balance and physical activity to prevent undesirable weight gain and thus maintain health. For a person who has identified health risk factors such as a family history of cardiovascular disease, nutrition education for the relationship between dietary saturated fat and LDL blood cholesterol may be appropriate, whereas the goal of nutrition intervention in patients who have already developed chronic diseases is to help reduce complications and prevent malnutrition. Even in

outcome measures—data used to evaluate the success of interventions; includes direct nutrition outcomes, clinical and health status outcomes, patient-/client-centered outcomes, and health-care utilization and cost outcomes outcomes management system—a system that evaluates the effectiveness and efficiency of the entire NCP: assessment, diagnosis, implementation, cost, and other factors; it links care processes and resource utilization with outcomes patient/client centered—describes care that considers patients’ cultural traditions, personal preferences and values, family situations, and lifestyles PES—problem, etiology, and signs and symptoms; the format used in the NCP to write a nutrition diagnosis; it clarifies a specific nutrition problem and logically links the nutrition diagnosis to nutrition intervention and to monitoring and evaluation screening and referral system—a supportive system to the Nutrition Care Process and Model that helps identify those persons who would benefit from nutrition care standardized language—a uniform terminology that is used to describe practice system factors—external factors (health care, education, and food supply systems) that influence the type of services that are available to individuals and how these services are delivered

palliative care, nutrition interventions assist with supporting quality of life and functional status.

Nutritional Status In addition to understanding the goal of nutrition care as it relates to a person’s health status, it is also important to evaluate and determine a person’s nutritional status. Assessing a person’s nutritional status involves not only comparing the amounts and types of nutrients that a person consumes to nutrient requirements at various stages throughout the continuum of growth, health, and illness but also examining the wide variety of factors that influence both nutrient intake and nutrient requirements. These same factors are listed in Table 2.1. If one consumes adequate amounts and types of nutrients to support and optimize a given health state, then nutrient intake and nutrient requirements are considered to be balanced. However, if there is an inadequate or excessive intake of nutrients, or the form of nutrients is not well utilized by the body, a nutrient “imbalance” is present. Nutrient imbalance can result in significant health consequences. An excess of kilocalories (kcal) and undesirable eating patterns are associated with the progression of a number of chronic diseases such as obesity, diabetes mellitus, coronary artery disease, and hypertension. Inadequate intake of kcal and Chapter 2  Overview: The Nutrition Care Process   19

Table 2.1 Factors Affecting Nutritional Status 1. Human Biological Factors (determine nutrient requirements— normal, increased, decreased, change in form, etc.)  

a. Biological factors (age, sex, genetics)

 

b. Physiological phases (growth, pregnancy, lactation, aging)

 

c. Pathological factors (disease, trauma, altered organ function or metabolism)

2. Lifestyle Factors (determine food, physical activity, and related choices)  

a. Attitudes/beliefs

 

b. Knowledge

 

c. Behaviors

3. Food and Nutrient Factors (determine the type and amount of nutrients available for use by the body)  

a. Intake/composition

 

b. Quantity

 

c. Quality

4. Environmental Factors (external influences that impact consumption and lifestyle)  

a. Social (cultural food practices and beliefs, parenting, peer influences)

 

b. Economic (household finances, economy of the community/ country)

 

c. Food safety and sanitation (contaminated or unwholesome food, unsafe food handling)

 

d. Food availability/access

5. System Factors (external influences that impact on delivery and services)  

a. Health care system

 

b. Educational system

 

c. Food supply system (industry, agriculture, institutions)

Source: Adapted from Splett P, Academy of Nutrition and Dietetics Task Force. Conceptual Framework for a Standardized Nutrition Language; 2004.

certain nutrients such as protein, on the other hand, can contribute to a compromised immune system and poor wound healing. Comparing nutrient intake to nutrient requirements alone, however, does not describe the broader picture of nutritional status. Even though nutrient balance implies that one is consuming all of the necessary nutrients in their appropriate amounts, assessing nutritional status is not merely a simple equation of intake compared to needs. A positive nutritional status implies that a number of internal and external factors that support optimal nutritional health are also present. Human biological factors such as age, sex, physiological stage, illness, and physical and functional abilities determine nutrient requirements. For example, a mother who is breastfeeding needs to consume more kcal and protein compared to a non-breastfeeding mother. Infants and children require a much higher kilocalorie level per kilogram than an adult in order to support appropriate growth and development. 20  Part 2  The Nutrition Care Process

Energy and protein needs are also increased following major surgery. Furthermore, the form of nutrient may need to be altered depending on the degree of organ function. A person who has had a large portion of the small intestine removed may not be able to digest or absorb large molecules such as triglycerides and would benefit from specialized nutrient forms such as medium-chain triglycerides. Lifestyle ­factors including attitudes, knowledge, and behaviors influence the type of choices that one makes about food and physical activity. For instance, understanding which foods contain saturated fat can influence what type and amount of meats and added fats a person consumes. Food and nutrient factors are the nutrients that are available for use by the body. Obtaining accurate information about a person’s dietary intake is essential to evaluating nutritional status and adequacy of their diet. Environmental factors such as social and cultural food preferences and practices are external influences that impact both food consumption and lifestyle choices. For example, people frequently consume more food than usual at a social event where food is served. It is also common that adults prefer the types of foods that were typically consumed in the household where they grew up as a child. Cultural background will introduce particular foods into one’s diet. Finally, system factors such as the health system, educational system, and food supply system impact the delivery of food, nutrition, and health services. A family whose income is near or at the poverty level or that lives in an area with limited food resources will likely purchase fewer fresh foods. Key Concepts: Health Status and Nutritional Status • Nutrition is important to promote health and prevent and treat ­disease states. • Adequacy of nutrient intake is important but does not completely describe nutritional status. • Determination of a person’s nutritional status is dependent on a wide variety of factors (biological, pathological, behavioral, ­cognitive, environmental, and systems).

It is important to determine both a person’s health status and nutritional status because these both guide the type of nutrition care provided. This chapter describes how dietetics practitioners use the NCP developed by the Academy of Nutrition and Dietetics (AND) to provide quality evidence-based nutrition care to individuals and groups to improve both health and nutritional status.

2.2  PURPOSE OF PROVIDING NUTRITION CARE The purpose of providing nutrition care is to restore a state of nutritional balance by influencing factors are contributing to the imbalance or altered state of nutritional status. Because of the wide variety of and interactions among the many variables discussed previously and listed in Table 2.1, identifying the underlying causes of a nutritional status imbalance can be a complex process. If a person’s caloric intake is less than desired, it is important to determine which, if any, of

the following are contributing to the cause of this problem: a disease condition that is increasing the nutrient needs, a lack of knowledge as to how many calories are in certain foods, a lack of resources (money, food preparation skills, transportation), or a cultural belief about limiting the intake of certain foods. Accurately determining the underlying, or “root,” cause of the problem will permit the selection of the most appropriate nutrition intervention. For example, if lack of financial resources is the main reason why a person is not consuming adequate kcal, providing only a list of expensive oral supplements will not be very effective. It might also be necessary to coordinate nutrition care and refer the client for support services and food aid. Thus, it is necessary to know the factors that influence a problem in order to provide nutrition interventions that are most likely to alleviate the problem. Key Concept: Nutrition Care • Providing nutrition care can influence and change the factors that contribute to an imbalance in nutritional status and thus restore nutritional health.

2.3  THE AND’S STANDARDIZED NCP The nutrition care process (NCP) is defined as “a systematic problem solving method that dietetics practitioners use to critically think and make decisions to address nutrition related problems and provide safe, effective, high quality nutrition care.”1 This NCP consists of four distinct but interrelated and connected steps: (1) nutrition assessment, (2) nutrition diagnosis, (3) nutrition intervention, and (4) nutrition monitoring and evaluation.1 Subsequent to the development of the NCP steps and model, workgroups were appointed to create a system of standardized language for each of the four steps of the NCP. A Nutrition Care Process/Standardized Language (NCP/SL) Committee continues to meet in order to evaluate and revise the language as needed. This committee also assists in the development of resources for implementation of the NCP, including the Academy of Nutrition and Dietetics. Nutrition Terminology Reference Manual (eNCPT): Dietetics Language for Nutrition Care.

Standardized Nutrition Language Standardized language refers to a uniform terminology that is used to describe professional practice. Many health professionals including physicians, nurses, and physical therapists use standardized terminology. Prior to the development of the NCP, the lack of a standardized nutrition language and common terminology made it very difficult for dietetics practitioners to communicate consistently with each other and other health professionals. Nutrition problems and interventions were often charted using broad, nonspecific language. For example, “poor nutritional status,” “at risk for malnutrition,” or “nutritional imbalance” might be noted in the chart as a red flag for nutrition care; however, these could refer to a number of conditions such as a change in weight, poor intake, or difficulty with chewing or swallowing. Nutrition

care plans likewise might have employed vague terms such as “complete nutrition assessment,” “monitor weight or dietary intake,” and/or “provide nutrition education.” These inconsistent terms made it difficult to establish specific and clear goals. In addition, there was no easy way to classify, measure, and report on the outcomes of nutrition interventions in various patient populations in order to demonstrate the effectiveness of nutrition care. The lack of specific uniform terminology also made it impossible to gather data needed for research, education, and reimbursement justification via outcomes analysis. Most notably missing was language that described specific nutrition problems. The standardized terminology now allows dietetics practitioners to make explicit that which had been implicit in the past. The standardized language consists of precise phrases (“terms”) that are organized into groups (“domains”) and assigned unique alphanumeric code numbers (e.g., “NC-1.1”). There are sets of standardized terminology: (1) nutrition diagnosis; (2) nutrition assessment; (3) nutrition intervention, and (4) monitoring and evaluation. The use of all sets of terms together connects each of the steps of the NCP. For instance, the assessment data of the food/nutrition-related history domain are likely to provide signs and symptoms that will confirm a nutrition diagnosis in the intake domain, whereas if a behavioral–environmental nutrition problem is suspected, then further data involving knowledge/beliefs and attitudes should be obtained to rule in or rule out the presence of that diagnosis. The standardized terms, their classifications, and their use within each step of the NCP are outlined in ­Figure 2.1 and discussed in more detail under “Steps of the NCP.”

Use of the NCP to Improve Quality of Care The NCP is a standardized process—a consistent structure and framework used to provide nutrition care—not standardized or “generic” care. When professionals use a systematic process with standardized language, there is less variation of practice and a higher degree of predictability in terms of outcomes. The Institute of Medicine defines quality as “the degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are consistent with current professional knowledge.”2 Quality performances can be assessed by measuring clients’ outcomes (end results of intervention and treatment) or the degree to which providers adhere to an accepted care process. Clients and patients want service that results in positive outcomes. Health care administrators, payers, and the government require cost-effective, high-quality service based on current evidence-based practice. Use of the NCP greatly increases the dietetics practitioner’s potential to provide high-quality nutrition care to individuals and groups. It combines the process of care (the systematic and consistent steps of the NCP) with the content of care (incorporation of evidence-based practice guides) to improve both quality of care and nutritional status (see Figure 2.2). The other significant benefit of using the NCP is the ability to clearly state patient goals and evaluate outcomes. Chapter 2  Overview: The Nutrition Care Process   21

Figure 2.1 Overview of the Nutrition Care Process Standardized Language Nutrition Diagnosis Terminology

Nutrition Intervention Terminology

Intake (NI) Clinical (NC) Behavioral-Environmental (NB) Other (NO)

Food and/or Nutrient Delivery (ND) Nutrition Education (E) Nutrition Counseling (C) Coordination of Nutrition Care (RC)

NCP Step 1: Nutrition Assessment

NCP Step 2: Nutrition Diagnosis

NCP Step 3: Nutrition Intervention

NCP Step 4: Nutrition Monitoring and Evaluation

Nutrition Assessment Terminology Food/Nutrition-Related History (FH) Anthropometric Measurements (AD) Biochemical Data, Medical Tests, and Procedures (BD) Nutrition-Focused Physical Findings (PD) Client History (CH) Comparative Standards (CS)

Figure 2.2 Demonstrating Quality

thinking skills. Critical thinking (see Chapter  1) integrates facts, informed opinions, active listening, Content of Care Process of Care Outcome and observations; it is creative and Best evidence Nutrition Care Improved quality rational, and it requires the ability Scientific principles Process and Model of care and health to conceptualize. Each step of the Protocols status NCP identifies unique and specific types of critical thinking that, when Source: Adapted from Slide #8 of ADA’S Nutrition Care Process and Model: Providing Quality Nutrition applied, improve the likelihood that Care in a Variety of Settings Power Point Prepared by ADA’S Nutrition Care Process Task Force, 2004. the process is being implemented in an effective manner. These specific critical thinking skills are described in Table 2.2. Key Concepts: The AND’s Standardized Nutrition Care Process The four steps of the nutrition care process (NCP) are: • Nutrition assessment • Nutrition diagnosis • Nutrition intervention • Nutrition monitoring and evaluation By using the NCP, dietetics practitioners can demonstrate that nutrition care improves outcomes because it: • Is a systematic method used to make decisions to provide safe and effective care. • Provides a common language for documenting and communicating the impact of nutrition care. • Relies on an evidence-based approach. • Uses specific critical thinking skills for each step.

Critical Thinking The NCP also enhances the quality of care provided by dietetics practitioners through the use of specific critical 22  Part 2  The Nutrition Care Process

2.4  BIG PICTURE OF NUTRITION CARE: THE MODEL The provision of nutrition care does not occur in a vacuum. The Nutrition Care Model in Figure 2.3 is a visual representation that reflects key concepts of each step of the NCP and illustrates the greater context within which nutrition care is provided. The model also identifies other systems that influence and impact the quality of care. It depicts the overlapping relationships of these components and how they interact to result in the best nutrition care possible.

Central Core Central to providing nutrition care is the relationship between the client and the dietetics practitioner or team of ­dietetics practitioners. The client’s previous e­ xperiences and ­readiness for change as well as the ability of the ­d ietetics practitioner to establish trust, demonstrate empathy, and communicate effectively with the client influence this

Table 2.2 Critical Thinking Used in the Nutrition Care Process Nutrition Assessment • Observe for nonverbal and verbal cues to prompt effective ­interviewing methods. • Determine appropriate data to collect.

client is aware of the purpose of care and participates in the decision-making process of goal setting and intervention selection. This central core reinforces the importance of providing care that is individualized and patient/­client centered.

• Select assessment tools and procedures.

Two Outer Rings

• Apply assessment tools in valid and reliable ways.

The outermost ring of the model identifies environmental factors—including practice settings, health care systems, social systems, and economics—that can have an impact on the ability of the client to receive and benefit from the interventions of nutrition care. Dietetics practitioners need to assess these factors and be able to evaluate the degree to which they may either be positive or negative influences on the outcomes of care. A health care plan that allows for up to three outpatient nutrition counseling sessions per year at low cost (e.g., copay only) to the client is a much more positive external influence than a health care plan in which the client has to pay all costs for each visit. The inner adjoining ring recognizes the strengths that dietetics practitioners bring to the NCP. These include professional knowledge/skills and competencies, code of ethics, evidence-based practice, and skills of critical thinking, collaboration, and communication. These are the knowledge and skills that registered dietitians and dietetic technicians obtain through accredited didactic and supervised practice programs. Providing nutrition care that is based on sound scientific evidence increases the likelihood that there will be a positive outcome for the client. Nutrition care also requires a great deal of collaboration with other health care professionals and community services.

• Distinguish relevant from irrelevant data. • Distinguish important from unimportant data. • Validate the data. • Organize and categorize the data in a meaningful framework that relates to nutrition problems. Nutrition Diagnosis • Find patterns and relationships among the data and possible causes. • Make inferences (e.g., “If this continues to occur, then this is likely to happen”). • State the problem clearly and singularly. • Suspend judgment (be objective and factual). • Make interdisciplinary connections. • Rule in/rule out specific diagnoses. • Prioritize the relative importance of problems. • Determine when a problem requires consultation with or referral to another provider. Nutrition Intervention • Set and prioritize goals. • Define the nutrition prescription or basic plan. • Make interdisciplinary connections. • Initiate behavioral and other interventions. • Match intervention strategies with client needs, diagnoses, and values. • Choose from among alternatives to determine a course of action. • Specify the time and frequency of care. Nutrition Monitoring and Evaluation • Select appropriate indicators/measures. • Use appropriate reference standards for comparison. • Define where patient/client is now in terms of expected outcomes. • Explain variance from expected outcomes. • Determine factors that help or hinder progress. • Decide between discharge or continuation of nutrition care.

relationship. If a person believes that changing her intake of saturated fat will decrease her risk of cardiovascular disease and has had previous nutrition counseling that was helpful, that person is more likely to want to meet again with a dietitian; in contrast, an individual who believes that lifestyle behavior changes will have little to no impact on the risk of disease will probably be less receptive. It is important for the dietetics practitioner to establish trust and be able to communicate effectively with others, and it is essential that the client be actively involved in the care whenever possible and if culturally acceptable. This means that the

Supportive Systems: Screening and Referral System and Outcomes Management System Although the two supportive systems—the screening and referral system and the outcomes management system— are essential to providing effective and efficient nutrition care, they are not considered steps of the NCP itself, primarily because they may not be accomplished solely by dietetics practitioners. A screening and referral system identifies those individuals or groups who would benefit from ­nutrition care provided by dietetics practitioners. Screening may be completed by nurses, by clients themselves, or through physician referral. Regardless of whether dietetics ­practitioners are actively involved in conducting the screening process, they are still accountable for providing input into the development of appropriate screening parameters to ensure that the right questions are asked. They should also evaluate how effectively the screening process identifies the clients who require nutrition care. Screening ­parameters need to be tailored to the population and to the n ­ utrition care services provided. A referral process may also ensure that clients are reliably connected with dietetics ­practitioners who will ultimately provide the nutrition care or medical nutrition therapy that is necessary. For example, using a nutrition screening tool at elderly congregate meal sites can identify those clients who are at risk and could then be seen by the dietetic practitioner employed at a senior center. Chapter 2  Overview: The Nutrition Care Process   23

Figure 2.3 Nutrition Care Process Model

The Nutrition Care Process Model

n oratio llab o C

&C

01

Nutrition Diagnosis P - Identify problem E - Determine etiology/cause S - State signs and symptoms

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ti c e Prac

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Nutrition Intervention Determine intervention and prescription Formulate goals and determine action Implement action

ce

of E

Nutrition Monitoring and Evaluation Select or identify quality indicators Monitor and Evaluate resolution of diagnosis

02

h Care Systems

Individual/ Population Interacts with Nutrition Professional

04

cie s

Healt

Nutrition Assessment and Reassessment Obtain/collect important and relevant data Analyze/interpret collected data

om pe ten

ation unic

Nutritio n&

Skills

mm Co

Die tet ics Kn ow l

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Economics

Identify risk factors Use appropriate tools and methods Involve interdisciplinary collaboration

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Screening and Referral System

Settings

-ba

Practice

03

Do

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Outcomes Management System Research NCP Use aggregated data to conduct research Conduct continuous quality improvement Calculate and report quality indicators

io n

l Th C r iti c a

in k

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S o ci a l S ys t e m s

Source: Swan WI, Vivanti A, Hakel-Smith NA, et al. Nutrition Care Process and Model Update: toward realizing people-centered care and outcomes ­management. J Acad Nutr Diet. 2017; 117: 2003–14; Figure 2, p. 2008.

Key Concepts: Nutrition Care Process and Model • Nutrition care is provided within the context of a larger model that includes a central core focused on individualized care and positive relationships. • Both external (environmental) and internal (resources of dietetics practitioner) factors influence the type of nutrition care provided. • The steps of the NCP are supported by two other systems: the screening and referral system and the outcomes management ­system. Dietetics practitioners participate in both of these systems, but may not have sole responsibility for accomplishing these tasks.

The other system supporting the NCP is the outcomes management system. An outcomes management system is used to evaluate the effectiveness and efficiency of the entire 24  Part 2  The Nutrition Care Process

NCP (assessment, diagnosis, interventions, outcomes, costs, and other factors) when nutrition care is provided to a number of patients. Outcomes management is different from the fourth step, nutrition monitoring and evaluation, which refers to the evaluation of a single patient’s/client’s progress in achieving goals and desired outcomes. Health care organizations use complex information management systems to manage resources and track performance. Selected information documented throughout the NCP is entered into these central information management systems and structured databases. Relevant aggregate data (data from a number of individual sources that have been summed together to create a larger whole) can then be collected and analyzed in a timely manner. Performance can be

adjusted based on this analysis in order to improve outcomes. For example, data collected over time might reveal that fewer than 45% of clients seen in an outpatient setting received ­follow-up appointments, and that of those 45%, fewer than half met desired outcome goals. These data would then be used to more closely examine the system of access and record keeping as well as the type of interventions used to provide care. Such an analysis can assist in the creation of policies for increasing the number of patients who receive follow-up care and in better achieving expected outcomes. When nutrition services have systems in place that can measure and evaluate data from many clients (aggregate data), these data can then be combined with data from other nutrition care providers and be part of evidence-based research that demonstrates the benefit and effectiveness of nutrition care and even contribute to additional research for population health. For example, registered dietitians using the NCP who have collected outcome data on the benefits of nutrition counseling on blood glucose control in patients with type 2 diabetes mellitus could then tabulate the data to summarize and report on a larger number of patients. The Academy of Nutrition and Dietetics Health Informatics Infrastructure (ANDHII) is a web-based system provided by the Academy for collecting health outcomes data from RDNs and NDTRs in practice. ANDHII is free to all members of the Academy and to all RDNs and NDTRs registered through the Commission on Dietetic Registration. Any RDN may contribute to the National Quality Improvement Tool, which is used to collect data on nutrition interventions and outcomes. For students and educators, there is also an Education and Practice project, which allows users to practice entering data and using the nutrition care process electronically (see Chapter 6).

2.5  STEPS OF THE NCP Step 1: Nutrition Assessment The first step of the NCP (see Table 2.3) provides important information that helps determine a person’s health and nutritional status. It is initiated by the referral and/or screening of individuals or groups for nutritional risk factors. A nutrition assessment is a systematic process of obtaining, verifying, and interpreting data in order to make decisions about the nature and cause of nutrition-related problems (see Chapter 3). It is an ongoing process that involves initial data collection and continual reassessment and analysis of a client’s needs and condition. The resulting data are used to accurately describe nutrition problems and facilitate a nutrition diagnosis at the next step of the NCP. Assessment data also provide a means to reevaluate the nutrition problem as part of nutrition monitoring and evaluation, the fourth step in the NCP. Nutrition assessment focuses on understanding the wide variety of factors (listed in Table 2.1) that influence a person’s nutritional status. Assessment data provide information about the types of nutrition problems present as well as their likely causes; they are also used to describe the severity of these problems. For example, if the nutrition problem is “undesirable food choices” or a specific type of food that is undesirable, such as “32 ounces of sugar-sweetened fruit drinks a day,” would be used to describe and quantify that problem.

Table 2.3 Overview of the Steps of the Nutrition Care Process Step One: Nutrition Assessment 1. Obtain and verify appropriate data. 2. Cluster and organize assessment data according to assessment domains and possible nutrition diagnoses. 3. Evaluate the data using reliable standards. 4. Calculate estimated nutrient needs (e.g., nutrition prescription as appropriate). Step Two: Nutrition Diagnosis 1. Identify possible diagnostic labels. 2. Complete nutrition diagnostic statements using the PES format. 3. Evaluate the quality of PES statements. Step Three: Nutrition Intervention 1. Prioritize the nutrition diagnoses. 2. Identify ideal goals and expected outcomes. 3. Plan the nutrition interventions using the standardized intervention language. 4. Implement the nutrition interventions. Step Four: Nutrition Monitoring and Evaluation 1. Monitor progress. 2. Measure outcomes. 3. Evaluate outcomes.

These data will then determine what types of outcomes are desired. In this case, the amount and type of beverages consumed would be tracked over time. Once a problem has been accurately defined and quantified, client goals can be established. If a client is consuming too many sugar-sweetened fruit drinks, the goal might be to consume 4 ounces of 100% fruit juice in place of one fruit drink and substitute water for the remainder. Each piece of nutrition assessment data is collected for a specific purpose. It helps answer the following types of questions: 1. What can be determined about this person’s nutritional status and all of the possible factors that contribute to nutritional balance? 2. What possible nutrition diagnosis/es are supported by the available evidence? 3. What additional data might be necessary to validate the suspected nutrition diagnoses? As dietetics practitioners collect data, they should simultaneously be thinking about the “why” (factors that contribute to or cause imbalance in nutritional status) and the “what” (possible nutrition diagnoses).

Obtain and Verify Appropriate Data  The specific type of data gathered in the assessment can vary depending on a number of factors such as practice setting or the individual’s/ group’s present health status. Dietetics practitioners who serve clients at a Women, Infants, and Children (WIC) clinic will obtain anthropometric data on head circumference and height and weight plotted on growth charts in order to assess the development of infants and children. Dietetics practitioners in outpatient clinics will obtain height and weight Chapter 2  Overview: The Nutrition Care Process   25

measurements for adults and may also gather data from a nutrition-focused physical examination. Recommended practices, as indicated in the AND’s evidence-based guidelines for practice or from other evidence-based research, will influence the type of data collected in a nutrition assessment. Lipid profiles would be appropriate for patients with type 2 diabetes and cardiovascular diseases, whereas BUN, creatinine, and serum phosphorus will be evaluated when providing nutrition care to patients with renal disease. The type of data collected also depends on whether an initial assessment or a reassessment is being conducted. For example, a thorough, detailed diet history is valuable during an initial assessment, but a brief investigation of intake of a specific nutrient such as fiber might be more valuable in a follow-up visit 3 weeks later, especially if inadequate intake of fiber was one of the nutrition problems identified during the initial appointment. The dietitian needs to know what type of data is most appropriate to collect and to be able to determine whether those data are valid and accurate. For example, a stated weight may or may not represent the current weight of a client. Accurate and valid diet history information is dependent on the ability of the dietitian to establish a trusting and nonthreatening relationship with the client. In all cases, the data that are reviewed should be related to the types of nutrition problems likely to be encountered.

Cluster and Organize Assessment Data  As shown in Box 2.1, the nutrition assessment standardized terms are grouped into five domains: (1) food-/nutrition-related history; (2) anthropometric measurements; (3) biochemical data, medical tests, and procedures; (4) nutrition-focused physical findings; and (5) client history. Organizing the data according to the five domains can reveal possible nutrition problem domains from which a nutrition diagnostic statement can then be more accurately formulated. The dietetics practitioner will examine anthropometric data (refer to Chapter 3) with the intended purpose of ruling in or ruling out the possibility of weight classification problems: underweight, unintended weight loss or gain, or BOX 2.1

overweight/obesity. Specific data from a dietary intake assessment reveal important information about the extent of possible intake domain nutrition diagnoses. Information gathered in an interview that reveals a person’s knowledge and beliefs about health and nutrition allows the dietetics practitioner to rule in or rule out possible problems in the knowledge and behavior classification of the behavioral-environmental domain. Each piece of assessment data helps answer a question regarding the presence, severity, and cause of a specific nutrition problem. Using an organized structure that focuses on nutrition problem areas assists dietetics practitioners to think critically about the meaning of the data and logically move into the next steps of the NCP.

Evaluate the Data Using Reliable Standards  It is not only important that data be linked to specific types of problems; it is equally important that the information obtained in a nutrition assessment be compared to evidenced-based standards or ideal goals. Reference standards located in this textbook or one your instructor may require should determine the nutrient needs of an individual. They include standards for energy, macronutrient, fluid, and micronutrient needs as well as recommendations for body weight and growth. Comparative standards are used to formulate the nutrition prescription; they may also need to be reevaluated after an intervention in the event that the plan is adjusted due to outcomes (either positive or not meeting goals). The estimated needs, once appropriately determined, provide the basis for nutrition goals and the standards by which to compare current dietary intake and weight to recommendations.3,4 Key Concepts: NCP Step 1, Nutrition Assessment • Nutrition assessment should ensure that appropriate and reliable data are collected for use in determining the existence of specific nutrition problems. • Organizing and categorizing data utilizing the five domains of the assessment standardized terms improves the efficiency and effectiveness of nutrition assessment and nutrition diagnosis.

CLINICAL APPLICATIONS

Nutrition Assessment Standardized Language: Domains and Examples • Food/Nutrition-Related History (FH): Food and Nutrient Intake (1), Food and Nutrient Administration (2), Medication and Complementary/Alternative Medicine Use (3), Knowledge/ Beliefs/ Attitudes (4), Behavior (5), Factors Affecting Access to Food and Food/ Nutrition-Related Supplies (6), Physical Activity and Function (7), and Nutrition-Related Patient/Client-­ Centered Measures (8) Examples: Total carbohydrate intake from the diet, fat and cholesterol intake, meal/snack pattern, area and level of knowledge, eligibility for

26  Part 2  The Nutrition Care Process

community programs, type of physical activity • Anthropometric Measurements (AD): Height, weight, body mass index (BMI), growth pattern indices/percentile ranks, and weight history Examples: Dosing weight, weight change, body mass index, measured height • Biochemical Data, Medical Tests, and Procedures (BD): Lab data (e.g., electrolytes, glucose) and tests (e.g., gastric emptying time, resting metabolic rate) Examples: BUN: creatinine ratio; fasting glucose; cholesterol, HDL

• Nutrition-Focused Physical Findings (PD): Findings from evaluation of body systems, muscle and subcutaneous fat wasting, oral health, suck/swallow/breathing ability, appetite. Examples: Loss of subcutaneous triceps fat; deltoid muscle atrophy; interosseous hand muscle atrophy • Client History (CH): Current and past information related to personal, medical, family, and social history Examples: Education, medical ­treatment/therapy, socioeconomic ­factors

Step 2: Nutrition Diagnosis Nutrition diagnosis, the second step of the NCP, consists of the identification of a nutrition problem that dietetics practitioners are responsible for treating independently. Nutrition diagnosis is the direct link between nutrition assessment and nutrition intervention. A nutrition diagnosis should not be confused with a medical diagnosis, which involves the art and science of distinguishing one disease from another and describes the nature of that disease. A disease is defined as any deviation from or interruption of the normal structure or function of a body part, organ, or body system. Treatment of a disease involves the management and care of a patient for the purpose of healing and or dealing with the disorder.5 Many diseases have profound effects on a person’s nutritional balance. The alteration of normal structure and function of organs can result in changes in nutrient intake, losses, requirements, and/or utilization. In some cases, nutrition therapy may be one of the most important ways of treating and managing the disease. In contrast to a medical diagnosis, a nutrition diagnosis is written in terms of a client problem for which nutrition-­ related activities provide the primary intervention. The goal of nutrition care is to improve the health and nutritional status of a client/patient by impacting the underlying cause of the nutritional problem. Nutrition diagnoses and care focus on nutrition issues that may be consequences of or contribute to diseases. Nutrition diagnoses also address behaviors that impact food choices. Nutrition diagnostic terms are grouped into three domains: (1) intake, (2) clinical, and (3) behavioral-environmental (see Box 2.2). The intake domain contains nutrition problems that are related to the intake of energy, nutrients, fluids, and bioactive substances through oral diet or nutrition support. Labels such as inadequate, excessive, or less than optimal intake of are used to describe the alteration in intake of a specific nutrient or substance (e.g., types of fats or carbohydrates). The clinical domain contains nutrition problems that are related to medical or physical conditions. These include functional problems such as swallowing, chewing, digestion, and absorption; biochemical problems; and weight

BOX 2.2

problems. The behavioral–environmental domain includes problems that are related to knowledge and beliefs, physical activity, and food safety and access. Within each of these domains, nutrition problems are further grouped according to classifications and subclassifications. Each nutrition diagnostic term has a term number and a standard definition. For example, “inadequate protein intake” (NI-5.6.1) is defined as “lower intake of protein-­containing foods or substances compared to established reference standards or recommendations based upon physiological needs.”3 The use of standard definitions helps dietetics practitioners use the language consistently within the profession. In addition to the numerical coding and standard definition, the AND has published a reference with each diagnostic term that also identifies possible etiologies and signs and symptoms commonly associated with that nutrition problem. These references provide tools that the practitioner may use to examine the appropriate data and ask key questions when determining whether a nutrition diagnosis is present or not. For instance, the sheet for the diagnosis “inadequate protein intake” names “Lack of or limited access to food” as a potential etiology, and “Report or observation of . . . estimated intake of protein insufficient to meet requirement” as a possible sign/symptom that might point to this diagnosis. As the dietetics practitioner gathers nutrition assessment data in order to determine whether or not a patient actually has a nutrition diagnosis of “inadequate protein intake,” she or he should attempt to obtain information from the diet and client history that will provide evidence of the problem. A problem should not be identified unless there is adequate evidence to support its presence. In this case, data describing the amount of protein that is consumed would be essential for determining how far below the recommendation the patient’s protein intake actually is. Other data from the assessment might provide clues about the cause of the problem, such as physiological reasons for increased need, lack of access to food, knowledge deficit, or psychological causes. By using these references, dietetics practitioners can ensure that the diagnostic terminology is used consistently and accurately.6

CLINICAL APPLICATIONS

Nutrition Diagnosis Standardized Language: Domains and Examples • Intake (NI): Domain that contains standardized nutrition diagnostic terms that describe actual problems related to intake of energy, nutrients, fluids, bioactive substances through oral diet or nutrition support Examples: Inadequate energy intake, excessive oral intake, inadequate fiber intake, inadequate vitamin intake (folate) • Clinical (NC): Domain that contains standardized nutrition diagnostic

terms that describe nutritional problems that relate to medical or physical conditions (functional, biochemical, weight, or malnutrition disorder). Examples: Swallowing difficulty, impaired nutrient utilization, unintended weight loss • Behavioral-Environmental (NB): Domain that contains standardized nutrition diagnostic terms that describe nutrition problems related to knowledge, attitudes/beliefs, physical

environment, access to food, and food safety Examples: Not ready for diet/lifestyle change, self-feeding difficulty, intake of unsafe food Reference Academy of Nutrition and Dietetics. ­Nutrition Terminology Reference Manual (eNCPT): Dietetics Language for Nutrition Care. http://www.ncpro.org, accessed July 31, 2018.

Chapter 2  Overview: The Nutrition Care Process   27

PES Statements  Nutrition diagnoses are written in a

PES (problem, etiology, signs/symptoms) format that lists the problem, its cause, and appropriate defining characteristics. The problem (P) is also referred to as the diagnostic label. It describes in a general way an alteration in the client’s nutritional status. Words such as excessive, inadequate, and less than optimal are frequently found in these labels. The etiology (E) or related factors are those that contribute to the cause or existence of a particular problem. Finally, the signs and symptoms (S) are the defining characteristics obtained from the subjective and objective nutrition assessment data. These data provide evidence that a problem exists and describe the severity of the problem. When these three parts are used to form the nutrition diagnostic statement, it is generally stated in the following way: the problem (P) related to the etiology (E) as evidenced by the signs and symptoms (S). For example, consider these nutrition diagnoses: • “Inadequate energy intake (P) related to changes in taste and appetite secondary to chemotherapy (E) as evidenced by average daily kcal intake 50% less than estimated needs (S)” • “Unintended weight loss (P) related to inadequate energy intake (E) as evidenced by 8 pounds (7% of UBW) weight loss within 4 weeks (S)” Let’s examine how these diagnoses were made. A comprehensive nutrition assessment reveals the following data: • Client is undergoing chemotherapy for cancer treatment (client’s medical history). • Client complains of meats tasting bitter and most beverages too sweet (subjective data from food/nutrient-related history). • Client states, “I have very little appetite and no desire to eat” (subjective data from food/nutrient intake history). • Three-day food records reveal average kcal intake of approximately 50% of estimated needs (objective dietary intake data compared to estimated needs). • Client has experienced weight loss of 8 pounds since last outpatient visit 1 month ago (objective anthropometric measurements). In order to evaluate the above nutrition assessment data, the dietetics practitioner applies a number of the critical thinking skills listed in Table 2.2. These include finding patterns and relationships between the data and possible causes, stating each problem clearly and singularly, ruling in/ruling out specific diagnoses, and prioritizing the importance of the diagnoses. From the relationships that exist among the assessment data just noted, “inadequate energy intake” and “unintended weight loss” are selected as relevant nutrition problems. It is essential to focus on problems for which nutrition interventions will be the primary treatment. Once the appropriate problems have been selected, the next step is to describe accurately the signs and symptoms. The signs and symptoms are used to validate and confirm the existence of problems. They also indicate the severity of the problems, answering the questions “How much?” and “How do I know?”

28  Part 2  The Nutrition Care Process

Finally, after the problem is validated by identifying the appropriate signs and symptoms, its etiology or cause is explored. To determine the etiology, related factors and additional data from the assessment are reviewed. It is important to seek the answer to the question “Why does this problem exist?” and explore all possibilities. It may even be necessary to frequently ask the question “Why?” to uncover the underlying root cause of the nutrition problem. To summarize: • The problem is the “What?” • The etiology is the “Why?” • The signs/symptoms are the “How do I know?” or “How severe is the problem?” In the present example, two important points about etiology are illustrated. First, even though medical diagnoses (cancer) and/or medical treatment (chemotherapy) contribute to nutrition problems, they should not be used as the primary etiology. Instead, it is best that a nutrition-related cause be part of the etiology. This is consistent with the guiding principle that distinguishes a nutrition diagnosis from other diagnoses. First, a nutrition diagnosis is written in terms of a client problem for which nutrition-related activities provide the primary intervention. Second, nutrition diagnostic terminology is always used to identify the nutrition problem (P). This language can also be used as etiology language. Behaviors and patterns of food and nutrient intakes that are undesirable (problems in and of themselves) can produce other problems such as changes in anthropometric, biochemical, or clinical findings. In the present example, inadequate caloric intake is the primary cause of unintentional weight loss. Traditionally, nutrition care has been driven by diet orders associated with certain disease conditions, such as diet orders for a “renal diet,” a “diabetic diet,” or a “weightloss diet.” With the advent of the standardized nutrition language and nutrition diagnoses, nutrition care can and should be driven by the extent of a nutrition problem rather than solely by a diet order or medical condition. Though medical conditions affect a person’s need for and ability to consume, digest, metabolize, and utilize nutrients, the nutrition diagnosis rather than the medical diagnosis determines the specific type of nutrition intervention. Instead of providing nutrition care/education as a result of a diet order for a diabetic or renal diet, the dietitian should carefully assess the nutritional status of each patient to specifically identify what, if any, nutrition problems (diagnoses) exist. For example, a patient with type 2 diabetes could conceivably have inconsistent carbohydrate intake, undesirable food choices, self-monitoring deficit, or limited adherence to nutrition-related recommendations. A complete assessment may reveal, however, the absence of any nutritional problems at all. In the case of a patient with chronic renal disease, there could be problems such as excessive potassium intake or excessive fluid intake; but again, a complete assessment may show there are no problems. Another scenario might be two patients with different medical diagnoses who present with a similar nutrition diagnosis, such as involuntary weight loss. In summary, using the nutrition diagnoses to clarify and identify specific nutrition problems may reveal (1) no nutrition problems at the present time, (2) different nutrition problems

for patients with similar medical diagnoses, or (3) similar nutrition problems for patients with different medical conditions. Note that in cases where a nutrition assessment reveals no nutrition problems, it is still necessary to document these findings in the patient’s record using the term “no nutrition diagnosis at this time.”

Criteria for Evaluating PES Statements  Since the

intent of nutrition diagnoses is to describe those problems for which nutrition intervention is the primary treatment, it is important to develop PES statements that accurately reflect that intent. The following questions and criteria were developed to ensure that nutrition diagnoses are well written and accurately represent the nutrition problems:3 Problem (P) • Can the dietetics practitioner impact, improve, or resolve the nutrition problem? • When all things are equal and there is a choice between stating the PES statement using two nutrition diagnoses from different domains, consider the intake domain as more specific to the role of the RDN. Etiology (E) • Is the etiology truly the root cause? • Is there an intervention that will address the root cause, thus increasing the likelihood that a positive change will result? BOX 2.3

• If it is not clear that the problem will be resolved by addressing the etiology, can an intervention at least reduce or lessen the significance of the signs and symptoms? Signs and Symptoms (S) • Are the signs and symptoms that are used to describe the problem specific enough to be measured? • Will measuring the signs and symptoms indicate if the problem is resolved or improved? PES Overall • Are the problems clearly and singularly stated? • Does the assessment data used to identify the nutrition diagnosis support and link to the diagnostic statement, etiology, and signs and symptoms? Box 2.3 demonstrates how these criteria are used to evaluate and refine PES statements for a client with diabetes.

Relationship of Nutrition Diagnosis to the Other Steps of the NCP  Figure 2.4 illustrates the relationship

of the nutrition diagnosis to the other steps of the NCP. As stated previously, the nutrition diagnosis links nutrition assessment to nutrition intervention. An accurate nutrition diagnosis is generated from a focused nutrition assessment and sets the stage for the next two steps of the NCP: Step 3, nutrition intervention, and Step 4, nutrition monitoring and evaluation.

CLINICAL APPLICATIONS

Evaluating a Nutrition Diagnosis When data are obtained from a nutrition assessment, a number of findings can provide clues to the presence of a particular nutrition diagnosis. The dietetics practitioner needs to distinguish among (1) data that are associated with a nutrition problem and/or may be a consequence of that problem, (2) data that will be used to document the specific signs and symptoms that describe and quantify that problem, and (3) data that will provide insight into the root cause of the problem. Which of the following nutrition diagnoses is preferred and why? A. Inconsistent carbohydrate intake related to not following a diabetic diet as evidenced by elevated blood glucose of 250 mg/dL B. Inconsistent carbohydrate intake related to inability to read labels correctly for carbohydrate content and lack of knowledge about amount of grams/carbohydrate units as evidenced by carbohydrate units in three meals of 1, 6, and 3

Evaluate the P: Can the dietetics professional impact, improve, or resolve the nutrition problem? In both examples, the nutrition problem “inconsistent carbohydrate intake” is one that can be improved or resolved. Evaluate the E: Is the etiology truly the root cause? Even though not following a diet plan is likely contributing to the inconsistent carbohydrate intake, there needs to be further understanding as to the reasons why a meal plan is not being followed. In other words, asking “why” uncovers the real reason for not following the plan and is more clearly stated in example B. Is there an intervention that will address the root cause, thus increasing the likelihood that a positive change will result? Developing an intervention using example A might lead prematurely to a more traditional diet education of a diabetic diet, whereas addressing the real reason for not being able to follow a meal plan gives both the provider and the client a more realistic and specific plan

for education. Focusing on the two topics in B should increase the likelihood that a positive change will occur compared with an education plan that is more general. Can an intervention reduce the significance of the signs and symptoms? In the case of example A, it is not clear that a change in carbohydrate intake alone will improve the blood glucose. There could be other factors that are impacting on the blood glucose levels such as medication, illness, and so on, whereas the signs and symptoms in B are more descriptive of the problem itself. Evaluate the S: Are the signs and symptoms used to describe the problem specific enough to be measured? In both cases, the signs and symptoms can be measured; however, improvement in carbohydrate units can be evaluated within a shorter time frame than can improvements in blood glucose. Furthermore, changes in meal patterns can be expected in direct response to the intervention, whereas changes in blood glucose are (continued)

Chapter 2  Overview: The Nutrition Care Process   29

Evaluating a Nutrition Diagnosis (continued) influenced by more variables and may not occur directly in response to the nutrition education provided. Evaluate the PES Overall: Are the problems clearly and singularly stated? In the case of example A, there are really two different types of problems embedded in this diagnosis: inconsistent carbohydrate intake and altered nutrition-related laboratory values. Example B describes a single problem in a straightforward manner,

allowing the dietitian to deal with one problem at a time. Does the assessment data used to identify the nutrition diagnosis support and link to the diagnostic statement, etiology, and signs and symptoms? Even though an elevated blood glucose level provides a clue that there may be a problem with carbohydrate intake, it does not specifically describe the nutrition problem itself. In this case the blood glucose may be a clinical consequence of the intake

Figure 2.4 Relationship of the Nutrition Diagnosis to the

Other Steps of the NCP

Reassessment

Step 1 Nutrition Assessment Identifies P, E, & S Step 2 Nutrition Diagnosis Problem (P) = diagnostic label for nutrition problem Etiology (E) = root cause of nutrition problem Signs & symptoms (S) = measurable evidence of nutrition problem

Provides rationale for intervention Provides rationale for ideal goals & outcomes

Step 3 Nutrition Intervention

Step 4 Nutrition Monitoring & Evaluation

Source: Adapted from Lacey K and Pritchett E, Nutrition Care Process and Model: ADA adopts road map to quality care and outcomes management. J Amer Diet Assoc. 2003; 103: 1061–72.

The signs and symptoms or defining characteristics represent subjective and objective data obtained from the nutrition assessment in Step 1. These data will provide evidence as to the existence of the problem and will help to qualify and/or quantify the severity of the problem. Subjective data, obtained either through patient interview or direct observation, can be used to qualify the problem. Adverbs or adjectives are helpful qualifiers, as when the cancer patient in the previous example complains of having “very little appetite.” Objective data, which can generally be measured or counted, quantify the problem. It is very important that the data used to define the signs and symptoms of the problem either quantify or qualify the specific problem. If the problem is an energy intake imbalance (either “inadequate energy intake” or “excessive energy intake”), then a measurement of kcal (percentage of estimated needs, average intake over time, an amount less than or more 30  Part 2  The Nutrition Care Process

problem but does not describe and/or quantify the intake problem. Therefore, after applying the criteria to each of the examples noted previously, example B is the preferred nutrition diagnosis. It states the problem clearly and singularly, and it provides a quantifiable description of the signs and symptoms from which specific goals can be established and measured. It also provides clear direction for a specific intervention targeted at the root cause of the problem.

than desired, etc.) best describes the energy problem; if the problem is one of weight, then an appropriate anthropometric measurement (BMI, relative weight, weight change over time, etc.) should be used to describe the weight problem. These signs and symptoms then become the basis for setting measurable goals as part of Step 3, nutrition intervention. They are also the outcome measures that are used to monitor and evaluate progress toward goals as part of Step 4, nutrition monitoring and evaluation. If kcal are inadequate by 50%, as in the previous diagnosis example, a desired goal might be to meet 75% of estimated caloric needs within 2 days. A kcal count or food record could then be used to track and evaluate that outcome. Key Concepts: NCP Step 2, Nutrition Diagnosis • Nutrition diagnosis is not the same as medical diagnosis. It describes a problem for which nutrition-related activities provide the primary intervention. • The desired format for writing a nutrition diagnosis is PES (problem, etiology, and signs and symptoms). • Critical thinking skills such as finding patterns and relationships, stating problems clearly and singularly, and ruling in/ruling out certain diagnoses are essential to making accurate nutrition ­diagnoses. • Accurate nutrition diagnoses set the stage for quality nutrition intervention (Step 3 of NCP) and nutrition monitoring and evaluation (Step 4 of NCP).

Finally, nutrition interventions as part of Step 3 should be logically linked to the cause of problems. If the root cause of inadequate intake is taste alteration and decreased appetite, interventions need to be linked to ways to enhance appetite and improve the taste of foods before a change in caloric intake will occur. When nutrition diagnoses are written as separate and distinct problems, even though one problem may actually cause another, the dietetics practitioner is able to prioritize which problem should be addressed first as part of Step 3, nutrition intervention. For example, when there is both an intake problem and a weight problem, caloric intake needs to change before a change in weight can be expected.

Step 3: Nutrition Intervention The third step of the NCP, nutrition intervention, involves both planning and implementing. It is a specific set of activities used to improve or resolve a problem. Nutrition interventions are actions purposefully designed to change a nutrition-related behavior, risk factor, environmental condition, or aspect of health status for an individual, target group, or the community at large.1 Dietetics practitioners work collaboratively not only with other health care professionals but more importantly with the client, family, or caregiver to create a realistic plan that has a good probability of positively influencing the diagnosed problem. This client-driven process is key to successful nutrition intervention, distinguishing it from previous planning steps that may or may not have involved the client to this degree.

Prioritize the Nutrition Diagnoses  A nutrition assessment will likely result in the identification and labeling of multiple nutrition diagnoses; therefore, before any action can be taken, it is essential to prioritize the diagnoses. The ranking of nutrition diagnoses permits dietetics practitioners to arrange the problems in the order of their importance and urgency for the client. Once they have been sorted for safety, they can be further prioritized based on criteria such as anticipated early response to an intervention, client preference, or the impact of one problem on another. Using the earlier example, it makes sense to first address the primary problem of energy intake before attempting to intervene on the secondary problem of weight: • “Inadequate energy intake (P) related to changes in taste and appetite (E) as evidenced by average daily kcal intake 50% less than estimated needs (S)” • “Unintended weight loss (P) related to inadequate energy intake (E) as evidenced by 8 pounds weight loss within 4 weeks (S)”

Write the Nutrition Prescription  An important part of the planning for nutrition intervention is concisely stating a nutrition prescription. A nutrition prescription is the recommended dietary intake of nutrients, energy, or specific foods/ selected products based on the use of appropriate standards, BOX 2.4

the nutrition diagnosis, and the current health condition. The prescription also helps to accurately identify ideal goals for the patient/client.

Set Goals  After prioritizing the nutrition diagnoses and

writing a nutrition prescription, it is necessary to identify patient-focused ideal goals/expected outcomes. Ideal goals are science-based values intended to control or improve specific health conditions. The AND’s evidence-based guides for practice and other practice guides provide resources to assist dietetics practitioners in selecting the appropriate goals for patients.7 Consuming less than 7% of kcal from saturated fat is an example of an evidence-based ideal goal for the nutrition treatment of hyperlipidemia; this level of intake is associated with the least cardiac risk.4 Expected outcomes are the desired change(s) to be achieved over time as a result of nutrition intervention. Expected outcomes are based on the nutrition diagnosis; for example, decreasing the intake of saturated fat by a specific amount or percentage of kcal is an expected outcome. Expected outcomes can also be defined in terms of a specific behavior that will result in the change in amount of saturated fat consumed; for example, the patient will substitute olive oil for solid margarine as the preferred spread on most bread. Though slightly different, ideal goals and expected outcomes are often used interchangeably. What is essential is that the goal or outcome—whichever is recorded in the chart—be written in observable and measurable terms that are clear and concise. Goals/outcomes should be client centered and realistically tailored to the client’s circumstances and expectations for treatment. Interventions to help a patient to meet these goals and achieve these outcomes are then planned.

Select the Nutrition Intervention  The final step of planning is selection of appropriate interventions. Like the standardized terms used for nutrition assessment and nutrition diagnosis, intervention terminology is organized into domains: (1) food and/or nutrient delivery, (2) nutrition education, (3) nutrition counseling, and (4) coordination of nutrition care by a nutrition professional. These four domains and the major types of interventions in each are summarized in Box 2.4.

CLINICAL APPLICATIONS

Nutrition Intervention Standardized Language: Domains and Examples • Nutrition Prescription: The client’s tailored recommended intake of energy and/or selected foods or nutrients based on current reference standards and evidenced based practice nutrition guidelines and related to client’s health and nutrition diagnosis. • Food and/or Nutrient Delivery (ND): An individualized approach for food/ nutrient provision including meals and snacks, enteral/parenteral nutrition, supplements, feeding assistance, feeding environment, and nutrition-related medication management

Example: Modify composition of meals/snacks • Nutrition Education (E): A formal process to instruct or train a patient/client in a skill or to impart knowledge to help patients/clients to voluntarily manage or modify food, nutrition, and physical activity choices to maintain or improve health Example: skill development • Nutrition Counseling (C): A supportive process characterized by a collaborative relationship to estabolis priorities, goals and individualized action plans.

Example: motivational interviewing • Coordination of Nutrition Care (RC): Consultation with, referral to, or coordination of nutrition care with other providers, institutions, or agencies that can assist in treating or managing nutrition-related problems Example: referral to community agencies/programs • Population Based Nutrition Care: Interventions designed to improve health of a population. Example: public policy change

Chapter 2  Overview: The Nutrition Care Process   31

Key Concepts: NCP Step 3, Nutrition Intervention • First and foremost is the need to prioritize the nutrition diagnoses, then write a nutrition prescription. • Ideal goals and expected outcomes need to be identified prior to implementing nutrition interventions. • Interventions are derived from accurate diagnoses and largely driven by client involvement. • The AND’s evidence-based guides for practice are tools that help dietetics practitioners promote quality service and demonstrate effectiveness of care.

All interventions must be based on scientific principles and rationales and must be grounded in quality research and evidence-based interventions when available. Once again, the AND’s evidence-based guides for practice and other practice guides are invaluable resources for both identifying science-based ideal goals and selecting appropriate interventions. These guides link external scientific evidence regarding nutrition care to a specific health problem, thus giving dietetic practitioners the confidence that they are making the best decisions when providing nutrition care. The ­evidence-based guides alone do not replace the expertise and judgment of dietetics practitioners, but rather enhance their value and increase the likelihood of a desired outcome.

Implement the Nutrition Intervention  Implementation is

the action phase of the NCP. It is during this phase that dietetics practitioners communicate the plan of action to the client and other professionals. Dietetics practitioners may directly carry out the intervention or may delegate or coordinate care provided by others. Once again, the central core of the Nutrition Care Model (relationship between patient/client/group and dietetics practitioner) recognizes that the client needs to be involved in this decision-making and action step of nutrition care.

Step 4: Nutrition Monitoring and Evaluation The purpose of monitoring and evaluation is to determine the degree to which progress is being made and the client’s goals or desired outcomes of nutrition care are being achieved. It is much more than merely “watching” what is happening. It requires an active commitment to measuring and recording the appropriate outcome indicators relevant to the nutrition diagnosis’ signs and symptoms. Progress should be (1) monitored, (2) measured, and (3) evaluated on a planned schedule. Systematic monitoring and evaluation provide consistency in practice, add value, and demonstrate effectiveness of care.

Monitor Progress  Monitoring refers specifically to deter-

mining that the goals and outcomes anticipated by the client and the dietetics practitioner are indeed being achieved. Specific activities that are associated with this level of monitoring include the following: • Determining whether the intervention is being implemented as planned • Checking the client’s understanding and attainment of goals • Identifying any changes in the client’s condition1

32  Part 2  The Nutrition Care Process

Monitoring in this way may require gathering additional information about possible reasons for any lack of progress. A nutrition diagnosis may be revised and/or a plan changed as a result of obtaining additional information. Therefore, the steps of the NCP may be performed more than once during the course of nutrition treatment.

Measure Outcomes  Measuring outcomes requires col-

lecting data over time. This is a critical component of the NCP. Interventions have too often been planned and acted upon with little regard for what has really happened as a result of the action taken. The key to measuring outcomes is knowing what needs to be measured. The NCP provides clear examples of the types of outcomes to be measured.1 These include the following (among others): • Direct nutrition outcomes such as knowledge gained, behavior changes, food or nutrient intake changes, and improved nutritional status • Clinical and health status outcomes such as laboratory values, anthropometry and body composition, blood pressure, and risk factor profile • Patient-/client-centered outcomes such as quality of life, satisfaction, self-efficacy, and self-management • Health care utilization and cost outcomes such as medication changes, special procedures, and planned/unplanned health care visits The specific outcomes that are measured are determined by the nutrition diagnosis, its etiology, and the signs and symptoms—that is, data that are obtained directly from the nutrition assessment. Therefore, the standardized terms from monitoring and evaluation are combined with nutrition assessment terms. There are only four domains that reflect the types of data to be monitored: (1) food/nutrition-related history; (2) anthropometric measurements; (3) biochemical data, medical tests, and procedures; and (4) nutrition-focused physical findings. Box 2.5 demonstrates how standardized terms are used to describe each step of the NCP; notice how the same parameters assessed in Step 1 are reassessed as part of Step 4.

Key Concepts: NCP Step 4, Nutrition Monitoring and Evaluation • This step requires an active commitment to measuring and recording changes in the client’s condition as they relate to the nutrition diagnosis signs and symptoms. • Progress should be monitored, measured, and evaluated on a planned schedule. • Direct nutrition outcomes, clinical and health status outcomes, patient/client-centered outcomes, and health care utilization outcomes are to be measured. • Data from this step can be used to create an outcomes management system and can contribute to the body of evidenced-based research.

Establishing a nutrition diagnosis that clearly describes the signs and symptoms establishes the type of outcome to

BOX 2.5

CLINICAL APPLICATIONS

Using Standardized Language to Describe Nutrition Care If a nutrition assessment reveals a fiber intake of 10 grams a day due to eating less than 1 cup of fruits or vegetables daily, the following standardized terms could be used in the NCP:

Step 1: Nutrition Assessment • Food intake: Amount and types of food = less than 1 cup fruits and ­vegetables daily • Fiber intake: Total fiber 15 4 Unsure 2 Have you been eating poorly because of a decreased appetite? No 0 Yes 1 Total  Score of 2 or more = patient at risk of malnutrition. Source: Ferguson M, Capra S, Bauer J, Banks M. The development of a valid and reliable malnutrition screening tool for adult acute hospital patients. Nutrition. 1999; 15: 458–464.

Figure 3.3 Example of a Validated Nutrition Screening Instrument: NRS-2002 The NRS-2002 is a validated screening method for identification of individuals at risk for malnutrition. Impaired nutritional status

Severity of disease (lower increase in requirements)

Score

Score

Absent: 0

Normal ­nutritional status

Absent: 0

Normal ­nutritional requirements

Mild: 1

Wt loss >5% in 3 month or food intake below 50–75% of normal requirement in preceding week.

Mild: 1

Hip fracture, Chronic patients, in particular with acute ­complications cirrhosis, COPD*, Chronic hemodialysis, diabetes, oncology

Moderate: 2

Wt loss >5% in 2 months or BMI 18.5–20.5 + impaired general condition or food intake 25–60% of normal requirement in preceding week.

Moderate: 2 Major abdominal surgery, Stroke, Severe ­pneumonia

Severe: 3

Wt loss >5% in 1 month (>15% in 3 months) or BMI 10)

Score (nutritional status) + score (disease severity) = total score Adjustment for age: if ≥70 years: add 1 to total score above S Age- adjusted total score Score 0: No risk: Weekly re-screening of the patient, if the patient is scheduled for major surgery, consider a preventive nutritional care plan Severity of disease Score 1–2: Enhanced risk: Weekly re-screening of the patient, if the patient is scheduled for major surgery, consider a preventive nutritional care plan Score ≥ 3: High risk: A nutritional care plan is initiated Source: Kondrup J, Rasmussen HH, Hamberg O, et al. Nutritional risk screening (NRS 2002): a new method based on an analysis of controlled clinical trials. Clin Nutr. 2003; 22: 321–36. For more information: http://www.forceval.co.uk/docs/BAPEN_must_full.pdf

44  Part 2  The Nutrition Care Process

3.4  FOOD- AND NUTRITION-RELATED HISTORY Typically, food and nutrition information is assessed either by collecting data retrospectively or by summarizing data ­gathered prospectively. All methods have their own strengths and limitations. The accuracy (or validity) of the information and the reliability of the data depend on the experience and skill of the clinician, the cooperation and accurate reporting of the client, and the type of assessment instrument that is used. Assessment instruments vary by the time frame assessed, the time that it might take to collect data, the need for an ­individual’s memory to be specific in nature, and the need for a higher cognitive ability. Information gathered will include, for example, dietary intake, food preparation, timing of meals, and meal environment and may also include physical activity or exercise (PA) patterns. There are numerous webbased assessment tools such as the ASA24 from the National Cancer Institute. Demonstration of the ASA24 can be found at https://asa24.nci.nih.gov/demo/. The ultimate goal of collecting dietary information is to determine the nutrient content of food that is consumed and then compare this to standard guidelines appropriate for that individual.

this method can be strengthened by the use of photographs, digital images, food models, or serving containers to improve recall of portion sizes.17,18

Figure 3.4 Data Collection A Registered Dietitian Nutritionist and client review a 24-hour recall during a nutrition counseling session.

Nutrition Care Indicator: Twenty-Four-Hour Recall When using a 24-hour recall as the dietary assessment Source: Courtesy of Marcia Nelms. method, the clinician guides the client through a recall of all food and drink that has been conFigure 3.5 24-Hour Recall Form sumed in the previous 24-hour period (see Figures 3.4 and 3.5). The clinician asks what food or beverage was 24-hour recall Date: Patient Name: consumed most recently prior to the Time Foods and Serving How Where Comments: interview and then works in reverse Beverages Size prepared order through the previous 24 hours. The clinician can question the client about activities during the period in order to stimulate the client’s memory. At the end of the recall, the clinician reviews the information to verify serving sizes and preparation methods and asks for clarification Sample Protocol for Completion of 24-Hour Recall if needed. The USDA multiple-pass approach, a variation of this method, is a widely accepted and validated 1. The 24-hour recall consists of obtaining information for food and fluid intake for the 24-hour period preceding the interview. It is assumed that this is a “typical” day. If not, clarify. method that includes five standardized reviews of information.13–16 2. Patient may not be able to remember all foods eaten. Begin by asking the sequence of Advantages of the 24-hour recall events for the previous 24 hours. For example, “Before speaking with me today, when was method include short administration the last time you ate or drank anything?”; “What was that ?”; “How much did you eat of time, minimal cost, and negligible ?” Then proceed backward from that time for the entire 24-hour period. risk for the client. One disadvantage is 3. Use food models and food containers to assist patients in clarifying the serving amounts. that a 24-hour recall does not always reflect typical eating patterns, since 4. A checklist may help the interviewer remember to ask or probe all information for each day-to-day dietary intake may vary food or beverage. considerably. A second disadvantage Components of 24-hour recall: is that clients may report information Note the time the food or beverage was consumed. they feel the clinician wants to hear. Record the food or beverage. Research indicates clients may over- or Determine serving size for food or beverage. underreport their intake. Reliance on Determine how the food was prepared. the client’s memory also may impact Determine where the patient had the food or beverage item. Include any relevant notes to the food or beverage report. the accuracy of the data. Accuracy of Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   45

Nutrition Care Indicator: Food Record/Food Diary In this method, the client documents his or her dietary intake as it occurs over a specified period of time. Typically, the record is kept over a 3- or 5-day period (see Figure 3.6) and should include a sampling of both weekdays and weekends. Clients estimate or measure their food intake. The advantage of this method is that it is not totally reliant on the client’s memory and may be much more representative of the client’s actual intake. Validity may be low, however, because underreporting is common, and the client may change food habits for the recording period. Accuracy is dependent on the client accurately reporting typical daily intakes. Additionally, there is a heavier burden on the client, who must make a commitment to record his or her intake. Many online tools and applications have been developed to assist the individual client in preparing a food record or tracking their intake electronically, such as “My Fitness Pal™.”19

Nutrition Care Indicator: Food Frequency The food frequency data collection method is a retrospective review of specific food intake. Foods are organized into groups, and the client identifies how often and in what ­quantities he or she consumes a specific food or food group (see Figure 3.7). The method can be self-administered. Many food frequency instruments are specialized and validated to identify food group intake for certain disease states such as cardiovascular disease (see Tables 13.10 and 13.11) or designed for use with specific populations. This is the data collection method used in the National Health and Nutrition Examination Survey (NHANES) dietary assessment and by the MEDFICTS questionnaire shown in Figure 3.7. Food frequency data can be collected via online applications using both narrative and pictorial representations of foods and quantities. Advantages of this methodology are that it is inexpensive and requires minimal time to administer. Disadvantages

Figure 3.6 Food Diary Date/Time

List all foods and drinks

Amount/serving size

Preparation/ cooking method

Seasonings/ Condiments

Where did you eat?

Who were you with?

Directions for Use of Food Diary READ THE FOLLOWING INSTRUCTIONS CAREFULLY Record amounts and descriptions of ALL food and drink (including water) for three consecutive days. These days should be “typical” to the way you eat on a normal basis. Please do not try to change your eating habits on the days you are recording. Please pick two weekdays and one weekend day that are most like your usual daily intake. Helpful Hints: • Record your intake immediately after you have eaten and NOT at the end of the day. This makes it much easier to remember and to record accurately. • Include all meals and snacks, granola bars, sandwiches, chocolate, sweets, ice cream, fruits—whatever you eat. • Include all drinks (e.g., water, tea, coffee, beer, sports drinks, and fruit juice). • Record any additions to food such as mustard, ketchup, mayonnaise, cream or sugar, steak sauce, salsa, dressings, gravy, pickles, honey, or butter. Describe foods accurately: • Record cooking methods (e.g., fried, baked, broiled, grilled, frozen, canned, added water, low sodium, and the amount of fat or oil used for cooking). • Record brand names and the descriptions (e.g., KRAFT, General Mills, Breyers, Campbell’s, Del Monte, and whether regular, 2% reduced fat, light, fat free, low carb, or sweetened). • Name the types of cheese, fish, or meat (e.g., cheddar, American, cod, tilapia, ground, sirloin, shredded). Describe the amounts as accurately as possible: • To help with measuring portion size, try to avoid terms such as “one bowl” or “a handful.” • Visualize the following comparisons when figuring portion size: • 3 ounces of meat is about the size of a deck of cards or audiotape cassette. • A medium-size piece of fruit is about the size of a tennis ball. • 1 ounce of cheese is about the size of 4 stacked dice. • 1/2 cup of ice cream is about the size of a tennis ball. • 1 cup of mashed potatoes or broccoli is about the size of your fist. • 1 teaspoon of butter is about the size of the tip of your thumb. • Use weights marked on packages (e.g., half of a 425-gram can of corn, half of a 16-ounce can, half of a 6-ounce bag of frozen corn). • Use cups, teaspoons, and tablespoons to record amounts.

46  Part 2  The Nutrition Care Process

Figure 3.7 Example of a Food Frequency Instrument: MEDFICTS In each food category for both Group 1 and Group 2 foods check one box from the “Weekly Consumption” column (number of servings eaten per week) and then check one box from the “Serving Size” column. If you check Rarely/Never, do not check a serving size box. See next page for score. Serving Size

Weekly Consumption Rarely/ never

3 or less

4 or more

Food Category

Score

Average Large Small ,5 oz/d 5 oz/d .5 oz/d 1 pt 2 pts 3 pts

Meats Recommended amount per day: 5 oz (equal in size to 2 decks of playing cards). Base your estimate on the food you consume most often. Beef and lamb selections are trimmed to 1/8" fat. Group 1. 10 g or more total fat in 3 oz cooked portion Beef—Ground beef, Ribs, Steak (T-bone, Flank, Porterhouse, Tenderloin), Chuck blade roast, Brisket, Meatloaf (w/ground beef), Corned beef Processed meats—1/4 lb burger or lg. sandwich, Bacon, Lunch meat, Sausage/knockwurst, Hot dogs, Ham (bone-end), Ground turkey Other meats, Poultry, Seafood—Pork chops (center loin), Pork roast (Blade, Boston, Sirloin), Pork spareribs, Ground pork, Lamb chops, Lamb (ribs), Organ meats†, Chicken w/skin, Eel, Mackerel, Pompano

3 pts

7 pts

1 pt

2 pts

Group 2. Less than 10 g total fat in 3 oz cooked portion Lean beef—Round steak (Eye of round, Top round), Sirloin‡ , Tip & bottom round‡, Chuck arm pot roast‡, Top Loin‡ Low-fat processed meats—Low-fat lunch meat, Canadian bacon, “Lean” fast food sandwich, Boneless ham Other meats, Poultry, Seafood—Chicken, Turkey (w/o skin)§, most Seafood†, Lamb leg shank, Pork tenderloin, Sirloin top loin, Veal cutlets, Sirloin, Shoulder, Ground veal, Venison, Veal chops and ribs‡, Lamb (whole leg, fore-shank, sirloin)‡

3 pts

6 pts

Eggs – Weekly consumption is the number of times you eat eggs each week

Check the number of eggs eaten each time

Group 1. Whole eggs, Yolks

1

2

$3

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

Group 2. Egg whites, Egg substitutes (1/2 cups) Dairy Milk—Average serving 1 cup Group 1. Whole milk, 2% milk, 2% buttermilk, Yogurt (whole milk) Group 2. Fat-free milk, 1% milk, Fat-free buttermilk, Yogurt (Fat-free, 1% low fat) Cheese—Average serving 1 oz Group 1. Cream cheese, Cheddar, Monterey Jack, Colby, Swiss, American processed, Blue cheese, Regular cottage cheese (1/2 cup), and Ricotta (1/4 cup) Group 2. Low-fat & fat-free cheeses, Fat-free milk mozzarella, String cheese, Low-fat, Fat-free milk & Fat-free cottage cheese (1/2 cup) and Ricotta (1/4 cup) Frozen Desserts—Average serving 1/2 cup Group 1. Ice cream, Milk shakes Group 2. Low-fat ice cream, Frozen yogurt

(continued) Source: NCEP, National Heart, Lung and Blood Institute, NIH Reference: NIH Publication no. 02-5215, Diet Appendix A; available from: https://www.nhlbi. nih.gov/health-pro/guidelines/current/cholesterol-guidelines/final-report.

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   47

Figure 3.7 Example of a Food Frequency Instrument: MEDFICTS (continued ) Serving Size

Weekly Consumption Rarely/ never

3 or less

4 or more

Food Category

Score

Small Average Large ,5 oz/d 5 oz/d .5 oz/d 1 pt 2 pts 3 pts

Frying Foods – Average servings: see below. This section refers to method of preparation for vegetables and meat. Group 1. French fries, Fried vegetables (1/2 cup), Fried chicken, fish, meat (3 oz)

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

3 pts

7 pts

1 pt

2 pts

3 pts

Group 2. Vegetables, not deep fried (1/2 cup), Meat, poultry, or fish—prepared by baking, broiling, grilling, poaching, roasting, stewing: (3 oz) Baked Goods – 1 Average Serving Group 1. Doughnuts, Biscuits, Butter rolls, Muffins, Croissants, Sweet rolls, Danish, Cakes, Pies, Coffee cakes, Cookies Group 2. Fruit bars, Low-fat cookies/cakes/pastries, Angel food cake, Homemade baked goods with vegetable oils, breads, bagels Convenience Foods Group 1. Canned, Packaged, or Frozen dinners: e.g., Pizza (1 slice), Macaroni & cheese (1 cup), Pot pie (1), Cream soups (1 cup), Potato, rice & pasta dishes with cream/cheese sauces (1/2 cup) Group 2. Diet/Reduced calorie or reduced fat dinners (1), Potato, rice & pasta dishes without cream/cheese sauces (1/2 cup) Table Fats—Average serving: 1 Tbsp Group 1. Butter, Stick margarine, Regular salad dressing, Mayonaisse, Sour cream (2 Tbsp) Group 2. Diet and tub margarine, Low-fat & fat-free salad dressing, Low-fat & fat-free mayonnaise Snacks Group 1. Chips (potato, corn, taco), Cheese puffs, Snack mix, Nuts (1 oz), Regular crackers (1/2 oz), Candy (milk chocolate, caramel, coconut) (about 1 1/2 oz), Regular popcorn (3 cups) Group 2. Pretzels, Fat-free chips (1 oz), Low-fat crackers (1/2 oz), Fruit, Fruit rolls, Licorice, Hard candy (1 med piece), Bread sticks (1–2 pcs), Air-popped of low-fat popcorn (3 cups) † ‡ ¥ §

Organ meats, shrimp, abalone, and squid are low in fat, but high in cholesterol. Only lean cuts with all visible fat trimmed. If not trimmed of all visible fat, score as if in Group 1. Score 6 pts if this box is checked. All parts not listed in Group 1 have ,10 g total fat.

Total from page 1 Total from page 2 Final Score

To Score: For each food category, multiply points in weekly consumption box by points in serving size box and record total in score column. If Group 2 foods checked, no points are scored (except for Group 2 meats, large serving = 6 pts). Example: 21 pts 3 pts

7 pts

1 pt

2 pts

3 pts

Add score on page 1 and page 2 to get final score. Key: $70

Need to make some dietary changes 40–70 Heart-Healthy Diet ,40 TLC Diet

48  Part 2  The Nutrition Care Process

include a tendency toward lower response rates because the instrument is self-administered. Additionally, foods on the preprepared list may be inappropriate for the individual who is completing the food frequency questionnaire. The instrument may not include ethnic or child-appropriate foods or quantities that are realistic for those eating larger amounts, such as athletes.

Nutrition Care Indicator: Observation of Food lntake/“Calorie Count” In an acute care or long-term care setting, actual food intake can be observed and recorded when a kilocalorie (kcal) or kcal-protein count is ordered. Specific procedures for this method vary from institution to institution. If very detailed information is required, as in the case of a research or metabolic study, food may be weighed before and after the meal is served. The patient’s food intake is then calculated from differences between the two. Any food consumed by family members or food brought in from outside the hospital will also need to be recorded. In most institutions, nursing or nutrition staff document what the patient eats from meal trays. The RDN or registered dietetic technician (NDTR) then calculates nutritional information such as kcal or protein content from this information. If the RDN or NDTR collects this information, it provides an excellent opportunity to assess the patient’s understanding of any dietary interventions and to teach specific nutrition information such as portion control strategies or nutrient content of the meal. This method also allows the RDN or NDTR to establish rapport and determine food preferences and tolerances.

3.5  EVALUATION AND ­INTERPRETATION OF DIETARY ANALYSIS INFORMATION After data are collected and analyzed, it is the clinician’s job to compare the information to established scientific r­ eference criteria. These criteria may include the ­individual patient’s needs (based on age, gender, and nutrition ­a ssessment) and may be as general as a comparison to the U.S. Dietary ­Guidelines or as specific as milligrams of vitamin C that should be consumed. 20 Limitations of each assessment method make the assessment of intake an estimation rather than an exact measurement, but in general, the appropriate criteria are determined by how the information will be used. For example, in order to determine whether an intervention to change the patient’s food choices has improved intake, a direct observation of food intake may be made and then analyzed by simply estimating the energy value and protein content of the food recorded, using an established method such as the Choose Your Foods: Food Lists for Diabetes. This is the data that can be used to support the documentation of a nutrition problem, shown in the Sample PES Statement box. Sample PES Statement for Intake Domain: Inadequate protein intake related to aversion to meat as evidenced by reported intake of 45% of estimated protein requirements (70–75 g/day).

Nutrition Care Criteria: Evaluation and ­Interpretation Using the U.S. Dietary Guidelines The 2015–2020 Dietary Guidelines for Americans, published by the Office of Disease Prevention and Health P ­ romotion of the U.S. Department of Health and Human Services (USDHHS), provide general recommendations for dietary intake that promote health and prevent disease. 20 These guidelines are based on decades of nutrition research and reflect the most up-to-date evidence-based information ­supporting the understanding of nutritional requirements. The guidelines include five broad recommendations for the general public designed to promote healthy eating patterns by emphasizing the choice of a variety of nutrient-dense foods. The guidelines stress the importance of substituting healthier food and beverage choices in order to reduce intakes of added sugars, saturated fats, and sodium. Although the U.S. Dietary Guidelines are an important tool in nutrition education and planning, they are not the most precise tool available for ­evaluating an individual’s diet, but they do provide broad guidance and examples of recommended food patterns.

Nutrition Care Criteria: Evaluation and Interpretation Using the USDA MyPlate Tools Dietary analysis using the MyPlate recommendations can quantify food consumed from each of the major food groups.21 These data give the clinician an overview of adequacy, variety, moderation, and balance. A food group–based analysis does not quantify macro- or micronutrients; on the contrary, when one simply looks at total energy and protein intakes, there is no way to determine the source of these nutrients. Using the USDA MyPlate eating plans in conjunction with macronutrient data allows the overall quality of the diet to be assessed (see Box 3.2).

Nutrition Care Criteria: Evaluation and Interpretation Using Choose Your Foods: Food Lists for Diabetes/Weight Management This method of analysis uses the food lists established jointly by the American Diabetes Association and the AND.22 Use of the lists provides a quick, rough estimate of kcal, ­protein, carbohydrate, and fat in the diet. Carbohydrate ­counting ­concentrates on estimation of carbohydrate and is used ­primarily by individuals with diabetes who are balancing their insulin dosages with dietary intake of carbohydrate. (See Chapter 17.)

Nutrition Care Criteria: Evaluation and Interpretation Using Individual Nutrient Analysis The USDA first published food composition values in 1896. The Nutrient Data Laboratory of the USDA maintains and updates the National Nutrient Databank System (NDBS). Historically, this information has been published in a series of Agriculture Handbooks, but now this information is available only online (http://ndb.nal.usda.gov).23 Other sources of data include other online databases, nutrition labels, food manufacturers, and restaurants and fast-food establishments. Data on food labels may not be 100% reliable, especially for products from small companies or imported foods.

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   49

BOX 3.2

CLINICAL APPLICATIONS

Comparison Assessment of Dietary Intake Consider these two meal records, which have similar kilocalorie values. Dietary assessment information may lead to very different results depending on the reference standards that are used.

Sample 24-hour recall Diet 1

Diet 1: 1 egg, 1 slice of toast, coffee with 2 tbsp half-and-half 2 oz ham sandwich on 2 slices of white bread with 1 tbsp mayonnaise 1 oz ­potato chips 4 oz chicken breast (fried), 1 roll, iced tea with 2 tbsp sugar Diet 2: 1 cup whole-grain cereal, 1 banana, 1 c. skim milk 2 oz ham sandwich, ½ cup chopped fresh vegetables on 2 slices of wholegrain bread with 1 tbsp mustard, 1 oz pretzels, 1 medium apple 4 oz chicken breast (baked), 1 cup fresh broccoli, asparagus, carrots stir-fried with 1 cup brown rice

Diet 2

Analysis for energy and protein (using the dietary exchanges) Nutrient

Total

Grains (5 oz with $3 oz whole grain)

4 oz

Kilocalories

1099.3

Vegetables (2 cups)

0 cups

Pro (g)

53.08

Fruits (1.5 cups)

0 cups

Fat (g)

51.15

Dairy (3 cups)

0 cups

Carb (g)

106.2

Protein foods (5 oz)

6 oz

Solid fats/added sugars

31

Grains (5 oz with ≥ 3 oz whole grain)

8.2 oz

Nutrient

Total

0 oz whole grain

5 oz whole grain

Kilocalories

1087.86

Vegetables (2 cups)

1.3 cups

Pro (g)

70

Fruits (1.5 cups)

2.4 cups

Fat (g)

24.02

Dairy (3 cups)

3 cups

Carb (g)

184.18

Protein foods (5 oz)

5.4 cups

Web-based Dietary Analysis  Nutrition profession-

als and consumers have access to many sources of digital dietary analysis programs. These programs vary significantly in terms of number of food items, nutrients included in the database, accuracy of the data, how often the information is updated, cost to access the program, and ease of use.

Nutrition Care Criteria: Evaluation and ­Interpretation Using Dietary Reference Intakes and Daily Values One method of evaluating dietary macro- and micronutrient amounts is use of the Dietary Reference Intakes (DRIs) and Daily Values (DVs). DRIs are standards established by the National Academy of Sciences. These standard reference values allow evaluation of energy, protein, vitamin, and mineral intakes for healthy people. There are four different sets of standards within the DRI: Adequate Intakes (AIs), Recommended Dietary Allowances (RDAs), Tolerable Upper Intake Levels (ULs), and Estimated Average Requirements (EARs). The RDA, AI, and UL can be used to assess diets of individuals.24,25 It is important when using these standards to understand the context in which the references are established. Values for RDAs are determined at approximately two standard deviations above the average (mean) requirement within the healthy population. This margin of safety allows the value of the RDA to meet the needs of most healthy people. Therefore, if the evaluated diet falls below the RDA or AI for a specific nutrient, it does not necessarily mean the client is deficient in this nutrient. Diagnosis of specific 50  Part 2  The Nutrition Care Process

Analysis for components of food intake pattern for 1600 kcal (using USDA Food Pattern)

nutrient deficiencies would require additional confirmation using other components of nutrition assessment. Still, DRIs serve as important benchmarks for evaluating the patient’s dietary intake, not only from food, but also from dietary supplements. The UL values assist in assessing a patient’s use of supplements and whether their current dosage poses any potential health risk. In the clinical setting, many patients have specific diseases or medical conditions that may have unique nutrient requirements. For example, an individual with a burn injury may require significantly higher doses of vitamin C and zinc to ensure appropriate wound healing. Additionally, medications and treatments may alter absorption, utilization, excretion, or storage of specific nutrients. In these situations, patients may need higher or lower levels of these nutrients. The DRI are established for the healthy population and hence may not be appropriate in clinical situations. Nonetheless, they can always be used as a starting point in dietary evaluation, and as the medical condition and subsequent nutrition therapy are established, adjustments can be made for specific nutrient requirements. The DVs were established by the Food and Drug Administration to assist consumers in interpreting nutrition labeling information. These standards set target goals for fat, saturated fat, cholesterol, total carbohydrate, fiber, sodium, potassium, and protein for a 2000- and 2500-kcal reference diet (note that these are different from the DRI goals). In general, the DVs are much more useful to the consumer purchasing groceries than the dietitian performing a nutrition assessment. The dietitian will use much more specific, individualized reference data for assessment but certainly may use the DVs as an educational tool.

3.6  ANTHROPOMETRIC/BODY

Figure 3.8 Measuring Infant Length

­COMPOSITION MEASUREMENTS “Anthropometry is the measurement of body size, weight, and proportions.”16 Body composition refers to the distribution of body compartments (e.g., muscle mass and body fat) as part of the total body weight. Evaluating both anthropometric and body composition data allows the clinician to fully assess these compartments. Because nutrition is a crucial component of normal growth and development, it is accepted practice to measure body compartments in order to evaluate infants and children for appropriate growth. In a normal, healthy individual, the relationships among body storage compartments are relatively stable. But when disease or stress is present, changes in the storage compartments are an important aspect of nutritional status and risk. Results of anthropometric assessment can be used to both identify goals for nutrition intervention and monitor changes that occur as a result of either those interventions or continued effects of disease and stress. NHANES, the U.S. nationwide survey used to obtain health and nutrition information, collects a variety of anthropometric measurements and provides standardized procedures for practitioners and researchers to apply as they use these techniques in health and disease assessment.26

Children under the age of 2 are measured using a stationary headboard and movable footboard.

Source: E. Whitney and S. Rolfes, Understanding Nutrition, 10e, Copyright ©2005, p. 591.

Figure 3.9 Stadiometer

Anthropometrics Nutrition Care Indicator: Height/Stature/Length 

Measurement of supine or standing height is ­necessary for monitoring growth of infants and children and for interpretation of weight in adults. For children under the age of 2 years, length is measured recumbently using a length board. This device has a stationary headboard and a movable footboard (Figure 3.8). This measurement requires two clinicians, one of whom holds the child’s head against the headboard while the other extends the leg and bottom of the heel to the footboard. The child is positioned correctly when the Frankfort plane is parallel to the fixed headboard. Length is recorded to the nearest 0.1 cm. It is recommended that a second measurement be taken and should agree with the first measurement within 1 cm or ¼ inch. Over the age of 2 years, standing height is measured using a tape measure or stadiometer as long as the child can follow instructions and remain standing for the measurement (see Figure 3.9). The procedure for measuring height is to have the client stand barefoot and look forward with shoulders, buttocks, and heels touching the vertical surface of either a wall or the stadiometer with the Frankfort plane.27 This ensures the head is not tilted incorrectly. Table 3.5 provides an example of a standardized protocol for obtaining length. Sometimes a client cannot stand for the measurement of height—for example, because he or she is disabled or confined to a wheelchair or bed. In these cases, any of several estimation methods may be used. One method is arm span: The client extends the arms from the body at a 90-degree angle and distance is measured between the tips of the two middle fingers. The length of the dominant arm can be measured in the same fashion and multiplied by 2 to estimate height. A limitation of this method is that it is an estimation of maximum adult height and not actual, current height.

Source: Courtesy of Marcia Nelms.

Knee height is another method of height estimation (­ Figure 3.10). Measurement of knee height, using a knee-height caliper, can be taken when the client is sitting or in a supine position. (Measuring supinely is considered to be more accurate.) The client lies supine with right knee and ankle flexed to 90 degrees. The clinician should place the fixed ­portion of the caliper under the heel and position the other blade over the anterior portion of the thigh above the knee. The shaft of the caliper is parallel to the tibia. The measurement (repeated

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   51

Table 3.5 Procedure for Taking the Recumbent Length 1. Cover the board with table paper. 2. Ask the assistant to remove hats, barrettes, shoes, and socks. “Big” hairstyles will need to be flattened as much as possible. If hair or barrettes interfere with placing the child’s head directly against the measuring board, make a note of this on the questionnaire. (Do not attempt to adjust the measurement.) 3. Provide a brief training to the assistant on how to hold the child’s head. 4. Place the sliding foot piece at the end of the measuring board and check to see that it is sliding freely. 5. Ask the assistant to lay the child down on his/her back on the measuring board and stand directly behind the child’s head. If it is not possible for the assistant to stand behind the child’s head, he/she may stand beside it. 6. Position yourself on the right side of the child so you can hold the foot piece with your right hand.  Note: While the infant is on the measuring board, you must hold and control the child so that he/she will not roll off or hit his/her head on the board. 7. Hold the child securely at the waist while the assistant positions the head. 8. Ask the assistant to cup her hands over the child’s ears. The assistant’s arms should be straight if possible and she should hold the child securely yet comfortably. Make sure that the assistant is cupping her hands. Her hands should not be flat against the child’s head and her thumbs should not be touching the child’s shoulders. 9. Ask the assistant to place the child’s head against the headpiece. 10. If the head is not against the headpiece, hold the child at the waist and lift or slide the child toward the headpiece. The assistant should hold the child’s head at all times and guide the head into position. 11. Check to be sure that the child’s head is in the correct position. The line from the hole in the ear to the bottom of the eye socket (Frankfort plane) should be perpendicular to the board or table. 12. Ask the assistant to place her head directly above the child’s head and watch the position of the child’s head during the entire measurement. Ask her to make certain that the child’s chin is not tucked in against his/her chest or stretched too far back. 13. Position the child’s body so that the shoulders, back, and buttocks are flat along the center of the board. 14. Place your left hand on the child’s knees. Hold the movable foot piece with your right hand and firmly place it against the child’s heels. A child’s legs and feet can be very strong. You may have to straighten them with your hands. 15. Check the child’s position: head against the headpiece with eyes looking straight up, body and legs straight and flat in the center of the measuring board, heels, and feet firmly against the foot piece. 16. When the child’s position is correct, read and call out the length measurement to the nearest 1/8". Continue to call out the measurement until the measurement is recorded. 17. Record the measurement on the data collection sheet under “Recumbent Length.” Check to make sure it is accurate and legible. Note: It is acceptable to take two measurements that agree within 1/8" and use either one of those measurements. Source: Indian Health Service. Infant guidelines. https://www.ihs.gov/HWM/infantguidelines/

Figure 3.10 Knee Height Knee-height calipers are used when height must be measured for an individual who cannot stand.

two to three times) is recorded to the nearest 0.1 cm. Height is then estimated using the following equations:28 Age 19–60 years: • White male = 71.85 + (1.88 × knee height) • Black male = 73.42 + (1.79 × knee height) • White female = 70.25 + (1.87 × knee height) – (0.06 × age) • Black female = 68.10 + (1.86 × knee height) – (0.06 × age) Age >60 years: • White male = 59.01 + (2.08 × knee height) • Black male = 95.79 + (1.37 × knee height) • White female = 75.00 + (1.91 × knee height) – (0.17 × age) • Black female = 58.72 + (1.96 × knee height)

Source: Courtesy of Marcia Nelms.

52  Part 2  The Nutrition Care Process

Height or length has been noted to be one of the most inaccurate measures. One study indicated that inaccuracies are introduced when shoes are not removed, a verbal report is taken instead of a measurement, or the head, shoulders, or heels are

This calculation allows weight to be compared to a criterion standard such as BMI. Weight is the most common measure of anthropometrics. Unfortunately, it is a gross measurement of all body compartments and does not distinguish body composition or fluid shifts. Nevertheless, due to its common availability and its relationship to growth, development, and health, it remains a vital component of nutrition assessment.

Figure 3.11 Measuring Weight Weight is the most common anthropometric measure.

Nutrition Care Criteria: Evaluation and ­Interpretation of Height and Weight in Infants and Children Growth Charts  Weight and height for infants and c­ hildren

Source: Courtesy of Marcia Nelms.

not in the correct position. In clinical settings, it is often either ­estimated or recorded from patient report.29–31 Nonetheless, accurate measurement is crucial because height is used to interpret weight, measure growth for children, calculate energy and protein requirements, and calculate creatinine height index (CHI).

Nutrition Care Indicator: Weight  Weight can be measured using a variety of scales, including balance beam (­Figure 3.11) and electronic scales. Bathroom scales and those that are moved frequently are not recommended due to poor calibration. Wheelchair and bed scales are available for nonambulatory patients. Ideally, the client should be weighed with minimal clothing and without shoes, at the same time daily, and after urination. For those patients with an amputation, weight has historically been adjusted using the following factors:32 • Hand: 0.8% • Forearm and hand: 3.1%

are evaluated using growth charts developed by the WHO, Centers for Disease Control and Prevention (CDC), and the National Center for Health Statistics (see  Box  3.3). ­D etermination of height for age and weight for age allows comparison of an infant or a child to a reference population. Data for the CDC growth charts are based on the NHANES and were most recently updated in 2000.33 It is ­recommended to use the WHO growth standards for infants and children less than two years of age and to use the CDC standards over age 2. When infants and children are either 97th percentile, further assessment should be made to confirm any health problems. Furthermore, shifts in patterns of growth should also alert the practitioner to either an error in measurement or a cause for concern for the child’s nutritional status. There are specific clinical diagnoses, such as genetic and endocrine disorders, that negate use of these standard growth charts. Alternative growth charts have been ­developed for children with specific health care needs such as cerebral palsy or Down’s syndrome. Weight for height and percentile weight for height can also be evaluated using CDC growth charts. These measurements allow evaluation to be independent of age and can be used to monitor acute malnutrition (95th percentile). An additional assessment using growth chart data is the calculation of a Z-score. Z-score or standard deviation score is equivalent to the observed value—the median value of the reference population divided by the standard deviation value of the reference population. A Z-score of 0 is the same as the 50th percentile, ± 1.0 plots at the 15th or 85th percentiles, respectively, ± 2 at roughly the 3rd or 97th percentiles.33

Body Mass Index  Revision of the CDC growth charts in

• Entire arm: 6.5% • Foot: 1.8% • Lower leg (below knee) and foot: 7.1% • Entire leg: 18.6% For example, for an individual who has had an entire leg amputated and currently weighs 165 lbs, weight would be adjusted by using the following equation: Adjusted body weight = actual measured weight divided by 100 — % amputation. The whole equation then is multiplied by 100. 165 lbs 3 100 5 202 lbs is the estimated body weight (100 2 18.6)

2000 added the measurement of BMI. BMI is weight (kg)/ [height(m)]2.33 Calculation and interpretation of BMI in children and adolescents has increased in recent years. Assessment is not based on adult standards, however; instead, overweight is defined as 85th to 95th percentile of BMI-for-age, and underweight is defined as  Age 2 BMI-for-Age Percentile

BMI Below 18.5

Weight Underweight

Status Health Risk

At risk for underweight

With ,16 suggesting possible eating disorder and other disease risk*

5–85th percentile

Normal

≥85th percentile but 10% in a 6-month period (see Table 3.8). The concept of unintentional weight loss is also included as a criterion in the

Table 3.8 Interpretation of Unintentional Weight Change Clinical Context Acute illness/injury

Weight Loss Indicating Severe Malnutrition >2% in 1 week >7.5% in 3 months >5% in 1 month >7.5% in 3 months >10% in 6 months >20% in 12 months

Social/behavioral/environmental circumstances

>5% in 1 month >7.5% in 3 months >10% in 6 months >20% in 12 months

Source: White JV, Guenter P, Jensen G, et al. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: characteristics recommended for identification and documentation of adult malnutrition (undernutrition). J Acad Nutr Diet. 2012; 112: 730–38.

proposed definitions of malnutrition.34 The absolute number of pounds or kilograms change is also used to describe rapid weight change as well.

Percent Usual Body Weight and Percent Weight Change  Percent usual body weight is calculated as: current body weight usual body weight

3 100

Percent weight change is calculated as: present body weight − usual weight usual body weight

weight (kg) ÷ [height (m)]2 or

>5% in 1 month Chronic illness

Body Mass Index  BMI or Quetelet’s Index, as stated ­previously, is calculated as:

3 100

or: % usual body weight – 100 = % change

Reference Weights  Height-weight tables and body weight

recommendations estimated from these data were initially ­created by the life insurance industry. These data have been criticized and their use is discouraged as the original population does not correlate with the current populations in the United States. Other criticisms of the development of these standards include the assumption of the weight of an individual’s clothes, use of a standard heel height on shoes, and estimation of frame size. Calculation of BMI (see the next two sections) is considered to be the only validated method for assessing healthy weight. Nonetheless, in many clinical settings, reference body weight is calculated using the Hamwi equation (shown below) even though it does not adjust for differences in age, race, or frame size.35 Men: 106 lbs for 5 foot + 6 lbs per inch over 5 foot or –6 lbs per inch under 5 foot Women: 100 lbs for 5 foot + 5 lbs per inch over 5 foot or –5 lbs per inch under 5 foot

weight (lbs) ÷ [height (inches)]2 × 704.5

BMI has been well correlated with overall mortality, disease and nutritional risk. It is crucial to remember that BMI does not distinguish between body compartments and, therefore, does not estimate body composition. Still, the BMI measurement is better at indicating obesity than mere height and weight alone. A client with a BMI >25 is considered to be overweight, and a client with a BMI 0.90 for men or ≥35 inches (88 cm) or >0.85 for women is considered to be predictive of obesity and chronic disease risk in Caucasian, African-American, Hispanic, and Native-American populations. Within Asian populations, risk is defined at ≥90 cm in men and ≥80 cm in women. Fat accumulation, primarily in the abdominal region (or android obesity), is linked to an increased risk of type 2 diabetes mellitus, metabolic syndrome, and other obesity-related diseases. The current recommendations from the National Heart, Lung, and Blood Institute/American Heart Association are that waist circumference should be used as a part of routine physical examination.36,37 Additional assessments using the waist circumference measurement are the waist-to-hip ratio and the waist-to-height ratio. These measurements are used to assess risk of obesity-related diseases that are associated with an android fat storage pattern (i.e., apple shape).37,38 Waist-tohip ratio is calculated by dividing the waist measurement by the hip measurement. Waist-to-height ratio is equal to waist measurement divided by height. See Figures 3.12 and 3.13 for guidelines for measurement of waist circumference and waist-to-hip ratio.

Body Composition Height and weight, though crucial components of nutrition assessment, are only gross measurements and cannot distinguish among body compartments. It is not unusual, then, for very muscular individuals to fall into the overweight or obese category when only height and weight are used in the nutrition assessment. Measurements of skinfolds, waist circumference, and other body composition techniques allow the clinician to make a more thorough and complete nutrition assessment. However, these are not routinely done in most clinical settings where acute care is the primary goal. In settings where clients are followed for a length of time, these assessments are clinically useful. Body composition refers to distribution and size of all components contributing to total body weight. In most clinical settings, body composition refers to two major components of total body weight: fat mass and fat-free mass. A more thorough definition would include fat and muscle mass, total body water, and osseous mineral (bones and teeth). Nutrition

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   55

professionals are most concerned about metabolically active tissue and fluid status. Techniques that allow assessment of these compartments support the design of appropriate nutrition interventions. Measurement techniques such as skinfolds and bioelectrical impedance use portable equipment and are

Figure 3.12 Measuring Waist Circumference The line shows the appropriate position for the tape measure.

easily accomplished in any setting. Other measurements using hydrodensitometry, air displacement plethysmography, dual-energy X-ray absorptiometry (DXA), computed tomography, or ultrasound are used in outpatient and research settings but not necessarily in the daily acute care setting. All these assessment methods are covered in this text because the basic understanding of these techniques allows one to compare various assessment methods for a variety of populations.39

Nutrition Care Indicator: Skinfold Measurements 

Skinfold measurement is used to estimate energy reserves— both fat and somatic protein—in subcutaneous tissue. Skinfold measurement involves measuring a double fold of skin and subcutaneous adipose tissue while excluding muscle tissue.39 Skinfolds are minimally invasive for the client, and require only calipers (Figure 3.14) and a tape measure. These advantages have led to the common use of skinfolds despite the availability of more accurate methods. It is important to

Figure 3.14 Skinfold Calipers

Source: National Heart, Lung, and Blood Institute Guidelines on ­Overweight and Obesity: Electronic Textbook. https://www.nhlbi.nih.gov/ health-pro/guidelines/current/obesity-guidelines/e_textbook/txgd/4142.htm

Source: Courtesy of Marcia Nelms.

Figure 3.13 Tape Placement for Waist Measurement Waist circumference should be measured around the abdomen at the level of the iliac crest.

Source: Courtesy of Marcia Nelms.

56  Part 2  The Nutrition Care Process

recognize, however, that it takes a significant amount of repetition and experience to obtain consistent, reliable results. Sites for skinfold measurement include the chest, triceps, subscapular, midaxillary, suprailiac, abdomen, thigh, and calf. Using more than one site for measurement may provide a more accurate “picture” of the individual. The most commonly used site is the triceps. Triceps skinfolds (TSFs) are taken on the nondominant arm, halfway between the olecranon and acromial processes. Additionally, midarm circumference measurement can be combined with TSF measurement to indirectly estimate arm muscle area and arm fat area (­Figure 3.15). Equipment needed for skinfold measurement includes a tape measure (Figure 3.16) and a skinfold caliper. The Harpendon or Lange calipers are generally recommended because these brands were used in development of reference standards and equations.

Nutrition Care Criteria: Interpretation and Evaluation of Skinfold Measurements  Skinfold and midarm circumference

Figure 3.15 Mid-Upper Arm Muscle Area in Adults

Clavicle Acromion process

Midpoint

Olecranon process Source: SR Rolfes, K Pinna & E Whitney, Understanding Normal and Clinical Nutrition 7e, Fig E7, p E8.

AMA for females 5

[MAC − (π 3 TSF)]2 43π

− 6.5

AMA 5 arm muscle area in mm2; MAC 5 midarm circumference in cm, and TSF 5 TSF in cm.

measurements—as well as the index calculations for mid-upper arm muscle circumference, mid-upper arm muscle area, and [MAC − (π 3 TSF)]2 − 10 AMA for males 5 mid-upper arm fat area—can be compared 43π to references that are based on NHANES summary data. Comparison data are age, AMA 5 arm muscle area in mm2; MAC 5 midarm circumference in cm, and gender, and race specific. They may also TSF 5 TSF in cm. be specific to frame size. Midarm circumference alone has not been considered a Source: Frisancho AR. 1990. Anthropometric standards for assessment of growth and nutrisensitive measure for malnutrition when tional status. Ann Arbor: University of Michigan Press. compared to other measures, but its use in Mid-Upper Arm Muscle Area in Adults epidemiological research has been increas40 Percentage of ing. An individual who is below the 5th Standard (%) Men (cm2) Women (cm2) Muscle Mass percentile or greater than the 95th percen100 ; 20* 54 ; 11 30 ; 7 Adequate tile may be at nutritional risk (Table 3.9). See Appendix D1, pp. A-73 to A-82 for these ref75 40 22 Marginal erence standards. 60 32 18 Depleted When interpreting these measurements 50 27 15 Wasted within a nutrition assessment, it is important to recognize that these reference standards *Mean mid-upper arm muscle mass ; 1 standard deviation. were developed using a healthy population and From National Health and Nutrition Examination Surveys I and II. should not be used for a patient in a disease state. Furthermore, a one-time skinfold calcu- Source: From the Merck Manual—Professional Version, Copyright 2018 by Merck & Co, Inc., lation may not really contribute any clinically Whitehouse Station, NJ. Available at https://www.merckmanuals.com/professional/SearchResults?query=Mid+upper+arm+muscle+area. Accessed July 31, 2018 useful information in the acute care setting. Hydration state, fluid shifts, and skin elasticity Percentiles for interpretation of Arm Muscle Area found in Appendix D1. (especially in older adults) can affect skinfold measurement. When the individual can serve Multiple-site skinfold measurements can be used to as his or her own control with repeated measures over time, estimate body density and body fat percentage. Numerous long-term changes in energy stores can be assessed to provide regression equations and protocols have been developed. The clinically useful information. Accuracy of measurement may regression equation originally designed for a population that be difficult to achieve if more than one clinician is performmost closely matches the client should be used. For example, ing the assessment, but error can be minimized when a single the Jackson–Pollock regression equation combines the triwell-trained clinician uses the same equipment and method ceps, suprailium, and thigh skinfolds to estimate body fat in each time the assessment is performed. Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   57

Figure 3.16 Measuring Tapes

Figure 3.17 Bioelectrical Impedance Analysis (BIA)

Using appropriate standardized equipment allows for consistent results when taking anthropometric measurements.

Source: Courtesy of Marcia Nelms.

Source: Courtesy of Marcia Nelms.

Table 3.9 Interpretation of Triceps Skinfold Measurements Comparing the percentile ranking of a specific individual for the various anthropometric measurements with a classification scheme is the basis for interpreting these values. Reference data in percentiles for triceps skinfold (TSF), arm muscle area (AMA), and arm fat area (AFA) appear in Appendix D1. Because reference data are those compiled by Frisancho from the NHANES I and NHANES II data, it is appropriate to use classification categories derived statistically from these data. The table below displays percentile categories and their interpretation for arm muscle and arm fat areas as well as total body weight. ­Percentile Rank

AMA

AFA

Total Body Weight

85

Above-average musculature

Excess fat

Excess total body weight

Sources: Based on Contemporary Nutrition Support Practice, Matarese L and Gottschlich M; Philadelphia: WB Saunders Company; 2003, box 3-1, p. 36; Ref : Frisancho AF: Anthropometric standards for the assessment of growth and nutritional status, Ann Arbor, Michigan: The University of Michigan Press; 1990: 28, 41, 51, 54, 60–63.

women and the chest, abdomen, and thigh for estimation of body fat in men. (See Appendix D for detailed instructions on skinfold measurements.)

Nutrition Care Indicator: Bioelectrical Impedance Analysis (BIA)  BIA is a common procedure used to

estimate body composition. It is considered to be a rapid, safe, portable, and noninvasive method of assessment. There are numerous types of equipment available to measure BIA, but they are all based on the same scientific principle. A small, low-frequency, alternating electrical

58  Part 2  The Nutrition Care Process

current is administered at one extremity of the body (see Figure 3.17). Measurement of impedance of the electrical current can then be used to estimate components of body composition, including body cell mass, fat-free mass, fat mass, and total body water. Tissues that contain little water such as fat and bone are poor conductors of electricity and therefore have a greater resistance or impedance to flow of the current. Other tissues that have greater water content, such as blood, muscle, and vital organs, are good conductors and therefore have lower impedance. More recent advances in technology provide for segmental measurement, which allows for estimation of regional body fat. Additionally, multiple-­f requency BIA may provide a more accurate assessment than a single frequency.

Nutrition Care Criteria: Interpretation and Evaluation of BIA Measurements  Regression equations used to

estimate body composition with BIA measurements include age, gender, weight, height, resistance, and reactance. From this information, components of body composition can be calculated. Additionally, equations have been validated specific to race and PA level.41 Even though the use of BIA has continued to expand in recent years, BIA should not be used to assess body composition in patients who have experienced major shifts in water balance and distribution. Phase angle, as a measure of body composition, has been used as an additional measure of prognosis in many chronic conditions. Current research uses BIA as the means to monitor fluid accumulation in clinical conditions such as renal failure. Published studies have utilized BIA to assess body composition in multiple clinical conditions. 42–45 Population-based reference data for BIA were previously unavailable, but NHANES data include new references for it.26

Nutrition Care Indicator: Hydrostatic (Underwater) Weighing  Underwater weighing is generally accepted

as the most accurate method of measuring body composition. Other body composition methods have historically been validated against underwater weighing results. Hydrostatic weight (hydrodensitometry) can be used to evaluate

body composition in the more traditional view, that of the two-compartment model. This method measures body volume (density) and relies on the assumption that the density of fat mass and components of fat-free mass are constant. Obviously, access to underwater weighing facilities is not readily available, and thus this method has limited clinical use. It is also a difficult procedure for the subject to complete. Additionally, the reference equations were based on only Caucasians and may need changes for use with other ethnicities. Other limitations of this methodology include the possible overestimation of fat mass due to the assumption that all components of fat-free mass are constant. A correction for residual lung volume must also be made, and this volume is difficult to estimate.

Figure 3.18 Dual-Energy X-Ray Absorptiometry DXA is increasingly being recognized as a reference method to assess body composition.

Nutrition Care Indicator: Dual Energy X-Ray Absorptiometry  DXA was first developed to measure

bone mineral content and density. DXA measures three compartments: mineral mass, mineral-free mass, and fat mass. In this method, the body is scanned with radiation photons at two different energy levels. Absorption of the photons by body tissues is then measured at each of these two levels. The absorption rate of different body tissues allows for calculation of the three body compartments (see Figure 3.18). Recognition of DXA as a reference method to assess body composition has grown.1,46–51 DXA is considered precise enough in assessing body composition and measuring total body fat for measurement of both short- and long-term changes for a variety of individuals and conditions.47 Unlike underwater weighing and air displacement plethysmography, but similar to skinfolds, DXA provides information on fat distribution among the right and left arms, legs, and trunk masses. Abdominal visceral fat is an important risk factor for metabolic syndrome, cardiovascular diseases, nonalcoholic steatohepatitis (NASH) and diabetes mellitus. DXA is increasingly being used as a less expensive alternative to computed tomography for obtaining a precise measure of visceral fat.50,51

Nutrition Care Indicator: Ultrasound  There is an

increasing recognition of the importance of muscle mass assessment, especially in the aging and critically ill populations. Previous assessments have not allowed for ease of use in either acute or outpatient settings. Increasingly, research is using bedside ultrasound (see Figure 3.19) as a method to assess loss of skeletal muscle, or sarcopenia.52,53 In the future, this emerging bedside ultrasound technique may offer practitioners a more reliable method with which to document and monitor sarcopenia.

Source: Courtesy of Marcia Nelms.

Figure 3.19 Portable Ultrasound Bedside ultrasound may be used to assess loss of skeletal muscle mass in the hospitalized population.

Nutrition Care Indicator: Air Displacement Plethysmography  In air displacement plethysmography, the cli-

ent’s total volume is measured indirectly by estimating the amount of air that is displaced within a sealed chamber. Since the early 1990s, the use of air displacement plethysmography has increased due to the availability of the equipment known as the BOD POD, shown in Figure 3.20. This method is recognized as comparable to hydrostatic weighing and DXA for measuring body composition in infants, children, and adults.54,55

Source: Pro3DArtt/Shutterstock.com

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   59

Figure 3.20 BOD POD The BOD POD is a popular method of body composition ­assessment.

normal energy deficits, additional energy is drawn from fat and glycogen stores. But when the body is under metabolic stress, it draws protein from the muscles to meet its needs (see Chapters 9 and 22). No specific laboratory value can determine the ­precise protein status of an individual. Each test has its own limitations. Therefore, a comprehensive nutrition assessment must use a battery of tests in order to delineate the changes that mark the development of a nutrient deficiency. Historically, protein assessment has focused on evaluation of two compartments: somatic and visceral. Somatic protein refers to skeletal muscle. Visceral ­protein refers to nonmuscular protein making up the organs, ­structural components, erythrocytes, granulocytes, and l­ymphocytes, as well as other proteins found in the blood.

Somatic Protein Assessment  In addition to using anthropometric measures such as midarm muscle area, midarm circumference, and overall body weight and SGA, biochemical tests such as CHI and nitrogen balance can be used to more specifically analyze somatic protein status.

Nutrition Care Indicator: Creatinine Height Index Creatinine is formed at a constant daily rate from muscle creatine phosphate. Creatine phosphate, which is stored in muscle, provides the phosphate group needed to regenerate adenosine triphosphate during high-intensity exercise. Creatinine is not stored in muscle but is cleared and excreted by the kidney. Daily urine output of creatinine can be correlated with total muscle mass. Source: Courtesy of Marcia Nelms.

3.7  BIOCHEMICAL ASSESSMENT AND MEDICAL TESTS AND PROCEDURES Assessment of data from numerous sources supports the appropriate nutrition intervention and plan of care. These data include information gathered during medical procedures such as a barium swallowing test as well as biochemical nutritional markers and indicators of organ function, which are found in blood, urine, feces, and tissue samples. Interpretation of biochemical measurements must be made in the context of diagnosis and medical treatment. Disease states, presence of inflammation, hydration status, and subsequent treatments can have considerable effects on the levels of the biochemical indices and thus dramatically affect their reliability as nutrition assessment measures.56,57 Reference values are established by the institution and may vary from lab to lab. Data should be interpreted using those values provided by the laboratory that conducted the tests.

Protein Assessment Protein’s unique function in supporting cellular growth and development elevates its significance in nutrition assessment. Even though a large amount of protein is stored in muscle and viscera, the body strives to protect it from being used as an energy source. Under healthy conditions or 60  Part 2  The Nutrition Care Process

Nutrition Care Criteria: Interpretation and Evaluation of CHI For this test, a 24-hour urine collection is performed and the total amount of creatinine excreted in that 24-hour period is compared with either a standard based on height or (as a percentage) to a standard excretion for a particular reference individual of a specific height, gender, and age. In Table 3.10, expected creatinine excretion is shown for various heights. CHI is usually expressed as a percentage of a standard value and is calculated with the following equation: CHI 5

24-hour urine creatinine (mg) expected 24-hour urine creatinine (cm)

3 100

A value calculated to be 60%–80% of the standard suggests mild skeletal muscle depletion, 40%–59% suggests moderate skeletal muscle depletion, and 3.5 g/dL. Synthesized by the liver (120–170 mg/ kg/day), albumin serves many significant functions within the body, most commonly as a transport protein and as a component of vascular fluid and electrolyte balance. Decreases

in serum albumin occur due to a decreased synthesis rate, an increased degradation rate, or a change in fluid distribution (either total volume or between compartments). Using albumin as a nutritional assessment marker in acute care is complicated by the fact that most patients are experiencing at least one of these factors; thus, albumin changes often reflect illness and not necessarily nutritional status.56 Nutrition Care Criteria: Evaluation and Interpretation of Albumin Albumin has been the subject of significant nutrition research and thus serves as a good prognostic screening tool, though it is not as reliable in the acute care setting as an overall indicator of protein and nutritional status due to the effects of disease, inflammation, hydration, and numerous other factors. Still, because it is easily measured and has an abundant body pool, albumin is readily available from lab reports in the acute care setting. Decreased albumin levels have been correlated with increased morbidity, mortality, and length of hospital stay. Albumin should still be considered as a longer-term marker for chronic malnutrition. Some of the same factors contribute to its limitations as well. Albumin has a long half-life (approximately 20 days), which decreases its sensitivity to short-term changes in protein status or to short-term interventions to improve protein status. Albumin synthesis is also affected by acute stress and the inflammatory response. Albumin loss occurs with burn injuries, nephrotic syndrome, protein-losing ­enteropathy, and cirrhosis. Other medical conditions that may result in hypoalbuminemia include infection, multiple myeloma, acute or chronic inflammation, and rheumatoid arthritis. Levels also decrease with aging. On the other hand, albumin levels will be higher with dehydration and when individuals are prescribed anabolic hormones and corticosteroids. Albumin levels must be interpreted carefully—the levels are a better indicator of stress and inflammation than of overall protein nutriture, even though they historically have been widely used for that purpose. Nutrition Care Indicator: Transferrin Synthesized by the liver, transferrin serves as a transporter for iron throughout the body. It can also serve as an indicator of protein status because it has a shorter half-life (8–10 days) and thus is

Table 3.11 Visceral Protein Assessment Overview Serum Protein

Normal Range*

Half-Life

Primary Function

Comments

Albumin

3.5–5.0 g/dL

17–21 days

Blood transport protein; Trauma, surgery, inflammation, and metabolic stress affect component of vascular fluid levels; affected by hydration status—decreases with overhydraand electrolyte balance tion, increases with dehydration

Transferrin

250–380 mg/dL F

8–10 days

Iron transport

Negative acute-phase respondent; affected by iron status

215–365 mg/dL M Prealbumin/ transthyretin

16–35 mg/dL

2–3 days

Transport of thyroxine

Negative acute-phase protein—decreases with illness, inflammation, infection, trauma, surgery, and metabolic stress; decreases with diagnoses of liver disease such as hepatitis or cirrhosis, malabsorption, and hyperthyroidism

Retinol-binding protein

2.1–6.4 mg/dL

10–12 hours

Transport molecule for vitamin A

Negative acute-phase respondent; elevated with renal failure; decreased with hyperthyroidism, cystic fibrosis, liver failure, vitamin A deficiency, zinc deficiency, and metabolic stress

*Reference values may differ by laboratory.

62  Part 2  The Nutrition Care Process

s­ ensitive to acute changes in protein intake or requirements. Normal serum levels are 215–380 mg/dL. Transferrin can be ­measured directly or calculated from total iron-binding capacity (TIBC) with the use of the following equation: Transferrin saturation (%) = (Serum iron level × 100%) ÷ TIBC. Nutrition Criteria: Evaluation and Interpretation of Transferrin Transferrin’s primary limitation is that its concentration is directly affected by iron status. When iron stores are decreased, transferrin levels will increase to accommodate the need for increased levels of transport. Other disease states such as hepatic and renal disease, inflammation, and congestive heart failure can also affect transferrin levels. Nutrition Care Indicator: Prealbumin (Thyroxine-Binding Prealbumin or Transthyretin) Prealbumin is another example of an acute-phase transport protein synthesized by the liver. Prealbumin is responsible for transport of thyroxine and is associated with retinol-binding protein (RBP). Nutrition Criteria: Evaluation and Interpretation of Prealbumin Research has shown that because of its very short half-life (2 days), prealbumin levels respond to short-term modifications in nutritional intake and interventions. Prealbumin is a more expensive test than albumin, but research has indicated that if it were used routinely during admission screening, approximately 44% more hospitalized patients would be identified as being at nutritional risk. The clinician evaluating prealbumin should recognize that levels are increased with renal disease and Hodgkin’s disease (a form of lymphoma), and decreased with liver disorders such as hepatitis or cirrhosis, malabsorption, and hyperthyroidism. Furthermore, like albumin, prealbumin levels may decrease as a result of illness and inflammation and not necessarily malnutrition.60,61 Nutrition Care Indicator: Retinol-Binding Protein RBP, synthesized by the liver, is an acute-phase respondent and serves as the transport molecule for vitamin A (retinol). RBP has the smallest body pool and shortest half-life (12 hours) of the serum proteins. Nutrition Criteria: Evaluation and Interpretation of RBP RBP is considered to be one of the more sensitive indicators of protein status in the non-critically ill. Theoretically, it should reflect short-term changes and responses to nutrition support interventions. Lee and Nieman note that it is most likely a better measure of recent dietary intake than an indicator of overall nutrition status.58 The literature does not support its use preferentially over other measures of serum proteins. Note that RBP levels are elevated with renal failure and decreased with hyperthyroidism, liver failure, vitamin A deficiency, zinc deficiency, and metabolic stress. Nutrition Care Indicator: C-Reactive Protein CRP is a positive acute-phase protein that is released during periods of inflammation and infection. As the levels of acute-phase proteins increase, hepatic reprioritization decreases synthesis of other transport proteins, such as prealbumin or albumin. Increasingly, CRP is being used to investigate the contribution of inflammation to malnutrition syndromes.

Since albumin and prealbumin levels may be reduced by the inflammatory process, they are not reliable prognostic indicators during periods of inflammation and infection; in these situations, the CRP level becomes a component of nutrition assessment. Higher CRP levels are associated with increased nutritional risk during stress, illness, and trauma.56,60

Immunocompetence Assessment Historically, evaluation of immunocompetence has been included as a part of any discussion of protein and nutrition assessment. This is logical, since adequate and appropriate immune function is dependent in part on adequate protein status. Protein deficiency routinely results in increased risk of infection as well as altered immune and inflammatory responses. But in clinical practice, the use of this type of nutrition assessment is complicated by the presence of disease and infection, which of course also affect all components of the immune system.

Nutrition Care Indicator: Total Lymphocyte Count (TLC)  When evaluating a complete blood count (CBC) and differential count, calculation for TLC can be completed as follows: TLC 5

WBC 3 % lymphocytes 100

TLC will be affected by presence of infection, trauma, stress, and diseases such as cancer and HIV, as well as medications that influence the immune system (e.g., chemotherapy and corticosteroids).

Nutrition Care Indicators for Hematological Assessment Evaluation of erythrocytes (red blood cells, or RBCs) can be an important component of nutrition assessment and is key to diagnosis of all anemia types. A CBC includes ­measurement of the total number of blood cells in the v­ olume of blood. Many types of anemias exist, including those caused by d ­ eficiencies of iron, folate, or vitamin B12 and those ­arising from chronic diseases such as renal failure and congestive heart failure. Anemias are diagnosed by evaluation of the CBC and by the microscopic evaluation of the size, shape, and color of erythrocytes. (See Chapter 19 for detailed information on hematological disorders.)

Hemoglobin (Hgb)  Hgb is a protein found in erythrocytes that functions to deliver oxygen to cells and to pick up carbon dioxide for expiration by the lungs. Measurement of Hgb is common in diagnosis of anemias, particularly iron-deficiency anemia. Additionally, Hgb is decreased in some chronic diseases and protein-energy malnutrition (PEM). Even though it is commonly measured, it is not the most sensitive or the most specific of hematological assessments of nutritional status. For example, in iron deficiency, iron stores may be depleted before serum Hgb levels will be affected. Hematocrit (Hct)  Hct is defined as the percentage of blood that

is actually composed of RBCs. Hct, like Hgb, will be decreased only in the final stages of iron deficiency. Hct is affected by other nutrient deficiencies as well as by hydration status.

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   63

Mean Corpuscular Volume (MCV)  MCV is a measure of

the average size of an individual RBC. A variety of anemias are characterized by changes in RBC size; for example, MCV is reduced in iron and copper deficiencies and elevated in folic acid and vitamin B12 deficiencies.

Mean Corpuscular Hemoglobin (MCH)  MCH is an estimate of the amount of Hgb in each cell. This value can reflect total serum Hgb levels. In some situations, however, MCH remains normal while the number of RBCs is low, resulting in low total Hgb. Abnormalities are generally specific to iron deficiency and other nutritional anemias. Mean Corpuscular Hemoglobin Concentration (MCHC)  MCHC also estimates the amount of Hgb in each RBC, but it expresses the value as a percentage.

Ferritin  Ferritin is a protein that serves as a storage form

of iron; therefore, serum ferritin is an estimate of iron stores. Ferritin is a sensitive and specific measure of iron status and will be one of the first indices to change in iron deficiency.

Transferrin Saturation  As discussed earlier under “Pro-

tein Assessment,” transferrin is a serum protein responsible for transport of iron systemically. Each molecule of transferrin can carry two molecules of iron. Under normal conditions, approximately 30% of iron binding sites on the transferrin molecule are saturated (i.e., have iron attached). The body’s requirement for iron and overall iron status will be reflected by changes in transferrin saturation. When iron status is low, transferrin is less saturated. Transferrin is calculated by using the ratio of serum iron levels to TIBC. TIBC is the test used to measure the saturation ability for transferrin. TIBC is higher during iron deficiency and lower after repletion. There are numerous equations to calculate transferrin from TIBC, but, as mentioned earlier, transferrin is not the most reliable indicator of protein status due to the effect of iron status.

Protoporphyrin  When there is inadequate iron available

for Hgb synthesis, zinc is substituted for iron within Hgb. Consequently, zinc protoporphyrin (the protein transporter for zinc) levels rise during iron deficiency and are considered a sensitive measure of iron-deficiency anemia.

Serum Folate  Coenzymes associated with folate are

­ ecessary for amino acid metabolism, including many onen carbon transfer reactions such as the conversion of h ­ istidine to glutamate. Folate coenzymes also play a c­ rucial role in the synthesis of purine needed for DNA. Folate d ­ eficiency can be diagnosed when megaloblastic, m ­ acrocytic RBCs are present and serum folate and red cell folate are decreased, while serum B12 remains within normal limits. If folate levels are inadequate for conversion of histidine to glutamate, an intermediate product, formiminoglutamate (FIGlu), is formed. Urinary levels of FIGlu are thus elevated in folate deficiency and serve as a diagnostic tool for the condition.

Serum B12  Anemia associated with B12 (cobalamin) defi-

ciency can be diagnosed in several ways. Clinically, it will be similar to folate deficiency but can be distinguished by measuring serum B12 levels, including serum total cobalamin and serum holo-transcobalamin II (the transport protein for B12). Biomarkers of B12 include homocysteine and methylmalonic 64  Part 2  The Nutrition Care Process

acid levels, which change early on in the development of B12 deficiency. Historically, the Schilling test allowed for determination of defective absorption (gastric vs. intestinal). In this test, B12 is given as an injection and the amount excreted in urine is measured. This allows problems with different steps of B12 absorption to be distinguished (see Chapter 16). The Schilling test is no longer used in clinical practice, though to date no other test has replaced its specific function.63

Vitamin and Mineral Assessment Laboratory tests are available for the assessment of most vitamins and minerals. These tests vary from high-performance liquid chromatography to antibody tests and microbiological, radioisotopic, and chemiluminescence assays. There is concern that different types of assays do not always provide comparable results. Clinicians should be aware that serum levels and tissue concentrations may also vary considerably, and take this into consideration when interpreting data for each specific vitamin or mineral. Common examples of situations where vitamins are routinely measured include serum vitamin D assessment in inflammatory bowel disease, osteoporosis, and renal disease; thiamin levels for individuals who are on long-term diuretics or who have a history of alcoholism; and B12 assessment for individuals with GI diseases or who are post-bariatric surgery.

Other Labs with Clinical Significance Many other biochemical labs are routinely assessed and monitored. These may include measures of lipid status such as LDL cholesterol, HDL-C, or triglycerides. Total cholesterol is often < 100 mg/dL in PEM or in conditions causing malabsorption. Electrolytes and measures of blood urea nitrogen (BUN), creatinine (Cr), and serum glucose are components of routine admission labs. The specific labs monitored by members of the health care team depend on the patient’s diagnosis, hydration status, and medical care. See Table 3.12 for a summary of routine admission laboratory measurements.

Table 3.12 Routine Admission Laboratory Measurements Chem—7 Panel BUN (blood urea nitrogen)

Glucose

Serum chloride

Serum potassium

CO2 (carbon dioxide)

Serum sodium

Creatinine Chem—20 Panel Albumin

Glucose

Alkaline phosphatase

LDH (lactate dehydrogenase)

ALT (alanine transaminase)

Serum phosphorus

AST (aspartate aminotransferase)

Potassium test

BUN (blood urea nitrogen)

Serum sodium

Serum calcium

Total bilirubin

Serum chloride

Total cholesterol

CO2 (carbon dioxide)

Total protein

Creatinine

Uric acid

Direct bilirubin Gamma-GT (gamma-glutamyl transpeptidase)

3.8  NUTRITION CARE CRITERIA:

3.9  NUTRITION CARE CRITERIA:

NUTRITION-FOCUSED PHYSICAL FINDINGS

­FUNCTIONAL ASSESSMENT

In addition to the physical examination performed by m ­ edical and nursing staff, the dietitian should routinely perform a nutrition-focused physical examination for at-risk patients. The purpose of this physical exam is to assess the patient for signs and symptoms consistent with malnutrition or specific micronutrient deficiencies. 64–68 Techniques of inspection, palpation, percussion, and auscultation are used to examine the body for these signs and symptoms. Inspection is a visual assessment of the body conducted in a systematic manner by the clinician in order to note any variations from normal features. Palpation is examination of the body using the sense of touch. Percussion involves the use of sound to identify deviations from standard sounds produced when the body surface is tapped by the fingers of the practitioner. The presence of body organs and cavities will change the resonance and quality of sounds. In the nutrition-focused physical assessment, percussion may be used to assess the status of the GI tract when assessing a feeding route or to identify fluid in the lungs, which may necessitate the need for medical intervention and possibly fluid restriction. Auscultation also uses the sense of hearing to identify deviations from standard sounds. In this technique, a stethoscope is used to evaluate sounds produced by the heart, lungs, and GI tract. An example is the identification of bowel sounds. The recently proposed criteria for diagnosis of malnutrition utilize physical assessment as a core component. These criteria include several characteristics of malnutrition that may be identified through a physical exam: loss of muscle mass, loss of subcutaneous fat, and localized or generalized accumulation of fluid.64 The methodology and interpretation for the nutrition-focused physical assessment are included in Appendices F–G. See Table 3.13 for example findings.

Functional assessment focuses on measurements that assess skeletal muscle function or strength. Additionally, functional assessment could be expanded to include those activities that require adequate strength. For example, in the SGA, questions that focus on activities and function are included. The SGA identifies the patient’s perception of his or her ability to accomplish self-care and the environment where the patient spends the majority of his or her time (e.g., bedridden, in a chair, or normal activity). Another method of functional assessment is the identification of specific ADL and instrumental ADL (IADL) related to nutritional status. Different scales have been developed to measure an individual’s ability to perform normal daily activities and are scored according to the specific assessment tool. Table 3.14 serves as an example checklist for these activities. A valuable assessment of muscle strength is handgrip dynamometry, used to determine handgrip strength. This is a standardized, simple, and quick means of assessing nutrition in relation to skeletal muscle function and is incorporated into the proposed criteria for malnutrition diagnosis.34 For this assessment, the patient is asked to grip the dynamometer device (see Figure 3.22) as tightly as possible. Handgrip standards are >35 kg for males and ≥23 kg for females but may vary depending on the instrument manufacturer’s guidelines. Handgrip measure has long been a part of fitness assessment and is also measured by both occupational and physical therapists. Communication with other team members will prove to be useful for this assessment. This evaluation is also useful for long-term follow-up in outpatient or rehabilitation settings. Additionally, more recent research is using handgrip strength as a predictor of malnutrition in multiple patient populations.69–71 The test is not valid in the presence of neuromuscular junction, muscle, or joint disease. Box 3.4 reviews functional assessment and other aspects of nutrition assessment of geriatric patients.

Table 3.13 Examples of Nutrition-Focused Physical Findings Exam Areas

Findings in Well-Nourished Patients

Potential Changes in Malnutrition

Orbital regions—surrounding the eye

Slightly bulged fat pads; fluid retention may mask loss

Hollow, dark circles, loose skin

Upper arm region—triceps/biceps

Ample fat tissue obvious between folds of skin

Reduced space between folds; fingers may touch when the hand encircles the upper arm

Thoracic and lumbar region—ribs, lower back, midaxillary line

Chest is full, ribs do not show; slight to no protrusion of the iliac crest

Can detect depressions between the ribs; iliac crest is visible

Temple region—temporalis muscle

Can see/feel well-defined muscle

Hollow, scooping, depression

Clavicle bone region—pectoralis major, deltoid, trapezius muscles

Not visible in male; visible but not prominent in female

Protruding, prominent bone

Clavicle and acromion bone region—deltoid muscle

Rounded curves at arm/shoulder/neck

Shoulder is squared; acromion protrusion is detectable

Scapular bone region—trapezius, supraspinatus, infraspinatus muscles

Bones not prominent; no significant depressions

Prominent visible bones such as ribs, scapula, shoulder or spine

Dorsal hand—interosseous muscle

Muscles protrude; bones not prominent

Depressed area between thumb and forefinger

Patellar region—quadriceps muscle

Muscles protrude; bones not prominent

Bones prominent; reduced muscle around knee cap

Anterior thigh region—quadriceps muscles

Well rounded, well developed

Reduced appearance of quadriceps

Posterior calf region—gastrocnemius muscle

Well-developed bulb of muscle

Thin—may have very little muscle

Source: Adapted from White JV, Guenter P, Jensen G, et al. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: characteristics recommended for identification and documentation of adult malnutrition (undernutrition). J Acad Nutr Diet. 2012; 112: 730–38.

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   65

Table 3.14 Activities of Daily Living (ADL) and Instrumental Activities of Daily Living (IADL) Activities of Daily Living Bathing, showering

Personal device care

Bowel and bladder management

Personal hygiene and grooming

Dressing

Personal mobility

Eating

Sexual activity

Feeding

Sleep/rest

Functional mobility

Toilet hygiene

Figure 3.22 Dynamometer Dynamometry, a common measurement of muscle strength, is one of the criteria that can be used for diagnosis of malnutrition.

Instrumental Activities of Daily Living Care of others

Health management and maintenance

Care of pets Child rearing Communication device use Community mobility Financial management

Home establishment and management Meal preparation and cleanup Safety procedures and emergency responses Shopping

Source: Adapted from: Lawton, MP, & Brody, EM Assessment of older ­people: self-maintaining and instrumental activities of daily living. ­Gerontologist. 1969; 9: 179–186. Graf, C. The Lawton Instrumental Activities of Daily Living Scale. Am J Nurs. 2008; 108(4): 53–62.

BOX 3.4

Source: Keith Brofsky/Photodisc/Getty Images

LIFE CYCLE PERSPECTIVES

Nutrition Assessment of Older Adult Populations Colette LaSalle, PhD, RD San Jose State University Nutrition assessment for the older adult utilizes a multidisciplinary approach to screen for nutritional risk factors. There are several unique features that must be considered when conducting a nutrition assessment on older individuals. Some of the main considerations are as follows: • Dental status: Does the person have natural teeth? If not, do dentures fit? Can he or she chew and form an appropriate bolus? Is there any pain when eating? Is saliva production adequate? Any altered taste perception? • Swallow function: Is swallow function adequate? Are fluids or solids lost while eating? Does the person exhibit signs and symptoms associated with aspiration such as choking or coughing when eating or drinking? Is there a diet order for texture modification or thickened fluids? • Body composition: Is there evidence of sarcopenia and/ or loss of lean body mass? Is hydration status within normal limits or is edema present? Using the nutrition focused physical examination as a standard component of the assessment will provide important data concerning muscle and fat loss. • Weight history: How does the current weight compare to norms (ideal body weight, BMI)? How does the current weight compare with usual or desired body weight? Have there been any recent significant or insidious changes in weight? • Diet history: Has the person received any diet education? Has he or she followed any diet restrictions in the past? What is his or her typical meal pattern (i.e., meal frequency,

66  Part 2  The Nutrition Care Process

•

•

• •

•

• •

preferred meal size, or inclusion of snacks)? Any food allergies or intolerances? Nutrient needs: What are the nutrient needs as individualized for age, gender, level of physical activity, disease state, and stress or trauma? How do estimated needs compare with intake? GI function: Is there a history of GI problems such as ­constipation, diarrhea, nausea, vomiting, gastroesophageal reflux disease, ulcer, celiac disease, diverticulosis, or GI ­surgery? Medical diagnosis: Will any medical diagnoses impact nutrient or fluid needs? Polypharmacy: How many medications are prescribed? Is there a potential for food–medication interactions? Do the medications affect appetite or GI function? Do they cause dry mouth, constipation, nausea, vomiting, diarrhea, gas, or bloating? Does the client use over-the-counter drugs or herbal or vitamin supplements? Social history: Is the client socially active? Does he or she have friends and family to assist with health care needs? Does he or she have access to medical care? Is there a history of alcohol or drug use? Cognitive function: Is there evidence of cognitive decline related to aging, Alzheimer’s disease, or substance abuse? Functional ability: Is the client able to purchase and prepare food? Is he or she able to perform the activities of daily living? Are there any functional barriers such as sensory impairments (vision, taste, hearing)? Are there difficulties

Nutrition Assessment of Older Adult Populations (continued) with ambulation or functional use of hands (arthritis, contractures)? Does he or she need assistance at mealtimes to monitor, cue, or feed? Is there additional data that can be obtained from measures of handgrip dynamometer or sit/ stand testing? • Physical examination: Is there evidence of altered ­hydration status (e.g., skin turgor and mucous membranes), wasting, or nutrient deficiencies? • Laboratory tests: Are labs indicative of altered protein ­status, inflammation, or chronic disease? Several validated nutrition screening questionnaires are ­available. Each is applicable to a slightly different geriatric ­population including both community dwellers and those ­residing in a care facility. Validated tools that are currently in use include the following: 1. Mini Nutritional Assessment (MNA) 2. Malnutrition Universal Screening Tool (MUST) 3. Short Nutritional Assessment Questionnaire (SNAQ) • SNAQ-65+for use in the community • SNAQ RC for use in residential/care homes 4. Subjective Global Assessment (SGA) 5. DETERMINE (The Nutrition Screening Initiative) References 1. Academy of Nutrition and Dietetics. Position of the Academy of ­Nutrition and Dietetics: individualized nutrition approaches for older adults: long term care, post-acute care, and other settings. J Acad Nutr Diet. 2018; 118: 724–35.

3.10  NUTRITION CARE CRITERIA: ENERGY AND PROTEIN REQUIREMENTS The final component of a nutrition assessment is determination of energy and protein requirements for the patient. This step is necessary in order to compare intake with needs and to establish nutrition goals. In most clinical settings today, protein and energy requirements are estimated using a variety of established equations. In some situations, it may be possible to measure energy needs by using indirect calorimetry and protein needs by performing a nitrogen balance study. The total amount of energy required by an individual is the sum of three basic components: basal energy ­expenditure (BEE) or basal metabolic rate (BMR) + energy for PA + ­thermic effect of food (TEF) = total energy expenditure (TEE). Basal energy expenditure is defined as energy used for physiological functions that maintain life, such as respiration and heartbeat, and accounts for approximately 60% of an individual’s energy requirement. BEE is assessed by measuring the oxygen consumed by an individual who has gone without food for at least 12 hours and has been lying down with little movement in a constant-temperature environment overnight.72 Additionally, during the actual measurement, the patient should not be moving, talking, sleeping, or using muscles other than those for breathing (i.e., be completely still and relaxed). Due to these strict measurement requirements, actual basal expenditure is

2. Bauer JM, Kaiser MJ, Sieber CC. Evaluation of nutritional status in older persons: Nutritional screening and assessment. Curr Opin Clin Nutr ­Metab Care. 2010; 13(1): 8–13. 3. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia: ­European consensus on definition and diagnosis: report of the E­ uropean ­Working Group on Sarcopenia. Age Ageing. 2010; 39(4): 412–23. Diekmann R, Winning K, Uter W, et al. J Nutr Health Aging. 2013; 17(4): 326–31. 4. Dorner B, Friedrich EK, Posthauer ME, American Dietetic Association. Position of the American Dietetic Association: Individualized nutrition approaches for older adults in health care communities [published c­ orrection appears in J Am Diet Assoc. 2010; 110(12): 1941]. J Am Diet Assoc. 2010; 110(10): 1549–1553. 5. Nutritional Screening Initiative. Determine Your Nutritional Health. vwwv.cdaaa.org/images/Nutritional_Checklist.pdf. Accessed November 13, 2013. 6. Guigoz Y, Vellas B, Garry PJ. Mini Nutritional Assessment: A practical assessment tool for grading the nutritional state of elderly patients. Facts and Research in Gerontology. 1994; 4: 15–59. 7. Loreck E, Chimakurthi R, Steinle NI. Nutritional assessment of the ­geriatric patient: A comprehensive approach toward evaluating and managing nutrition. Clin Geriatr. 2012; 2: 20–26. 8. BAPEN. Malnutrition Universal Screening Tool. http://www/.bapen​ .org.uk/ screening-for-malnutrition/must/introducing-must. Accessed ­November 13, 2013. 9. Nestle Nutrition Institute. Mini Nutritional Assessment. Available at http://wvw/.mna-elderly.com/forms/mini/mna_mini_english.pdf. ­Accessed November 13, 2013. 10. Skates JJ, Anthony PS. Identifying geriatric malnutrition in nursing practice: the Mini Nutritional Assessment (MNA®)—An evidence-based screening tool. J Gerontol Nurs. 2012; 38: 18–27. 11 Fight Malnutrition. Short Nutrition Assessment Questionnaire. http:// www/.fightmalnutrition.eu/fight-malnutrition/screening-tools/snaqtools-in-english/. Accessed November 13, 2013. 12. Stratton RJ, Hackston A, Longmore D, et al. Malnutrition in hospital outpatients and inpatients: prevalence, concurrent validity and ease of use of the “malnutrition universal screening tool” (“MUST”) for adults. Br J Nutr. 2004; 92(5): 799–808.

in a practical sense theoretical and thus d ­ ifficult to measure. Therefore, in many discussions regarding energy requirements, the term resting energy expenditure (REE) or resting metabolic rate (RMR) is used. Resting refers to measurement conditions where the individual is resting in a comfortable position without any other restrictions. RMR is usually estimated to be approximately 10% higher than BMR/BEE.72 PA is the most variable portion of an individual’s energy needs and fluctuates depending on the type, duration, and intensity of PA. In most individuals, PA accounts for approximately 15%–20% of energy requirements. TEF is estimated to be approximately 10% of an individual’s caloric intake and represents the energy needed for absorption, transport, and metabolism of nutrients. In hospitalized and other diseased populations, many individuals are hypermetabolic and have additional energy and protein requirements. These are discussed here and covered in additional detail for specific disease states in the appropriate chapters within this text.

Measurement of Energy Requirements The most accurate method of measuring REE/RMR in a clinical setting is to use indirect calorimetry.72–74 The equipment (metabolic carts; see Figure 3.23) used for this process has steadily become more sophisticated over the last

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   67

(­ specific numbers of kcal per mL of oxygen consumed). These values are then converted to REE/RMR using computer ­s oftware within the equipment. Calculations are based on the Weir equation: REE(kcal/day) = 1.44 × (3.9 × VO2 + 1.1 × VCO2).75 The literature recommends that nutrition support be provided at 100% of the measured RMR with the f­ ollowing substrate recommendations: carbohydrate at 50%, lipid at 20%–30%, and protein at 15%–20% of total kcal. An established protocol for use of indirect calorimetry and careful interpretation will be necessary for the clinician to effectively use the data.76

Figure 3.23 Indirect Calorimetry The most accurate method of assessing resting energy ­requirements is indirect calorimetry.

Estimation of Energy Requirements

Source: Courtesy of Marcia Nelms.

several decades, but the basic principles for measuring REE/ RMR remain the same. The amount of oxygen and carbon dioxide in both inspired and expired air (VO2 and VCO2 or ­respiratory quotient [RQ]) are measured, and the volume (V) of gas exchanged is equated to known energy constants

As stated previously, the use of indirect calorimetry is increasing, although cost and availability of equipment continue to limit its routine use in many institutions. It is more common in clinical situations to calculate an estimation of an individual’s energy requirements and, therefore, clinicians must rely on prediction equations. The method of estimation will vary depending on whether the patient is an adult or child; in a steady healthy state or acutely ill; and independently breathing or mechanically ventilated (see Figure 3.24). For the nonacutely ill overweight or obese individual, it is recommended to use the Mifflin–St. Jeor equation.77 The newest critical care nutrition guidelines state that while there are more than 200 published equations, their

Figure 3.24 Applying Evidence-Based Guidelines for Estimation of Energy Needs No Is patient eligible for indirect calorimetry based on protocol? Yes • Follow protocol for indirect calorimetry. • Use measurement taken in steady state (during a 5-min period, VO2 and VCO2 change ,5%). • Calculate kcal requirements using 100% of measured RQ. • If RQ ,0.67 or .1.3, measurement error is likely.a

Is patient mechanically ventilated?

Yes

Use Penn State equation.a,b

No Does patient’s clinical condition affect energy requirements?

Yes

Adapt appropriate equation based on available evidence regarding clinical condition.

Yes

• Pediatric: Schofield equation with stress factorse,f • Adult: No consistently reliable equation. Options to use include the following:a,b,g • 20–35 kcal/kg body wt for normal-wt pt • 20–35 kcal/kg IBW for obese pt

No Is patient acutely ill? No • Pediatric: WHO equationc or RDAd • Adult: 10–12 kcal/lb body wt or 22–25 kcal/kg body wt or Mifflin–St. Jeor equationa,b

a

Frankenfield D. Energy. In: Mueller C, Ed. The ASPEN Adult Nutrition Support Curriculum 3e. Silver Spring, MD: ASPEN; 2017. Academy of Nutrition and Dietetics. Evidence Analysis Library. Energy Expenditure: Systematic Review. 2013-2014. Available from: https://www.andeal​ .org/topic.cfm?menu=5299&cat=4320. Accessed August 4, 2018.

b

c

Food and Nutrition Board: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. ­Washington, DC: National Academies Press; 2005.

d

Sax HC, Scuba WW. Nutritional goals and macronutrient requirements. In: The ASPEN Nutrition Support Practice Manual. Silver Spring, MD: ASPEN; 1998:1–5; and Page CP, Hardin TC, Melnik G, eds. Nutritional Assessment and Support—A Primer 2nd ed. Baltimore, MD: Williams and Wilkins; 1994: 32.

e

Schofield WN. Predicting basal metabolism rate, new standards and review of previous work. Hum Nutr Clin Nutr. 1985; 39C: 5–91. Corkin MR. Pediatric Nutrition Support Handbook. Silver Spring, MD: ASPEN; 2011. g McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). J Parenter Enteral Nutr. 2016; 40: 159–21 f

68  Part 2  The Nutrition Care Process

accuracy is highly variable—each patient’s needs are highly individualized, and this affects the accuracy of any equation used.74 The 2016 ASPEN/SCCM critical care guidelines recommendation is: “Based on expert consensus, in the absence of IC (indirect calorimetry), we suggest that a published p ­ redictive equation or a simplistic weight-based equation (25–30 kcal/kg/d) be used to determine energy requirements.”74 Additionally, it is recommended that the patient be followed closely and his/her energy requirements reassessed more than weekly.74 Historically, the first established equation was the ­Harris–Benedict equation, first published in 1919.78 The Food and Agriculture Organization (FAO) of the United Nations and the WHO have also established equations to estimate basal energy requirements, which are also gender and age specific. All equations are outlined in Table 3.15. There are differing recommendations and practices for choosing the body weight used with each of these equations.79–81 Either actual body weight, ideal body weight, or adjusted body weight for obese patients could potentially be used to calculate energy requirements. Certainly, it is more difficult to accurately predict energy requirements in either the underweight or obese patient. For example, in the American College of Chest ­Physicians equation, BMI determines the weight that is used in the ­calculation (see Table 3.15). As discussed earlier in this section, lean body mass is the most metabolically active tissue and represents the largest proportion of the REE. Historically, the rationale for use of an adjusted body weight was based on the assumption that 20%–25% of fat mass is metabolically inactive. As Walker and Heuberger point out in their review, there is no research to support this calculation.81 ­Clinicians, including the MD and RDN, feel that the risk of initially overfeeding in the critically ill justifies the use of ideal body weight in overweight or obese patients. Otherwise, in normal-weight individuals, actual body weight is used in the calculations for REE.

Energy Requirements Based on DRI  The DRIs for macronutrients are standards of intake that are age and gender specific and are designed to meet the nutrient requirements of about 98% of the healthy population.82 The DRI also include estimated energy requirements (EERs) that provide guidelines to meet the energy needs of approximately 50% of the healthy population. Because energy requirements vary considerably from individual to individual, the EER values are not meant to be goals of nutrient intake for individuals and hence are not recommended for estimating patients’ energy requirements in a clinical setting. See the back inside cover of this book for these values. Activity Factor  After REE has been determined, energy

used in activity also must be estimated in order to estimate total energy requirements. Previously activity and stress ­factors have been used to account for the metabolic stress of certain disease states and injuries. These have not been ­validated and are not recommended for practice.83 There are many methods used to estimate the amount of energy needed for PA, especially in the nonhospitalized population. One total energy requirement formula developed by the Food and Nutrition Board incorporates a PA

Table 3.15 Estimation of Energy Requirements Harris–Benedict Equation REE for females = 655.1 + 9.6 W + 1.9 H – 4.7 A REE for males = 66.5 + 13.8 W + 5.0 H – 6.8 A [W, weight in kg; H, height in cm; A, age in years]

Mifflin–St. Jeor Equation Men: RMR = (9.99 × weight) + (6.25 × height) – (4.92 × age) + 5 Women: RMR = (9.99 × weight) + (6.25 × height) – (4.92 × age) – 161 [weight in kg; height in cm; age in years]

American College of Chest Physicians Equation REE = 25 × weight (kg) [If BMI = 16–25, use usual body weight; If BMI >25, use ideal body weight; and if BMI 50

22–25 kcal/kg IBW

Schofield Equation for use in Pediatrics—Acute Care Men

Women

Male

Female

Age

Equation (kcal/day, weight in kg)

10% in 6 months

>7.5% in 3 months

>5% in1 month

Severe Malnutrition

2. White JV, Guenter P, Jensen G, et al. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: Characteristics recommended for identification and documentation of adult malnutrition (undernutrition). J Acad Nutr Diet. 2012; 112: 730–38.

1. Tappendan KA, Quatrara B, Parkhurst ML, Malone AM, Fanjiang G, Ziegler TR. Critical Role of Nutrition in Improving Quality of Care: An Interdisciplinary Call to Action to Address Adult Hospital Malnutrition. MEDSURG Nursing. May–June 2013; 22(3): 147–65.

Sources:

• Serum proteins, such as serum albumin or prealbumin, are not included as defining characteristics of malnutrition because recent evidence analysis shows serum levels of these proteins do not change in response to changes in nutrient intake.

•  The National Center for Health Statistics defines chronic as a disease/condition lasting ≥3 months.

•  Refeeding and/or nutrition support may stabilize but not significantly improve nutrition parameters in the presence of inflammation.

Not applicable

Mild fluid accumulation

Mild depletion of muscle mass

Mild depletion of body fat

5% in 1 month

Severe Malnutrition

1-2% in 1 week

Non-Severe Malnutrition

In Context of Chronic Illness

•  A minimum of two of the six characteristics above is recommended for diagnosis of either severe or non-severe malnutrition.

Notes:

Loss of muscle, i.e., temples, clavicles, shoulders, scapula, thigh, and calf.

Muscle mass

Body fat

Loss of subcutaneous fat, i.e., Moderate depletion orbital, triceps, fat overlying ribcage. of body fat

Physical assessment:

≤50% energy intake compared to estimated energy needs for ≥5 days

RD obtains diet history and ­estimates energy needs. Suboptimal intake is determined as a percentage of estimated needs over time.

Intake

Severe Malnutrition

Evaluated in light of other clinical >2% in 1 week findings including hydration. Weight >5% in 1 month change over time is reported as >7.5% in 3 months a percentage of weight lost from baseline.

ICD-10 Codes E40-46

Weight loss

Criterion

In Context of Acute Illness/Injury

Table 3.17 Characteristics and Documentation for Malnutrition Diagnosis

CHAPTER REVIEW QUESTIONS 1. What is the difference between nutritional status and nutritional risk? 2. How is nutritional screening different from nutritional assessment? 3. Describe the difference between subjective data and objective data that are collected for a nutritional assessment. List three pieces of objective information and three pieces of subjective information that could be collected for nutritional assessment. 4. Name and describe briefly four methods used to collect dietary

assessment data. List the advantages and disadvantages of each method. 5. Describe two resources that are used to interpret dietary intake. 6. Which anthropometric measurements are collected for nutritional assessment? Describe briefly each measurement and explain the accuracy of each in determination of body composition and/or health status. 7. List four blood proteins used in nutrition assessment. Describe the

effectiveness of each as markers in measuring nutritional status and the contribution of inflammation to their interpretation. 8. Describe how energy requirements can be determined or estimated. How is the energy requirement affected by stress? 9. Outline the etiology-based definitions for malnutrition and the components of nutrition assessment that are included as characteristics for diagnosis.

REFERENCES 1. Academy of Nutrition and Dietetics. ­Nutrition Terminology Reference Manual (eNCPT): Dietetics Language for Nutrition Care. http://www.ncpro.org. Accessed July 31, 2018.

11. Patel V, Romano M, Corkins MR, et al. Nutrition screening and assessment in hospitalized patients a survey of current practice in the United States. Nutr Clin Pract. 2014; 29: 483–90.

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13. Conway, JM, Ingwersen, LA, Moshfegh, AJ. Effectiveness of the USDA 5-step multiple-pass method to assess food intake in obese and nonobese women. Am J Clin Nutr. 2003; 77: 1171–78. 14. Conway, JM, Ingwersen, LA, Moshfegh, AJ. Accuracy of dietary recall using the USDA five-step multiple-pass method in men: an observational validation study. J Am Diet Assoc. 2004; 104(4): 595–603. 15. Blanton CA, Moshfegh AJ, Baer DJ, Kretsch MJ. The USDA automated multiple-pass method accurately estimates group total energy and nutrient intake. J Nutr. 2006; 136(10): 2594–99. 16. Lee RD, Nieman DC. Measuring Diet. In: Lee RD, Nieman, DC, eds. Nutritional Assessment. 6th ed. New York, NY: McGraw-Hill; 2013: 74–108. 17. Sharman SJ, Skouteris H, Powell MB, Watson B. Factors related to the accuracy of self-­ reported dietary intake of children aged 6–12 years elicited with interviews: a systematic review. J Acad Nutr Diet. 2016; 116: 76–114. 18. Kirkpatrick SI, Potischman N, Dodd KW, et al. The use of digital images in 24-hour recalls may lead to less misestimation of portion size ­compared with traditional interviewer-­ administered recalls. J Nutr. 2016; 146: 2567–73. 19. My Fitness Pal™. Available from: https:// www.myfitnesspal.com/. Accessed July 20, 2018. 20. U.S. Department of Health and Human Services. Office of Disease Prevention and Health Promotion. 2015–2020 Dietary ­Guidelines for Americans. http://www.health.gov/­ dietaryguidelines/. Accessed July 27, 2017.

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62. Johnson AM, Merlini G, Sheldon J, Ichihara K. Clinical indications for plasma protein assays: transthyretin (prealbumin) in inflammation and malnutrition. Clin Chem Lab Med. 2007; 45: 419–26

47. Shepherd JA, NK Bennett NK. Sommer MJ, Heymsfield SB. Body composition by DXA. Bone. 2017; 104: 101–105. 48. Andreoli A, Scalzo G, Masala S, Tarantino U, Guglielmi G. Body composition assessment by dual-energy X-ray absorptiometry (DXA). Radiol Med. 2009; 114: 286–300. 49. Williams JE, Wells JC, Wilson CM, Haroun D, Lucas A, Fewtrell MS. Evaluation of Lunar Prodigy dual-energy X-ray absorptiometry for assessing body composition in healthy persons and patients by comparison with the criterion ­4-component model. Am J Clin Nutr. 2006; 83: 1047–54. 50. Direk K, Cecelja M, Astle W, et al. The ­relationship between DXA-based and anthropometric measures of visceral fat and morbidity in women. BMC Cardiovasc Disord. 2013; 13: 25–38. 51. Kaul S, Rothney MP, Peters DM, et al. Dual-energy X-ray absorptiometry for quantification of visceral fat. Obesity. 2012; 20: 1313–18. 52. Mourtzakis M, Wischmeyer P. Bedside ultrasound measurement of skeletal muscle. Curr Opin Clin Nutr Metab Care. 2014; 5: 389–395. 53. Ticinesi A, Meschi T, Narici MV, Lauretani F, Maggio M. Muscle ultrasound and sarcopenia in older individuals: a clinical perspective. J Am Med Dir Assoc. 2017; 18: 290–300. 54. Gibby JT, Njeru DK, Cvetko ST, et al. Wholebody computed tomography-based body mass and body fat quantification: a comparison to hydrostatic weighing and air displacement plethysmography. J Comput Assist Tomogr. 2017; 41: 302–308. 55. Bedogni G, Agosti F, De Col A, et al. Comparison of dual energy X-ray absorptiometry, air displacement plethysmography and bioelectrical impedance analysis for the assessment of body composition in morbidly obese women. Eur J Clin Nutr. 2013; 67(11): 1129–32. 56. Ferrie S, Allman-Farinelli. Commonly used “nutrition” indicators do not predict outcome in the critically ill: a systematic review. Nutr Clin Pract. 2013; 28: 463–84. 57. Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. NEJM. 1999; 448–54. 58. Lee RD, Nieman DC. Biochemical Assessment. In: Lee RD, Nieman, DC, eds. Nutritional Assessment. 6th ed. New York, NY: McGraw-Hill; 2013: 317–52. 59. Sherwood L. Body Defenses. In: Sherwood L, Human Physiology from Cells to Systems. 9th ed. Belmont, CA: Brooks-Cole/Cengage; 2016: 404–44.

63. Carmel R. Cobalamin. In: ross AC, Ballabero B, Cousins RJ, Tucker KL, Zeigler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Philadelphia, PA: Lippincottt, Williams and Wilkins; 2014: 369–89. 64. Hipskind P, Galang M, Jevenn A, Pogatschnik C, Hamilton C, ed. Nutrition Focused Physical Exam: An Illustrated Handbook. Silver Spring, MD: ASPEN; 2016. 65. Fischer M, JeVenn A, Hipskind P. Evaluation of muscle and fat loss as diagnostic criteria for malnutrition. Nutr Clin Pract. 2015; 30: 239–48. 66. Esper DH. Utilization of nutrition-focused physical assessment in identifying micronutrient deficiencies. Nutr Clin Pract. 2015; 30: 194–202. 67. Green Corkins K, Teague EE. Pediatric ­nutrition assessment. Nutr Clin Pract. 2017; 32: 40–51. 68. Becker P, Carney LN, Corkins MR, et al. Consensus statement of the Academy of Nutrition and Dietetics/American Scoiety for Parenteral and Enteral Nutrition: indicators recommended for the identfication and documentation of pediatric ­malnutrition. Nutr Clin Pract. 2015; 30: 147–61. 69. Olguin T, Bunout D, de la Maza MP, et al. Admission handgrip strength predicts functional decline in hospitalized patients. Clin Nutr. 2017; 17: 28–32. 70. Norman K, Stobaus N, Gonzalez MC, et al. Handgrip strength: outcome predictor and marker of nutritional status. Clin Nutr. 2011; 30: 135–42. 71. Sharma P, Rauf A, Matin A, et al. Handgrip strength as an important bedside tool to assess malnutrition in patient with liver disease. J Clin Exp Hepatol. 2017; 7: 16–22. 72. Gropper SS, Smith JL. Body ­composition, energy expenditure, and energy balance. In: Human Nutrition and Metabolism. 7th ed. ­Belmont, CA: Wadsworth/Cengage Learning; 2018: 273–93. 73. Frankenfield D. Energy. In: Mueller C.ed. The ASPEN Adult Nutrition Support Curriculum. 3rd ed. Silver Spring, MD: ASPEN; 2017. 74. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). J Parenter Enteral Nutr. 2016; 40: 159–211. 75. Weir JB de V. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol. 1949; 109: 1–9.

76. Haugen HA, Chan L-N, Li F. Indirect calorimetry: a practical guide for clinicians. Nutr Clin Pract. 2007; 22: 377–88. 77. Mifflin MD, St Jeor ST, Hill LA, Scott BJ, Daugherty SA, Koh YO. A new predictive equation for resting energy expenditure in healthy individuals. Am J Clin Nutr. 1990; 51: 241–47. 78. Harris JA, Benedict FG. A Biometric Study of Basal Metabolism in Man. Publication No. 279. Washington, DC: Carnegie Institute; 1919. 79. Krenitsky J. Adjusted body weight: pro: evidence to support use of adjusted body weight in calculating calorie requirements. Nutr Clin Pract. 2005; 20: 468–73. 80. Ireton Jones CS, Turner WW. Adjusted body weight, con: why adjust body weight in

energy-­expenditure calculations. Nutr Clin Pract. 2005; 20: 474–79. 81. Walker RN, Heuberger RA. Predictive equations for energy needs for the critically ill. Respr Care. 2009; 54: 509–21. 82. Food and Nutrition Board. Dietary Reference Intakes for Energy Carbohydrates, Fiber, Fat, Protein, and Amino Acids. Washington, DC: National Academy Press; 2002. 83. Kudsk K. Nutrition support for the patient with surgery, trauma, or sepsis. In: Ross AC, Baballero B, Cousins RJ, Tucker KL, Zeigler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2014: 1273–88.

84. U.S. Department of Health and Human ­Services, Public Health Service, Centers for ­Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Division of Nutrition and Physical Activity. Promoting Physical Activity: A Guide for Community Action. Champaign, IL: Human Kinetics; 1999. 85. Ainsworth BE, Haskell WL, Leon AS, et al. Compendium of physical activities: classification of energy costs of human physical activities. Med Sci Sports Exerc. 1993; 25(1): 71–80. 86. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, Geneva: World Health Organization; 2016. Available at www.who​ .int/classifications/icd/en. Accessed July 31, 2018.

Chapter 3  Nutrition Assessment: Foundation of the Nutrition Care Process   75

CHAPTER 4

Source: Courtesy of Marcia Nelms.

Nutrition Intervention, Nutrition ­Monitoring and Evaluation Marcia Nahikian-Nelms, PhD, RDN, LD, FAND The Ohio State University

LEA RNING O B JECTIV ES LO 4.1  Identify etiologies that impact nutritional status. LO 4.2  Identify the two activities involved in nutrition intervention. LO 4.3  Describe types of food, nutrients, and dietary interventions that are used to help prevent and treat malnutrition and other diagnoses.

76

LO 4.5  Differentiate between nutrition education and nutrition counseling, and identify effective skills and strategies for each. LO 4.6  State how coordination of nutrition care can be implemented.

LO 4.7  Identify the four categories of nutrition care outcomes and their significance.

G LOSSARY clear liquid diet—diet consisting of liquids that contribute minimal residue to the gastrointestinal tract; includes fruit juices without pulp, carbonated sodas, broth, tea, coffee, water, popsicles, fruit ice, Jell-O (gelatin), and liquid nutritional supplements (e.g., Boost Breeze®) dysphagia—difficulty swallowing evidence-based dietetics practice—dietetics practice in which systematically reviewed scientific evidence is used to make food and nutrition practice decisions

full liquid diet—diet consisting of all beverages allowed on clear liquid diets with addition of milk, ice cream, yogurt, and liquid nutritional supplements (e.g., Ensure® and Boost®) hyperosmolar—having a higher osmolality than body fluids (>300 mOsm/kg) isotonic—having the same osmolality as body fluids (approximately 300 mOsm/kg) medical foods—food administered under the supervision of a physician and intended for the specific dietary management of a disease for

which distinctive nutritional requirements are established NPO—nil per os, which is Latin meaning “nothing per mouth” osmolality—number of water-attracting particles per weight of water in kilograms (expressed as mOsm/kg)

4.1 INTRODUCTION

Figure 4.1 Collaboration

Medical nutrition therapy (MNT) as defined under Medicare Part Β refers to “nutritional diagnostic, therapy, and counseling services provided by a registered dietitian nutritionist (RDN) or nutrition professional for the purpose of disease management.”1 The responsibility and scope of practice for the RDN center on the provision of nutrition care utilizing the nutrition care process or NCP (refer to Chapter 2). The specific purpose of nutrition intervention, the third step in the NCP, is to resolve or alleviate the nutrition problem that has been identified in the nutrition diagnosis (PES statement). This is accomplished by planning and implementing appropriate nutrition interventions that are tailored and individualized to the patient’s/client’s needs.2 Intervention strategies are directed at the etiology or cause of the nutrition diagnoses. If the etiology cannot be influenced through nutrition therapy, then the interventions should be directed at improving the signs and symptoms of the nutrition problem. Etiologies can generally be classified into one or more of the following categories: (1) beliefs or attitudes, (2) cultural, (3) physical function, (4) knowledge, (5) physiological, (6) psychological, (7) social-personal, (8) treatment, (9) access, or (10) behavioral. 2 Nutrition interventions are intended to positively change (1) food and/or nutrient delivery and intake, (2) nutrition-related knowledge or behavior, (3) environmental conditions, or (4) access to ­supportive care and services. These changes are represented by the four domains of the standardized intervention language: (1) food and/or nutrient delivery, (2) nutrition education, (3) nutrition counseling, and (4) coordination of nutrition care (refer to Chapter 2). The registered dietitian nutritionist (RDN) may recommend, implement, or order various types of nutrition interventions. He or she may also ­i nitiate, modify, or discontinue a nutrition intervention. The u ­ ltimate goal of the nutrition intervention will, of course, be to improve the individual’s overall nutritional status and to support the medical care of that individual (see Figure 4.1). Once the nutrition intervention is conducted, it is equally important to evaluate its effectiveness. This is accomplished

Collaboration with colleagues allows for appropriate nutrition intervention.

Source: Courtesy of Marcia Nelms.

in the fourth step of the nutrition care process (NCP): ­nutrition monitoring and evaluation. This chapter provides an overview of the various types of nutrition i­nterventions that RDNs provide and briefly discusses resources and tools that help the practitioner to effectively evaluate the impact of the nutrition intervention. Specific interventions for patients requiring enteral and parenteral nutrition are covered in Chapter 5. Further examples of interventions a­ ppropriate for patients with specific diseases are included in Part 4 ­(Chapters 12–25).

Chapter 4  Nutrition Intervention, Nutrition ­Monitoring and Evaluation   77

4.2  NUTRITION PRESCRIPTIONS As noted previously, nutrition intervention involves two components: planning and implementation. The nutrition ­p rescription, an important part of the planning, outlines nutritional needs for the patient and supports the medical care that is prescribed by the health care team. “The nutrition prescription concisely states the patient/client’s i­ ndividualized recommended dietary intake of energy and/or selected foods or nutrients based on current reference ­standards and dietary guidelines and the patient/client’s health condition and ­nutrition diagnosis.”2 The nutrition ­prescription also should either provide the path for the nutrition intervention or frame BOX 4.1

the context within which the intervention is implemented. As discussed in Chapter 1, the Academy of Nutrition and Dietetics (AND) defines evidence-based dietetics practice as “the incorporation of systematically reviewed scientific evidence into food and nutrition practice decisions. It integrates professional expertise and judgment with client, customer and community values and evaluates outcomes.”3 Throughout this text, as pathophysiology and nutrition therapies are discussed, evidence is provided to support the efficacy of an appropriate nutrition prescription. Box 4.1 discusses evidence-based guidelines. The role of the RDN in planning and implementing nutrition interventions is summarized in Table 4.1.

RESEARCH TO PRACTICE

Evidence-Based Guidelines Ethan A. Bergman, PhD, RD, CD, FADA ­ entral ­Washington University C Susan N. Hawk, PhD, RD  Central Washington University It is important that the RDN use the most up-to-date i­nformation when providing care for patients. This i­nformation must be based on evidence supported by well-controlled research ­studies and clinical practice. Evidence-based recommendations or ­guidelines are scientifically developed to assist health care professionals in making appropriate decisions about patient care. The following are sources of evidence-based research designed to help health care professionals choose the best clinical approach to patient care: 1. Academy of Nutrition and Dietetics (AND) Evidence Analysis Library (EAL): Available at www.andeal.org/. The EAL has been created to summarize the best available research in dietetics and nutrition. Access to the AND Evidence Analysis Library is free to AND members but requires a subscription for nonmembers.

2. National Guideline Clearinghouse (NGC): Available at www.guideline.gov. The NGC is a resource for evidence-based clinical practice guidelines for physicians, nurses, and other health care professionals, including dietitians. 3. Cochrane Library: Available at www.cochranelibrary. com/. The Cochrane Library publishes Cochrane Reviews, which are based on the best available information about health care interventions. The reviews explore the evidence for and against the effectiveness and the appropriateness of various types of medical treatment. 4. Agency for Healthcare Research and Quality (AHRQ): Available at www.ahrq.gov. AHRQ is the research arm of the U.S. Department of Health and Human Services (HHS). It examines how people access health care, its cost, and the results of this care. The main goals of AHRQ are to identify the most effective ways to organize, manage, finance, and deliver high-quality health care.

Table 4.1 Standards of Practice: The Registered Dietitian’s Role in Nutrition Intervention Each RD/RDN Plans the Nutrition Intervention

Each RD/RDN Implements the Nutrition Intervention

• Prioritizes the nutrition diagnoses based on problem severity, safety, patient/client needs, likelihood that nutrition intervention will influence the problem, and patient/client perception of importance

• Collaborates with colleagues, interdisciplinary team, and other health care professionals

• Bases intervention plan on best available evidence (e.g., national guidelines, published research, evidence-based libraries, and databases) • Refers to policies and program standards • Confers with patient/client and caregivers, interdisciplinary team, and other health care professionals • Determines patient-/client-centered plans, goals, and expected outcomes • Develops the nutrition prescription • Defines time and frequency of care, including intensity, duration, and follow-up • Utilizes standardized language for describing interventions • Identifies resources and/or referrals needed

• Communicates and coordinates the nutrition intervention/plan of care • Initiates and individualizes the nutrition intervention/plan of care • Assigns activities to dietetic technicians, registered (DTR) and other administrative support and technical personnel in accordance with qualifications, organization policies, and applicable laws and regulations • Continues data collection • Follows up and verifies that nutrition intervention is occurring • Adjusts intervention strategies, if needed, as response occurs • Documents: Date and time; specific treatment goals and expected outcomes; recommended interventions; adjustments to the plan and justification; client/community receptivity; referrals made and resources used; other information relevant to providing care and monitoring progress over time; plans for follow-up and frequency of care; rationale for discharge, if applicable

Source: Academy Quality Management Committee. Academy of Nutrition and Dietetics: Revised 2017 Standards of Practice for Registered Dietitian ­Nutritionists. J Acad Nutr Diet. 2018; 118: 141–65.

78  Part 2  The Nutrition Care Process

4.3  FOOD AND/OR NUTRIENT

Modification of Meals and Snacks

­DELIVERY (ORAL DIETS)

Modifications of a general diet are often recommended as part of the nutrition prescription for patients under the care of a RDN. These changes result in “modified diets” that have several important functions. They may be used to ­maintain or restore health and nutritional status. They may also ­accommodate changes in appetite, digestion, absorption, or organ function. These diets can provide the appropriate nutrition therapy to support weight loss or gain, or to assist with treatment of a particular diagnosis. For ­example, ­m odified diets may be created by altering the ­k ilocalorie (kcal) level, levels of individual nutrients, method of ­preparation, food or ingredient composition, and/or ­number, size, or ­f requency of meals and snacks of the “house” or ­“regular” diet. Texture and consistency can also be adjusted (i.e., softer foods served) to alleviate mechanical problems for patients with impaired chewing or swallowing ability. Texture-­ altered diets contain foods that are easy to chew and usually omit raw fruits and vegetables. Individuals with dysphagia ­(difficulty swallowing) may require more specific modifications of ­texture and consistency. Diets for these individuals are ­discussed more thoroughly in Chapter 14. For very short periods (two or three meals), liquid diets consisting of broth, juice, cream soups, and milk may be served to patients who are beginning to eat after a long period without food (nil per os, or NPO). These diets are often referred to as clear liquid diets or full liquid diets. A clear liquid diet is intended to provide fluid and energy in a form that requires minimal digestion and limits residue in the ­gastrointestinal (GI) tract. It may be used during acute GI distress, during GI medical testing (such as a ­colonoscopy), or prior to surgery. Clear liquid diets are inadequate in kcal, ­p rotein, vitamins, and minerals, so they should be used only when medically necessary. Historically, the clear ­liquid diet has been used as a progression toward solid food after a ­surgical procedure or when the GI tract required ­minimal stimulation. Newer research has demonstrated that e­ arlier feeding with avoidance of this historical progression is ­a ssociated with decreased hospitalization time with no ­a dditional complications. 7 A recent meta-analysis of the ­literature reveals that, unfortunately, current practice is not consistent with the evidence.8,9 A full liquid diet also has been used as a transitional diet between liquids and solid foods. This nutrition i­ntervention, like the similar use of the clear liquid diet, is outdated. Because a full liquid diet includes milk and milk products, it may cause intolerance due to the large amounts of ­lactose. Table 4.2 outlines the basic principles of these liquid diets, but be aware that these nutrition interventions may no l­onger be warranted in the future as more and more research d ­ emonstrates that the restrictions are not necessary. An important component of ensuring tolerance to oral diets, especially clear and full liquid diets, is the consideration of the osmolality of the particular liquids that are provided. Hyperosmolar liquids may not be tolerated during these transitional periods or when the GI tract has not been stimulated (see Chapter 14). This is additional evidence that these nutrition interventions should not be used in most practice settings. Table 4.3 provides the osmolality of common liquids

The first step in prevention or treatment of malnutrition is an adequate supply of acceptable food composing a diet that has been individualized to age, height, weight, activity level, nutritional status, and medical condition. Malnutrition in acute care may be the result of chronic illness experienced by patients before admission or an acute response to inflammation and metabolic stress, but it is also exacerbated by pain, anxiety, depression, medical testing, and unfamiliar foods or meal schedules associated with admission to a health care setting. Insufficient food intake may be related to the factors depicted in Figure 4.2. Therefore, it is important that these factors be carefully assessed prior to planning nutrition interventions. In a recent article, a survey assessing indicators for reduced food intake in 56 countries revealed that the most common factors that could predict food intake were reduced intake during previous week, confinement to bed, females at either end of the age spectrum, and low body mass index.4 This type of research provides additional information to identify those individuals at risk for inadequate oral intake. In many instances, a healthful diet—commonly referred to as “regular” or “house” diet is served in hospitals and postacute care in a minimum of three meals each day and will meet a patient’s nutritional needs. Menus are written and approved by a RDN and are designed to provide the Dietary Reference Intake for all nutrients. Restaurant-style menus, room service ordering systems, à la carte food carts, and individual-unit kitchens and galleys are all examples of methods to ensure patient satisfaction and choice in menu selection.5,6 When patients have the option to select the food items they prefer, as they do in most institutions, one of the simplest yet most helpful interventions may be to assist a patient with menu selection. Offering suggestions and appropriate substitutions can be an efficient method of ensuring that the patient’s diet remains adequate and acceptable. A 2016 study examined meals ordered within a pediatric hospital and found that the majority did not meet optimal nutritional guidelines, which further emphasizes the need for guidance in menu selection.6

Figure 4.2 Factors Affecting Nutritional Intake during

Insufficient Food Intake

Inappropriate Diet Orders

Pain

r ilia es am ul nf d U che S

Fe An ar xi and et y

Medical Testing

U

ns io at

ic ed

M

na cc Fo ep od tab le

Illness

Chapter 4  Nutrition Intervention, Nutrition ­Monitoring and Evaluation   79

Table 4.2 Principles of Clear and Full Liquid Diets Diet Clear liquids

Purpose

Foods Acceptable

Intended to supply fluid and energy in a form that requires ­minimal digestion and stimulation of the GI tract

• Clear fluids or foods that are liquid at body temperature and leave minimal residue • Clear fruit juices • Bouillon, consommé, clear broth • Gelatin, fruit ice, plain hard candy, sugar, honey

Limitations • Not nutritionally adequate • Should be limited to 24–48 hours unless supplements are added • Research evidence does not support long term use of this diet.

• Commercially prepared low-residue, lactose-free nutritional supplements Full liquids

Transition between clear liquids and solid food

• Consists of foods or fluids that are or become liquid at body temperature

• May present problem with large amounts of lactose

• All clear liquids

• Research evidence does not support long term use of this diet.

• Cream soups • Milk, ice cream, pudding, yogurt

Table 4.3 Osmolality of Selected Liquids Beverage

mOsm/kg

Beverage

mOsm/kg

Milk*

 275

Prune juice

1265

Malted milk

 940

Grape juice

 863

Ice cream

1905

Apple juice

 683

Eggnog

 695

Orange juice

 614

Fruit yogurt

 871

Tomato juice

 595

Sherbet*

 125

Punch with sugar

 448

Ensure/Boost

590/640

Sugar-free punch*

  29

Ensure Plus/Boost Plus

680/720

Mineral water*

  74

Boost Breeze

 920

Broth

 445

Enlive!

 840

Polycose

 900

 750

Flavored gelatin

 735

Popsicles

 720

Resource fruit beverage Enteral formulas

250–710

Note: Beverages with an asterisk (*) are considered isotonic. Source: Rees Parrish C. The clinician’s guide to short bowel s­ yndrome. Nutrition issues in gastroenterology, series #31. ­Practical ­Gastroenterology. 2005: 88–89.

that are used in these diets. Choosing those with a lower osmolality may help promote tolerance during the transition to oral feeding. Nutritional intake may be modified to prepare patients for a specific medical test. For example, when a patient is tested for gastroparesis, a specific test diet is ordered so that there is a reference value for the test results (see Chapter 14). Details of the types of diets served are recorded in an institution’s policies and procedures or within a reference such as the AND’s Nutrition Care Manual. Given adequate appetite along with sufficient resources to purchase and prepare food, most malnourished individuals can be rehabilitated with oral diet alone. But maximizing oral intake within the hospital setting is often challenging because this environment is not always conducive to eating. Add to this environment the stress, fear, pain, and isolation of illness and it is a wonder that anyone who is hospitalized can eat adequately. For these individuals, a number of alternatives exist. A primary function of nutrition services in health care institutions is to be the patient’s nutrition advocate. 80  Part 2  The Nutrition Care Process

When patients present with a suboptimal intake, nutrition services staff members work with the patient and health care team to provide a variety of nutritional options. If a patient’s nutrient needs are not being met, it may be necessary to enhance oral intake with between-meal or evening supplemental feedings of nutrient-dense foods acceptable to the individual patient. For these supplemental feedings, traditional foods such as fruit, crackers, sandwiches, milkshakes, custards, or puddings may be served. Increasing nutrient density without actually increasing volume can be an effective tool for the individual who is suffering from decreased appetite. For example, instead of using skim milk, the patient could receive whole milk with the addition of a protein supplement such as Beneprotein or 2 tbsp of dry milk powder to boost both kcal and protein. Adding peanut butter to toast for breakfast is an simple method to increase both kcal and protein. Table 4.4 provides examples of methods to increase nutrient density using readily available foods, and Figure 4.3 presents two breakfast meals that were modified in this manner.

™

Table 4.4 Nutrition Interventions to Increase Nutrient Density Increasing Energy Content • Add butter or margarine to cooked cereals, soups, vegetables, or casseroles. • Add jam, jelly, or honey to toast or other breads and crackers. • Use whole milk or cream with soups, casseroles, creamed vegetables, or shakes and smoothies. • Add sour cream or yogurt to soups, casseroles, creamed vegetables, or shakes and smoothies. • Add nut butters or cream cheese to raw vegetables, bread, or crackers. Increasing Protein Content • Add powdered milk to any beverage, soup, or casserole. • Add liquid egg substitutes to shakes, soups, vegetables, or casseroles. • Wherever possible, add nuts, nut butters, chopped meats, cooked eggs, cheese, or yogurt to prepared foods. • Add tofu or soy crumbles to any prepared vegetable, soup, or casserole.

Figure 4.3 Nutrient-Dense Breakfasts (a) Mint-chocolate chip avocado green smoothie. Nutrient analysis: 525 kcal, 33 g fat, 35 g carbohydrate (net 13 g), 22 g fiber, 34 g protein, and 9 g sugar. Ingredients: 1 avocado, 2 tbsp chia seeds, 1 cup almond milk, 1 scoop chocolate-flavored protein powder, 2 cups fresh spinach, and 2 tbsp dark chocolate chips. (b) Cinnamon apple oatmeal with walnuts. Nutrient analysis: 600 kcal, 29 g fat, 82 g carbohydrate (net 70 g), 12 g fiber, 16 g protein, 15 g sugar. Ingredients: 1 cup dried rolled oats, ¼ cup walnuts, 1 cup almond milk, 1 medium apple.

(b)

(a)

Source: Photography copyright of McKel Hill, MS, RD, LDN Nutrition Stripped, nutritionstripped.com

All of these various types of modifications as well as a general diet are listed within the meals and snacks section of the food and nutrient delivery domain.2 Examples of possible nutrition diagnoses for which these interventions may be appropriate include the following:

Figure 4.4 Oral Supplement Beverages A selection of commercial oral supplement beverages.

• Increased energy expenditure • Excessive or inadequate (specify) nutrient intake • Inconsistent carbohydrate intake • Excessive or inadequate energy intake • Less than optimal intake of types (specify) of nutrients (e.g., fats, carbohydrates, and proteins) • Malnutrition

Supplements Medical Food Supplements  Another classification of

possible interventions within the food and delivery domain is medical food supplements. Medical food supplements are defined as commercial or prepared foods or beverages intended to supplement energy, protein, carbohydrate, fiber, and/or fat intake.2 Liquid meal replacement formulas such as those shown in Figure 4.4 may provide a convenient alternative to between-meal snacks. These products typically come in single-portion containers providing 250–350 kcal with 7–15 grams of protein in 250 mL, and may be available in a variety of flavors. They are lactose free. Some contain fiber, and others are more calorically dense or higher in protein. Examples of these products include Ensure , Boost , MightyShakes , Resource Health Shake , and Carnation Breakfast Essentials . Manufacturers have introduced many variations of these products for specific medical conditions, such as wound

® ®

™

®

®

®

Source: Courtesy of Marcia Nelms.

healing or diabetes. Oral supplements may be available in liquid form, as puddings, or as cereal-type bars. Because unopened supplement packages do not require refrigeration, these products may be served at a time convenient to the patient. In long-term care facilities, they may be

Chapter 4  Nutrition Intervention, Nutrition ­Monitoring and Evaluation   81

administered in place of water with medications as a means of increasing nutrient intake. Commercial supplements are popular because of their convenience and also because patients and caregivers may be familiar with them due to direct-to-consumer marketing. However, acceptability and intake are highly individual. Patients receiving oral supplements frequently develop “taste fatigue” after supplements are initiated, and supplement intake then decreases. It is also important to remember that merely providing supplemental feedings will not increase appetite; in fact, many patients complain that extra portions, frequent meals, and supplemental snacks are overwhelming and reduce appetite. This is why it is essential to include the patient in the decision-making process for changes in the meal plan. The patient needs to understand why oral supplements are being offered and how they could improve his or her current medical status. Providing supplement taste tests could be one way to help patients decide which product they would prefer to add to their diet. Developing a rotation for snacks or supplements and setting portion goals with the patient may also improve acceptance. Regular follow-up and monitoring are necessary in order to coordinate successful interventions and minimize waste associated with unused products.

Modified Beverages and Foods  Another means to

improve nutrient density within food choices is to add single nutrients such as protein or fiber through the use of “modular” products. Manufacturer websites can provide specific information about the specific products that are available. Protein modulars, such as ProMod or Beneprotein , can be added to both foods and beverages but will need to be

®

BOX 4.2

®

mixed well. They change the taste and consistency slightly, as do lipid modulars such as medium-chain triglyceride (MCT) oil. In general, modulars are not as cost-efficient as other types of supplements, and they also increase the labor costs. Box 4.2 provides more information about the MCT supplement. Common nutrition diagnoses for which medical food supplements might be necessary include the following: • Inadequate energy intake • Increased protein needs

Vitamin and Mineral Supplements  If the nutrition

assessment reveals that the patient’s diet is inadequate in essential vitamins and minerals, supplements of these nutrients should be discussed with the health care team and recommendations made (see Figure 4.5). Additionally, many medical conditions interfere with digestion, absorption, or utilization of these micronutrients. Thus, making appropriate, evidenced-based recommendations for supplementation of vitamins and/or minerals is an expected step in nutrition intervention and is within the RDN scope of practice.10 For example, if the patient is diagnosed with osteopenia, the RDN, along with the medical providers, could recommend supplementation for calcium and vitamin D using appropriate reference standards and evidence-based guidelines. Furthermore, the RDN, along with the pharmacist, would support this recommendation with instructions on appropriate sources of supplements to maximize absorption and utilization as well as any specific guidelines on potential drug–nutrient interactions. This is an excellent example of the importance of interprofessional care where

CLINICAL APPLICATIONS

A Review of the MCT Modular Supplement Medium-chain triglycerides (MCTs) are 8- and 10-carbon-chain fatty acids, ­liberated from coconut oil and then re-esterified to glycerol. Because MCTs do not depend on pancreatic lipase or emulsification for digestion, they are used clinically to supply kcal to patients with a variety of pancreatic and gastrointestinal disorders. MCTs are hydrolyzed more readily than long-chain triglycerides (LCTs) by lipase, even in the absence of emulsification by bile salts. After transport into the enterocyte, they are not packaged into chylomicrons but instead are absorbed into the portal bloodstream and transported bound to albumin to the liver, where they can be metabolized to release energy.

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Medium-chain fatty acids (MCFAs) and long-chain fatty acids (LCFAs) also differ in their metabolism. In the liver, LCFAs must be transformed into acyl carnitine derivatives before they can enter the mitochondria for subsequent beta-oxidation. Carnitine acyl transferase I (CAT I) and carnitine acyl transferase II (CAT II) on the inner mitochondrial membrane are both necessary for the entry of LCFAs into the mitochondria. MCFAs do not need CAT I or CAT II for entry and their subsequent beta-oxidation. The oxidation of MCFAs in the fed or fasted state will result in increased production of acetoacetate, 3-hydroxybutyrate, and acetone, three molecules known as ketone bodies. LCFAs only produce ketones in the fasted state since m ­ alonyl-CoA, an intermediate of

carbohydrate metabolism, inhibits CAT I, thus decreasing the entry of LCFAs into the mitochondria in the fed state. Although ketones have a “bad” reputation as a result of their high blood concentrations during diabetic ketoacidosis, they can be efficiently utilized as oxidative fuels and converted to fatty acids. Examples of supplements that contain MCTs include MCT Oil (Nestlé), MCT Fuel (Twinlab), and MCT Power (GT Nutrition USA). One tablespoon provides 4–15 grams of MCTs and 65–135 kcal. Abbot Nutrition has developed a structured lipid featuring a combination of MCTs and LCTs on one triglyceride. This allows the delivery of MCTs to the peripheral tissues where they can be used directly as substrate within cells.

Figure 4.5 Vitamin and Mineral Supplements

Figure 4.6 Bioactive Substance Supplements

The registered dietitian nutritionist should make recommendations for supplementation using the latest evidence-based research.

Benecol is an example of a bioactive substance supplement prescribed as part of the nutrition therapy for hyperlipidemia.

Source: Courtesy of Marcia Nelms. Source: Courtesy of Marcia Nelms.

Feeding Assistance and Feeding Environment recommendations from numerous providers should support the patient care plan. Common examples of nutrition diagnoses for which vitamin and mineral supplements might be appropriate include the following: • Inadequate or excessive vitamin/mineral intake • Food–medication interaction • Food-and nutrition-related knowledge deficit

Bioactive Substance Management  Bioactive substances are defined as food substances added to a food product or taken as supplements that have a specific intended health purpose. Examples of commonly used bioactive substances include plant stanol or sterol esters (see Figure 4.6), soy protein, psyllium, beta-glucan, and pro-/ prebiotics. A patient with hyperlipidemia may be instructed to consume stanol esters as a supplement. The RDN, using the American Heart Association’s guideline for the National Cholesterol Education Program, would instruct the patient on the amount of stanol esters recommended for the intended reduction of lipid levels. Next, the RDN would describe the current products available for purchase and assist the patient with the incorporation of the products into his or her dietary plan. Throughout this text, many bioactive substances are discussed as a component of nutrition therapy and medical care. Many of the nutrition diagnoses for which bioactive substances are prescribed are similar to those for vitamin and mineral supplements as noted above; however, additional appropriate diagnoses include the following: • Suboptimal or excessive bioactive substance intake • Excessive alcohol intake

During nutrition assessment and the subsequent identification of nutrition problems, it is not uncommon to discover that even though the appropriate and adequate diet is available to the patient, he or she is unable to consume adequate amounts. Changing the environment to allow for food choice—for instance, organizing family-style meals in a rehabilitation facility—can significantly improve the patient’s ability to eat. Preparing the patient to eat may include helping him or her to sit at the appropriate height and distance from the tray, optimizing pain medication delivery, or scheduling appropriate mouth care for the patient prior to the meal. Other nutrition interventions may include recommendations for adaptive equipment and providing assistance with eating. Ensuring an appropriate and conducive environment is a team effort requiring the expertise of occupational and physical therapists, speech-language pathologists, pharmacists, and all levels of nursing care. Communication is key to ensure that all components of the nutrition intervention will be successful. These interventions are generally used to address the following types of nutrition diagnoses: • Inadequate energy intake • Unintended weight loss • Disordered eating pattern • Self-feeding difficulty

Nutrition-Related Medication Management During nutrition assessment, each patient’s medications are evaluated for possible drug–nutrient interactions. Chapter 11, “Pharmacology,” covers this topic in depth. Interventions can address the effects of dietary intake on drug dissolution, absorption, metabolism, and excretion.

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Additionally, interventions may target the effects of prescribed drugs on nutrient ingestion, absorption, metabolism, and excretion. The RDN may also be involved in the coordination of medications with meal planning. A common example would be the development of insulin-to-carbohydrate ratios as the RDN assists the patient with the more complex components of medical nutrition therapy for diabetes (see Chapter 17). Another example would be the use of pancreatic enzyme dosages with meals. The RDN provides specific instructions for dosing of enzymes for individuals with cystic fibrosis or other conditions of pancreatic insufficiency. Chapter 15 discusses the role of pro-/prebiotics as a complement to other nutrition therapies and medical care for a number of GI conditions— just one more example of the crucial role the RDN plays in coordination of patient care. For patients who are unable to eat enough food to maintain their weight, it is necessary to identify other factors that impair intake. Non-nutritional causes of poor intake range from poorly fitting dentures to lack of interest in unfamiliar foods to depression. If these factors cannot be resolved and poor intake persists, drugs that stimulate appetite are sometimes ordered. These drugs, including megestrol acetate and dronabinol, are available by prescription.11,12 Like all drugs, appetite stimulants can produce significant side effects in some patients. Megestrol acetate has been shown to improve appetite and increase weight, especially in patients experiencing anorexia-cachexia syndrome. The drug is expensive, ­h owever—it can cost several hundred dollars per month. Moreover, a recent review found that the use of this drug was associated with an increased risk of blood clots, sudden difficulty in breathing, and fluid retention. Approximately one in four patients will experience an increase in appetite and one in 12 will gain weight while taking megestrol acetate. Data on the long-term safety of its use are limited.12 Dronabinol is a derivative of marijuana that may improve appetite, but it has not been associated with weight gain. Dronabinol is expensive, and users have experienced nausea, vomiting, and mental status changes, including euphoria and somnolence. As new information becomes available, drug doses may change. Thus, recommendations to use appetite stimulants should be preceded by a discussion with a pharmacist on your health care team and a thorough review of updated dosing and complication information from reliable sources such as Drug Facts and Comparisons13 or the American Hospital Formulary Service’s AHFS Drug Information.14,15 For more information on appetite stimulants and other interventions, see Chapters 22 and 23. Common examples of nutrition diagnoses for which nutrition-related medication management might be used include the following: • Altered GI function • Impaired nutrient utilization • Altered nutrient-related laboratory values • Food–medication interaction

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4.4  NUTRITION EDUCATION In addition to the many types of nutrition interventions that focus on the delivery of food and/or nutrients and the prevention of malnutrition, the RDN also provides nutritionrelated information to patients and clients in order to change or reinforce eating behaviors. This can be provided as either nutrition education or nutrition counseling; however, it is important to recognize that these are very different processes. Nutrition education focuses “on instruction or training intended to lead to nutrition-related knowledge” and/or “instruction or training intended to lead to nutritionrelated result interpretation and/or skills.” 2 Nutrition counseling typically involves more in-depth behavior change strategies. Both nutrition education and nutrition counseling are intended to maintain or improve health. Nutrition counseling is discussed in further detail in the next section of this chapter. Opportunities for providing education to patients and clients arise in nearly ever y encounter and with nearly every nutrition diagnosis. Nutrition education may occur in a variety of environments or through various mediums including a group class, individual instruction, written instructions, or via telephone or electronic communication. The acute care setting is certainly not as conducive to education as the outpatient setting can be. Unfortunately, many patients will have contact with the RDN only while hospitalized. Furthermore, illness, pain, and an uncomfortable environment can hinder the educational process. It is also difficult to adjust to illness and even more difficult to understand numerous pieces of information from a variety of individuals. If adequate education or follow-up is needed, referral to an outpatient RDN is optimal. While in the hospital, the RDN may initially provide basic education that will allow the patient to develop “survival skills” until further education is available. Basic guidelines for providing nutrition education regardless of the setting or diagnosis include the following: • Clearly communicate the purpose of the education. • Prioritize the nutrition issues or problems so that education is not too complex. • Explain the relationship of nutrition to health/disease. • Tailor the education to fit the individual patient by understanding his or her level of baseline knowledge, skills, and learning style. The goal of both types of nutrition education is for the patient to make appropriate dietary and nutritionrelated changes that promote positive health and nutrition outcomes. The skills and resources needed by the RDN include effective communication, use of terms that can be understood by patients, appropriate reading materials, visual aids to support the verbal information provided, and sensitive listening skills. Box 4.3 provides an overview of writing skills required for developing nutrition education materials.

BOX 4.3

CLINICAL APPLICATIONS

Writing for Nonmedical Audiences: Instructional Materials for Patients, Their ­Families, and the Public Ralph G. Nelms, PhD  Wright State University Writing to the community of health professionals within your institution or agency will become easier with practice. But writing for other health professionals is not the only kind of writing you may be called on to do. You may also find yourself writing for various nonprofessional audiences, including the public in general. This section describes some of the most common of these forms of writing. The purpose of these materials is to inform, sometimes with the goal of persuading the reader to take action, if necessary, after reading the material. Examples include informational material outlining nutrition therapies and lifestyle changes. The audience for such materials obviously differs greatly from the professional audience that charting addresses. You should avoid most medical abbreviations because your readers will simply not be familiar with them. You cannot use professional or even academic jargon. Words such as data will need to be replaced with more generally understood words such as information. In other words, use commonsense language. Remember, the goal here is to instruct.

Your reader cannot be instructed if she or he cannot understand what is being said. Establish the appropriate reading level and even have a member of your target audience evaluate your instructional material.

Tips for Writing Instructional Materials Ask nonprofessionals you know to give you feedback on the instructional materials you write before you prepare them for distribution so that you can revise the text if it is unclear to your test audience. You can also establish a focus group that is representative of your intended audience for the purpose of evaluating and responding to your writing. Their insight can help ensure that you will meet the audience’s needs. Use numbering and bullets to create easy-to-read lists. As a model, consider the way bullets and numbers are used in this textbook. Spend time planning the document you want to produce before beginning to actually write it. Put together a rough plan for organizing the information.

4.5  NUTRITION COUNSELING Nutrition education and nutrition counseling share the common goal of assisting the patient to make appropriate diet and lifestyle changes to improve his or her health and nutrition status. Nonetheless, there are significant differences in how education and counseling are provided. As discussed previously, nutrition education primarily involves the transfer of knowledge and/or skill building. That does not imply that nutrition education isn’t important or relevant; however, having information and/or knowing how to complete a specific task such as label reading or recipe modification alone does not necessarily translate into a behavior that is sustainable. In other words, “knowing is not always doing.” Nutrition counseling is defined as: “A supportive process, characterized by a collaborative counselor–patient/client relationship to establish food, nutrition and physical activity priorities, goals, and individualized action plans that acknowledge and foster responsibility for self-care to treat an existing condition and promote health.”2 The role of the RDN as counselor has

This prewriting planning will make writing a lot easier. Leave yourself plenty of time to revise the document once it is drafted. Read through it first to make sure you included all the information (the content) that you planned to convey. Read through it a second time to make sure that the organization makes sense—that information introduced early in the document, for example, is explained immediately rather than much later in the document. Read through the document a third time to check the language and make sure it is understandable to your audience. Make sure you check your spelling, too. A warning: There is one important similarity between writing to professional peers and writing to nonmedical professionals: the need for clarity. Sometimes, when shifting from technical writing intended for the professional community to writing for nonprofessionals, writers also shift from an ideal of clarity in their writing to an ideal of eloquence. Eloquence is fine for novelists, but it is irrelevant here. Be clear, be concise, and use language appropriate for your audience.

evolved from that of a clinician who mainly provides information on what and how to eat to that of one who is able to evaluate and take into consideration the complex social and physiological factors that influence food and lifestyle choices. It is important that the counselor develop a collaborative relationship with the patient/client that enables careful examination of nutrition problems to establish goals and plans. The ultimate goal of counseling is for the patient/client to take responsibility for behaviors that improve his or her nutritional status in order to treat an existing condition and promote health.2

Counseling Skills Effective nutrition counseling is greatly influenced by the relationship between the patient/client and the dietetic practitioner, as illustrated in the central core of the Nutrition Care Model (see Chapter 2). The definition of nutrition counseling in the standardized nutrition intervention terminology supports the importance of this relationship by noting the

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following important assumptions and characteristics of the role of the RDN as counselor: • Supportive: The counselor’s role is to encourage and positively guide the patient as changes are made. Being a champion of change and advocating for the benefits of a healthy lifestyle can be especially useful to patients who are undergoing dietary changes.

• Process: Counseling is not a one-time encounter in which everything important about nutrition can be explained. Counseling is a process that involves important follow-up and continued contact in order to be most effective. The AND’s “Evidence-Based Guidelines for Medical Nutrition Therapy for Diabetes Mellitus (DM)” conclude that there is strong support for the effectiveness of an initial series of three to four encounters with an RD/RDN, each lasting 45–90 minutes. These encounters should be completed within 3–6 months of diagnosis of DM. Furthermore, at least one follow-up encounter is recommended annually to reinforce lifestyle changes and to evaluate and monitor progress.16 • Collaborative: Because effective counseling requires working together with the patient/client as a partner to solve problems, the role of the counselor is more subordinate than authoritarian. Changes are more likely to be made when the patient values the benefits of the change and can take personal ownership rather than only being told what to do.

• Relationship: Developing a professional relationship with the patient/client that is built on trust and honesty is extremely valuable. Sharing information about one’s dietary and lifestyle behaviors is very personal. Many persons are already aware that some of their practices are not necessarily beneficial to health, and they may feel ashamed or fear being judged when answering diet history questions. Therefore, characteristics and communication skills that demonstrate good listening and acknowledgment of the client are essential to building trust and promoting openness. Tables 4.5 and 4.6 illustrate many of these important characteristics and communication skills. • Individualized: Unlike nutrition information that describes healthy eating guidelines for a group or population, such as the Dietary Guidelines for Americans, nutrition counseling can take on many different shapes and forms, based on well-known and researched counseling theories and strategies that are tailored to an individual’s needs and environment.

• Self-care: Even though the nutrition counselor is a champion of change and a partner in this process, the long-term expectation is that the client him- or herself will be able to maintain appropriate changes and solve problems in order to make the diet and lifestyle choices long lasting. That does not limit the opportunity for ongoing support and follow-up by the counselor in order to evaluate and monitor progress. As important as building a positive relationship and demonstrating active listening are, it is equally important

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Table 4.5 Characteristics of Counselors That Promote a Positive Relationship • Behave naturally: Appear authentic and sincere; encourages spontaneity and openness on the part of the client. • Have a sense of humor: Helps the client to not take problems too seriously; helps break down barriers between the counselor and the client. • Be flexible: Do not have unrealistic expectations. • Be optimistic and hopeful: Clients respond well and appreciate the support. • Encourage clients to talk: They may not have had opportunities to in the past; provide verbal and nonverbal responses such as nods and occasional “hmms.” • Maintain appropriate eye contact: Look at clients but do not stare. • Develop attentive body language: Use relaxed gestures and sit or stand with an open, welcoming, and calm posture. • Listen with an open mind and spirit of inquiry: Be sure that responses and nonverbal language are not judgmental. • Respect, value, care, and trust others: Conveys the message that clients are valued and respected. Source: Adapted from Bauer K, Liou D, Sokolik C. Nutrition Counseling and Education Skill Development. 2nd ed. Belmont, CA: Cengage; 2012.

Table 4.6 Effective Communication Skills That Demonstrate Active Listening and Undivided Attention to Clients Clarifying (Probing): Confirm the accuracy of a client’s statement by asking a question or prompting the client to continue talking. • “Can you explain further. . .?” • “Tell me more about. . .” Paraphrasing (Summarizing): Lets clients know that the counselor is listening; allows the client to clarify any misunderstanding. • “Let me summarize what I think you just said . . .” Responding with empathy: Demonstrates that a counselor understands what a person feels from their frame of reference; clients can feel they are no longer alone. It is not effective to simply state that you know how another person feels. • “It sounds like . . .” • “It seems like . . .” Conveying respect: Show consideration and appreciation for the time and information that the client shares. • “I am impressed with how you . . .” • “You have done a great job of . . .” Source: Adapted from Bauer K, Liou D, Sokolik C. Nutrition Counseling and Education Skill Development. 2nd ed. Belmont, CA: Cengage; 2012.

to obtain adequate and accurate information from patients and clients. Therefore, developing communication skills of inquiry and appropriate questioning techniques such as motivational interviewing are also essential for the counselor. Examples of these types of questions and skills are summarized in Box 4.4.

BOX 4.4

CLINICAL APPLICATIONS

Effective Communication Skills for Obtaining Accurate Information from Clients Questioning When used appropriately, questioning can be very effective; however, it is important to know when to ask a question and what type of question best meets the need of inquiry at a particular point in time during the interview or counseling session. As a general rule, it is advisable to avoid questions that begin with “why,” as they are often perceived as judgmental and accusatory. Clients can become defensive and less willing to provide accurate and truthful information if they feel that they need to defend their answer. Following are examples of common types of questions used by nutrition counselors: • Closed-ended questions: Questions designed to obtain either a yes or no response or a very brief answer. It is generally recommended that use of this type of question be limited, as a closed-ended question tends to prompt a response the client thinks is correct or preferred. • Examples of how these questions may begin: “is,” “are,” “did,” “how many” • Open-ended questions: Although these types of questions are valuable in that they allow the responder to provide a great deal of information and do not limit a response to a short answer, they do require that the

counselor listen very carefully to what is being said. Answers may become lengthy and it may be necessary to redirect the client. The major advantage to using open-ended questions is that clients are less likely to feel threatened and more likely to provide honest responses. They may also provide information that guides appropriate secondary and probing questions. • Examples of how these questions may begin: “how,” “what” • Secondary questions: These are questions that stem from information that has been provided by the client, about which further detail is needed. These types of questions are very similar to the clarifying or probing questions described in Table 4.6. • Examples of how these questions may begin: “tell me more,” “can you explain further” • Funneling questions: These are questions that are logically arranged so that a broad topic is first introduced and then subsequent questions narrow the subject or topic into more specific and detailed information. Unlike secondary questions that can be asked at any point in the interview, funneling questions assume a more logical and sequential order. • Examples of how these questions may be structured:

Theoretical Basis/Approach for Nutrition Counseling

• “What is your usual meal and snack pattern throughout the day?” • “Given that you generally eat lunch at work, what would you typically have?” • “What kind of salads and dressings are you likely to purchase at work?”

Giving Feedback or Noting Discrepancies Occasionally it is necessary to confront a client who may be providing information that is either inconsistent or contradictory or excuses for not making changes. This form of questioning is especially valuable if a client is in denial or is expressing resistance to change. Bauer et al. note a variety of ways that the counselor can bring these discrepancies to the attention of the client. • State an observation without adding “but”; use “and” as the connector. Following the “and” is the observation of the discrepancy. • Begin the statement with “on the one hand . . .on the other hand . . .” • Directly say “I see/hear an inconsistency . . .” Adapted from Bauer K, Liou D, Sokolik C. Nutrition Counseling and Education Skill Development. 2nd ed. Belmont, CA: Cengage; 2012.

Counseling Strategies

The foundation and supporting principles used to facilitate behavior change in nutrition counseling draw from numerous areas of research within the realms of education and psychology. Behavior change theories and models provide a research-based rationale for designing and tailoring nutrition interventions to achieve the desired effect. For example, if during a nutrition assessment interview the patient acknowledges that he or she does not believe that making significant behavior changes will result in a better health outcome, principles of the health belief model as well as awareness of the stages of change should influence how the counselor proceeds and what type of information is appropriate to promote a change in belief and movement to the next stage of change. Table 4.7 provides a summary of the major theories that support nutrition education and counseling methods.

RDNs can and should use a number of strategies to assist the client in achieving healthful behavior change. Whereas a theoretical basis provides guidance to better understand a person’s motivation and readiness to change, strategies are the tools that can help facilitate change. Strategies include motivational interviewing, self-monitoring, and cognitive restructuring. For example, the major motivational strategies are giving advice, identifying and removing barriers, providing choices, decreasing desirability of a present behavior, practicing empathy, providing feedback, clarifying goals, and active helping.16 Self-monitoring may include using a food diary to increase the client’s awareness of actual food intake. Cognitive restructuring teaches the client appropriate steps in addressing failures in behavior change. Providing positive approaches to particular dietary changes facilitates the client’s efforts to deal with problem behaviors.17 Boxes 4.5 and 4.6 explore the unique attributes of nutrition education and counseling for pediatric and geriatric patients.

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Table 4.7 Examples of the Theoretical Basis/Approach for Nutrition Counseling and Education Theory

Assumptions/Principles

Application in Nutrition Counseling/Education Interventions

Cognitive-behavioral

Uses the concept that behavior is learned and is directly related to both internal and external factors

Nutrition counseling and education should focus on ­interventions that will change environment and/or focus on ways to change a pattern of negative thinking

Health belief model

Predicts a person’s decisions about health-related ­behavioral changes; identifies the client’s perceived ­ability to accomplish a behavior change

May benefit from explanation of disease risks and link to diet or exploration of the pros and cons of actions

Social learning theory

Builds on concepts of modeling; people learn through observing others who are doing well

Share success stories; refer to appropriate support groups; engage clients in group classes

Transtheoretical/stages of change

Focuses on the concept that behavior change occurs in stages of motivation as client moves through five stages in order to take action

Treatment interventions need to be tailored to client’s stages of change

Sources: Adapted from Snetselaar L. Overview of nutrition counseling. In: Nutrition Counseling Skills for the Nutrition Care Process. 4th ed. Boston, MA: Jones and Bartlett; 2009: 10–17. Bauer K, Liou D, Sokolik C. Frameworks for understanding and attaining behavior change. Nutrition Counseling and Education Skill Development. 2nd ed. Belmont, CA: Cengage; 2012: 18–22, 28–29.

BOX 4.5

LIFE CYCLE PERSPECTIVES

Unique Features of Pediatric Nutrition Education/Nutrition Counseling Colette LaSalle, PhD, RD  San Jose State University Unique aspects of pediatric nutrition counseling and education include consideration of the age-related cognitive development of the child and the importance of relaying the nutrition-related message to the parent and/or caregiver. The complexity of the intervention is also dependent upon the setting (school-based, group, individual, or acute care) and the level of risk associated with the nutrition message. Nutrition efforts should be targeted and age appropriate. For example, a nutrition intervention designed to improve vegetable intake should be conducted in a multilevel manner in which educational objectives are geared toward both adult and child. This could be accomplished in a group setting with both adult-oriented dialogue and child-centered “storytelling” or actions that convey the importance of eating vegetables. While adult learners (parents) need informative, goal-oriented education, children prefer a colorful, simple message with a specific learning objective. To accomplish this, the lesson plan could include information on the significance of vegetable intake for growth and development and suggestions for incorporating vegetables into the child’s diet for the adult learner, along with a “storytelling” component for the child. The latter would include “hands-on” experiences such as a seed-planting demonstration in conjunction with tools (a jar, dirt, and seeds) that can be taken home so that children can grow their own vegetables or a taste testing with vegetables that are new to the child.

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School-based nutrition education and counseling have been found to be successful, especially if nutrition education is integrated within the curriculum and school food service. It is also important that the child is provided with information in such a way that he or she can transfer this knowledge home to the family. Pediatric nutrition education is still dependent on the caregiver supporting any of the nutrition interventions that are recommended. References 1. Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: nutrition guidance for healthy children ages 2 to 11 years. J Acad Nutr Diet. 2014; 114: 1257–76. 2. Cluss PA, Ewing L, King WC, Reis EC, Dodd JL, Penner B. Nutrition knowledge of low-income parents of obese children. Transi Behav Med. 2013; 3(2): 218–25. 3. Folliard JN, Duncan-Goldsmith DM. Opportunities to improve snacks and beverages in schools. J Acad Nutr Diet. 2013; 113(9): 1145–51. 4. Hoelscher DM, Kirk S, Ritchie L, Cunningham-Sabo L, Academy Positions Committee. Position of the academy of nutrition and dietetics: interventions for the prevention and treatment of pediatric overweight and obesity. J Acad Nutr Diet. 2013; 113(10): 1375–94. 5. Patino-Fernandez AM, Hernandez J, Villa M, Delamater A. Schoolbased health promotion intervention: parent and school staff perspectives. J Sch Health. 2013; 83(11): 763–70. 6. Post RC, Haven J, Eder J, Johnson-Bailey D, Bard S. MyPlate reaches more frontiers. J Acad Nutr Diet. 2013; 113(8): 1014, 1016–17. 7. Ruel MT, Alderman H, Maternal and Child Nutrition Study Group. ­Nutrition-sensitive interventions and programmes: how can they help to accelerate progress in improving maternal and child nutrition? Lancet. 2013; 382(9891): 536–51. Erratum in: Lancet. 2013; 382(9891): 506.

BOX 4.6

LIFE CYCLE PERSPECTIVES

Unique Features of Geriatric Nutrition Education/Nutrition Counseling Colette LaSalle, PhD, RD  San Jose State University While older Americans are a heterogeneous group, they share a high prevalence of chronic diseases. For example, it is estimated that 80% of older adults have one chronic disease and 50% have two or more; the average 75-year-old has three chronic diseases and takes five prescription drugs. Interestingly, 9 out of 10 of these individuals have conditions that could be improved through nutrition education and counseling. This illustrates the importance of focused nutrition interventions in this population. Clients range widely in age, education, cognitive function, and previous level of nutrition education regarding diet restrictions and reside in very different environments. Some are free-living community dwellers, whereas others live in assisted-care (including with family) or long-term care facilities. Thus, the type and format of nutrition interventions must be tailored to the client. For example, interventions for individuals with diminished cognitive capacity must be directed toward the caregiver and incorporate goal-oriented, specific, measureable, and achievable tasks that will optimize nutrition status. In contrast, for community-based interventions ­targeted toward free-living adults who are capable of defining personal objectives and setting their own nutrition-related goals, nutrition education should be well planned and messages should be limited in number, simple, targeted, practical, and reinforced. Geriatric learners do well in group nutrition education classes where they can interact with peers.

­ essages should be ethnicity specific and incorporate M “hands-on” application of new skills, such as “heart-healthy” cooking classes where the sensory experience increases learning and retention. References 1. Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: Individualized nutrition approaches for older adults: long-term care, post-acute care, and other settings. J Acad Nutr Diet. 2018; 118: 724–35. 2. Office of Disease Prevention and Health Promotion. Older Adults. Available from: https://www.healthypeople.gov/2020/topics-objectives/topic/older-adults. Accessed: August 2, 2018. 3. Raghupathi W, Raghupathi V. An empirical study of chronic diseases in the United States: a visual analytics approach to public health. Intl J Environ Res Public Health. 2018; 15: 431–55. 4. Gopinath B, Russell J, Flood VM, et al. Adherence to dietary guidelines positively affects quality of life and functional status of older adults. J Acad Nutr Diet. 2014; 114(2): 220–29. 5. Fitzgerald N, Morgan KT, Slawson DL. Practice paper of the Academy of Nutrition and Dietetics abstract: the role of nutrition in health promotion and chronic disease prevention. J Acad Nutr Diet. 2013; 113(7): 983. 6. Hsiao PY, Mitchell DC, Coffman DL, et al. Dietary patterns and relationship to obesity-related health outcomes and mortality in adults 75 years of age or greater. J Nutr Health Aging. 2013; 17(6): 566–72. 7. Breedveld-Peters JJ, Reijven PL, Wyers CE, et al. Integrated ­nutritional intervention in the elderly after hip fracture. A process ­evaluation. Clinical Nutrition. 2012; 31: 199–205. 8. Slawson DL, Fitzgerald N, Morgan KT Position of the Academy of Nutrition and Dietetics: the role of nutrition in health promotion and chronic disease prevention. J Acad Nutr Diet. 2013; 113(7): 972–79.

4.6  COORDINATION OF

4.7  NUTRITION MONITORING

NUTRITION CARE

AND EVALUATION

The fourth and last domain of nutrition interventions is coordination of nutrition care. Providing health care is a team effort. RDNs work with numerous other health care professionals with the ultimate goal of improving the lives and health of their patients (refer to Chapter 1). The coordination of care encompasses those steps necessary to ensure a successful transition from the health care facility to the patient’s home or any of the types of post-acute care facilities. Depending on the specific nutrition intervention outlined in the nutrition care plan, the coordination of care can include referrals to community agencies for access to food or nutrition support, or to another RDN who specializes in a particular nutritional intervention. Many health care facilities regularly coordinate the care of their patients through team meetings where all health goals and interventions can be addressed. Interprofessional care has routinely supported an improved outcome for patients. Learning about the members of the interprofessional team and observing that collaboration should be an important of your dietetics training.18 See Box 4.7 for additional information.

As discussed in Chapter 2, the purpose of monitoring and evaluation is to determine the degree of progress being made and whether the client’s goals or desired outcomes of nutrition care are being achieved. Monitoring and evaluation of nutrition care outcomes answers the question, “Is the nutrition intervention strategy working to resolve the nutrition diagnosis, its etiology, and/or its signs or symptoms?”2 A nutrition diagnosis should identify both an etiology that is the cause of or a contributing factor to the nutrition problem and the signs and symptoms describing the severity or consequences of the problem (refer to Chapter 2). An appropriate nutrition intervention not only impacts the etiology but also improves the signs and symptoms of the nutrition problem. The nutrition outcomes are the basis through which a body of research establishing the effectiveness of nutrition interventions can be built. As outlined in Box 4.1, evidence-based practice guides and protocols should be utilized in the selection of interventions and identification of science-based goals and expected outcomes. Nutrition care outcomes can be grouped into four categories that parallel four domains of the assessment language:2

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BOX 4.7

CLINICAL APPLICATIONS

Interprofessional Core Competencies The accepted definition of interprofessional education is the event that “occurs when two or more professions (students, residents and health workers) learn with, about, and from each other to enable effective collaboration and improve health outcomes.” Both interprofessional health care and interprofessional education and training have been topics of discussion over the past five decades. The literature tells us that patients do better when their care is coordinated through a team. It is therefore hoped that providing training in team-based health care will translate into improved health outcomes for our patients. In 2016, the following core competencies for interprofessional education were developed through a collaboration

of the major educational fields within the health sciences. Mastery of these competencies among RDNs will move us closer to improving health care in the United States. • Values/Ethics: Work with individuals of other professions to maintain a climate of mutual respect and shared values. • Roles/Responsibilities: Use the knowledge of one’s own role and those of other professions to appropriately assess and address the health care needs of patients and to promote and advance the health of populations. • Interprofessional Communication: Communicate with patients, families, communities, and professionals in

• Food-/nutrition-related history data (improved nutrient intake and administration, knowledge, behavior, access, and ability and nutrition quality of life) • Anthropometrics (improved body composition measures) • Biochemical data, medical tests, and procedures (normalization of biochemical data and tests) • Nutrition-focused physical findings outcomes (normalization of physical findings) Improvement in the food-/nutrition-related domain often precedes changes in the other types of outcomes. For example, a decrease in caloric intake over time can not only result in a change in weight but also improved blood glucose control or blood pressure. Furthermore, these changes will often lead to positive health care outcomes such as decreased risk of disease conditions, decreased hospitalization and health care costs, and improved overall quality of life. In order to successfully monitor and evaluate an outcome of a nutrition intervention, a nutrition reassessment must be completed. This reassessment should focus on the changes in the factors contributing to and signs and symptoms of the nutrition problem. As data are continually collected and recorded, the patient’s progress should also be documented. The following nutrition diagnosis status terms can be used to accurately report progress: (1) resolved—nutrition problem no longer exists; (2) improvement shown—nutrition problem still exists with positive progress to goal; (3) unresolved—no improvement shown; or (4) no longer appropriate—change in condition. If the status is either “improvement shown” or “unresolved,” further reassessment will be needed to evaluate any conditions or factors that continue to contribute to a suboptimal nutrition outcome. This might result in a change in intervention or identification of additional nutrition problems. Regardless of the clinical setting or length of care, realistic nutrition goals and expected outcomes can be determined. 90  Part 2  The Nutrition Care Process

health and other fields in a responsive and responsible manner that supports a team approach to the promotion and maintenance of health and the prevention and treatment of disease. • Teamwork: Apply relationship-­ building values and the principles of team dynamics to perform effectively in different team roles to plan, deliver, and evaluate patient/population-­ centered care and population health programs and policies that are safe, timely, efficient, effective, and ­equitable. Source: Interprofessional Education Collaborative. Core Competencies for Interprofessional Collaborative Practice: Report of an Expert Panel. Washington, DC; 2016. Retrieved from: https://www.ipecollaborative.org/resources.html

Once nutrition diagnoses are identified and prioritized, some of the problems (e.g., those in the clinical or behavioralenvironmental domains) may need to be resolved over a longer time, thus benefiting from the coordination of nutrition care. Prior to the development of the standardized language now used in the NCP, RDNs often participated in collecting institutionalized data such as length of stay or reduction in health-related risk factors; however, nutrition-specific outcomes were measured less frequently. With the advent of the standardized language, dietitians can now track ­nutrition-related outcomes and provide data that contribute to evidenced-based practice supporting the use of medical nutrition therapy. As mentioned in previous chapters, ANDHII is a web-based system provided by the Academy for collecting health outcomes data from RDNs and NDTRs in practice. See Chapter 6 for more details.

4.8 CONCLUSION This chapter focused on providing further information regarding the third and fourth steps of the NCP: nutrition intervention and nutrition monitoring and evaluation. The various types of nutrition interventions defined within the standardized language have been introduced; specific interventions that are commonly used to provide nutrition care to patients with certain diseases and health conditions are included in subsequent chapters. One of the most important concepts in this chapter is that the selection of an appropriate nutrition intervention begins with a well-written and accurate nutrition diagnosis and that before an intervention can be implemented, it is necessary to develop a nutrition prescription and/or expected goals or outcomes, which in turn become the basis for monitoring and evaluating progress toward the resolution of the nutrition problem.

CHAPTER REVIEW QUESTIONS 1. Describe two ways that the house or regular diet can be modified to accommodate patient needs. 2. What is the difference between clear and full liquid diets? When are they used, and what are their limitations? 3. Identify at least two steps to increase energy and protein in a regular diet.

4. Nutrition interventions can include changes to the environment that could improve nutritional intake. Give examples of interventions that can assist with improving nutritional intake within the environment.

6. Give an example of a closed-ended question and an open-ended question that might be used during a patient encounter. In what situation would it be best to use an open-ended question?

5. What is the major difference between nutrition education and nutrition counseling?

REFERENCES 1. U.S. Department of Health and Human Services. Medicare program; revisions to payment policies and five-year review of and adjustments to the relative value units under the physician fee schedule for calendar year 2002. CMS-1169-FC. Federal Register. 2001; 66(212): 55246–503. 2. Academy of Nutrition and Dietetics. eNutrition Care Process and Terminology (eNCPT) Academy of Nutrition and Dietetics, https://www​ .ncpro.org/. Accessed July 31, 2018. 3. Academy of Nutrition and Dietetics. Evidence Analysis Library. Available at http://www​ .adaevidencelibrary.com. Accessed July 31, 2018. 4. Schindler K, Themessl-Huber M, ­Hiesmayr M, et al. To eat or not to eat? Indicators for reduced food intake in 91,245 patients hospitalized on nutritionDays 2006–2014 in 56 countries worldwide: a descriptive analysis. Am J Clin Nutr. 2016; 104: 1393–402. 5. Burns J, Gregory S. Changing foodservice systems: a balancing act between patient satisfaction and cost. J Foodservice Business Research. 2007; 20: 63–78. 6. Keller M. That’s progress. Advancements in hospital foodservice. Today’s Dietitian. 2009; 8: 28–31.

7. Huang JS, Chu S, Cheung C, Poon L, ­Terrones L. The nutritional value of food service meals by hospitalized children. Clin Nutr ESPEN. 2016; 15: 122–125. 8. Willcutts KF, Chung MC, Erenberg CL, Finn KL, Schirmer BD, Byham-Gray LD. Early oral feeding compared with traditional timing of oral diets after upper gastrointestinal surgery: a systematic review and meta-analysis. Ann Surg. 2016; 264: 54–63. 9. Rattray M, Roberts S, Marshall A, Debrow B. A systematic review of feeding practices among postoperative patients: is practice in-line with evidence based guidelines. J Hum Nutr Diet. 2017; https://doi.org/10.1111/jhn.12486. 10. Academy Quality Management Committee. Academy of Nutrition and Dietetics: Revised 2017 Standards of Practice for Registered Dietitian Nutritionists. J Acad Nutr Diet. 2018; 118: 141–65. 11. Yeh SS, Lovitt S, Schuster MW. Pharmacological treatment of geriatric cachexia: evidence and safety in perspective. J Am Med Dir Assoc. 2007; 8: 363–77.

Megestrol acetate for treatment of anorexiacachexia syndrome. Cochrane Database Syst Rev. 2013; Issue 3: CD004310. 13. Prescribers’ Digital Reference. Available from: http://www.pdr.net/. Accessed July 31, 2018. 14. Drug Facts and Comparisons 2017. St. Louis, MO: Walters Kluwer; 2017. 15. AHFS Drug Information 2017. Bethesda, MD: American Hospital Formulary Service; 2017. 16. Franz MJ, Powers MA, Leontos C, et al. The evidence for medical nutrition therapy for type 1 and type 2 diabetes in adults. J Am Diet Assoc. 2010; 110:1852–1889. 17. Holli B, Beto JA. Nutrition Counseling and Education Skills for Dietetics Professionals. 8th ed. Baltimore, MD: Wolters Kluwer, 2018. 18. Interprofessional Education Collaborative (2016). Core Competencies for Interprofessional Collaborative Practice: Report of an Expert Panel. Washington, DC. Retrieved from: https://www .ipecollaborative.org/resources.html.

12. Ruiz Garcia V, López-Briz E, Carbonell Sanchis R, Gonzalvez Perales JL, Bort-Marti S.

Chapter 4  Nutrition Intervention, Nutrition ­Monitoring and Evaluation   91

CHAPTER 5

Source: istock.com/Yobro10

Enteral and Parenteral Nutrition Support Kristen Roberts, PhD, RDN, LD, CNSC Marcia Nahikian-Nelms, PhD, RDN, LD, FAND The Ohio State University

LEA RNING O B JECTIV ES LO 5.1  List consequences of malnutrition. LO 5.2  Discuss the difference between enteral and parenteral nutrition. LO 5.3  Identify disadvantages and possible complications of enteral and parenteral nutrition. LO 5.4  Describe the types of enteral nutrition and their indications. LO 5.5  Describe the three types of enteral feeding delivery methods.

92

LO 5.6  Explain refeeding syndrome, how it can be avoided, and which patients are at highest risk.

LO 5.9  Calculate estimated nutrient needs for parenteral and enteral ­nutrition prescriptions.

LO 5.7  Apply the nutrition care process to develop enteral and parenteral nutrition prescriptions.

LO 5.10  Determine amounts of ­calories and macronutrients provided by ­parenteral and enteral prescriptions.

LO 5.8  Explain the steps involved in determining the enteral and parenteral nutrition prescriptions.

LO 5.11  Determine criteria for ­monitoring and evaluating enteral and parenteral feedings.

GLO SSARY aspiration—inspiration of foreign matter into the lung bolus feedings—rapid administration of 250–500 mL of formula several times daily central venous catheter (CVC)— vascular access device inserted into large veins such as the subclavian, jugular, or femoral veins in the center of the body colonocyte—epithelial cell of the large ­intestine or colon continuous feedings—administration of ­formula for 10–24 hours daily, using a pump to control the feeding rate enteral nutrition (EN)—feeding through the gastrointestinal tract using a tube, catheter, or stoma that delivers nutrients distal to (or beyond) the oral cavity gastrostomy—an opening into the stomach hydrophilic—water loving, or attracting water implantable port—vascular access device that is completely under the skin, is placed in the vein on the upper chest wall, and exits the body near the xyphoid process, axilla, or abdominal wall intermittent feedings—administration of formula several times daily, over 20–30 minutes intravenously (IV)—by vein, in reference to administration of drugs or nutrients intravenous lipid emulsion (ILE)—the type of fat that is administered as part of a parenteral nutrition solution

jejunostomy—an opening into the jejunum nasogastric feeding tube—a tube that is inserted nasally (through the nose) into the stomach nasointestinal feeding tube—a tube that is inserted nasally (through the nose) past the stomach into the intestine NPO—nil per os, which is Latin meaning “nothing by mouth” orogastric feeding tube—a tube that is inserted orally (through the mouth) into the stomach osmolality—number of water-attracting particles per weight of water in kilograms (expressed as mOsm/kg) osmolarity—number of millimoles of liquid or solid in a liter of solution ostomy—an artificial opening created by ­surgical procedure parenteral nutrition (PN)—administration of nutrition directly into the circulatory system (formally known as total parenteral nutrition [TPN] and intravenous hyperalimentation [IVH], which has been replaced by central parenteral nutrition [CPN]) percutaneous endoscopic gastrostomy (PEG)—a procedure used by a physician to insert a feeding tube through the skin and into the stomach using an endoscope peripheral parenteral nutrition (PPN)— administration of nutrition into a small vein in the arm or back of the hand (also known as peripheral venous nutrition [PVN])

5.1  INTRODUCTION: PLANNING AND IMPLEMENTATION OF NUTRITION INTERVENTIONS WITH ENTERAL AND PARENTERAL NUTRITION SUPPORT With increased focus on the issues of overweight, obesity, and chronic disease in health care, it is important not to lose sight of the fact that insufficient food intake and the resulting protein-energy malnutrition are of significant concern. As many as 30%–50% of hospitalized patients and up to 95% of nursing home patients exhibit some signs of malnutrition. Furthermore, almost 70% of hospitalized patients will exhibit a decline in nutritional status during hospitalization and up to one-third of these patients will become malnourished.1–4 The Healthcare Cost and Utilization Project (HCUP) analyzed U.S. hospitalizations that involved a diagnosis of malnutrition. This group estimated approximately 2 million admissions that involved the diagnosis of malnutrition.5 In the United Kingdom, costs associated with malnutrition are as high as $13 billion, which is twice the cost of health care associated with obesity.6 Estimations for malnutrition in children admitted to acute care hospitals range from 6% to 14% in G ­ ermany, France, the United Kingdom, and the United States.7

peripherally inserted central catheter (PICC)—vascular access device inserted into the arm and threaded into the subclavian vein to the vena cava propofol—lipid-based drug that is used to maintain sedation during mechanical ventilation refeeding syndrome—metabolic alterations that may occur during nutritional repletion of starved patients specialized nutrition support (SNS)—provision of nutrients orally, enterally, or parenterally with therapeutic intent. stoma—an opening structured lipid—commercially produced lipid that alters fatty acids to allow for ­absorption as a medium-chain triglyceride stylet—wire guide within the enteral tube that assists with insertion surgical gastrostomy—an opening into the stomach that requires a surgical procedure tunneled catheter—intravenous access device that is placed in the vein on the upper chest wall and exits the body near the xyphoid process, axilla, or abdominal wall vascular access device—a device inserted into a vein, which permits ­administration of intermittent or continuous infusion of ­parenteral solutions of medications viscosity—thickness of a liquid

The consequences of inadequate nutrition and subsequent malnutrition include increased risk of infection, delayed wound healing, and delayed return to home, work, or baseline activities of daily living following hospitalization.1,2,5,7–11,12 All these consequences contribute to increased health care costs and diminished quality of life. Health care institutions—and in particular, interdisciplinary clinicians (such as the physician, nurse, registered dietitian nutritionist [RDN], and pharmacist)—work to prevent or treat malnutrition and other diseases by providing the patient with appropriate specialized nutritional support. As discussed in Chapter 4, this support can be provided through an oral diet designed to meet the patient’s specific nutritional requirements and modified to meet his or her specific physical needs. This might include modification of the type or amount of food and nutrients within meals or at specified times between meals, or the addition of medical food supplements and/or vitamin and mineral supplements. Recent data collected in 56 countries for the nutrition survey, nutritionDays 2006–2014, identified factors associated with placing a patient at risk for malnutrition that were associated with inadequate oral intake during hospitalizations. Worldwide, factors that placed a patient at risk were older women with low body mass index (BMI) who were confined to bed Chapter 5  Enteral and Parenteral Nutrition Support   93

and who had reduced dietary intake the previous week. 13 Any time that individuals cannot meet their nutritional needs through an oral diet, they should be evaluated for enteral nutrition (EN) (or tube feeding) and/or parenteral nutrition (PN) administration. Building on the nutrition intervention principles discussed in Chapter 4, this chapter focuses on food and nutrient delivery for the primary purpose of preventing or treating malnutrition when nutrient needs cannot be met with an oral diet. The use of nutrition support (in particular, EN support) is now recognized as an integral component of the medical care for patients that can blunt the stress response, reduce infections and other medical complications.12 Nutrition support via enteral and parenteral nutrition is a life-sustaining alternative for patients who are unable to maintain their nutritional status using oral diets or supplements. PN support became an important nutrition intervention in the 1970s, as methods were developed to provide adequate feedings by vein. Since then, research and economic necessity have yielded significant technical advancements. Nutrition support has developed rapidly, and practice is challenging as clinicians strive to keep up with changes in the field. See Box 5.1 for a brief history of nutrition support. A comprehensive nutrition assessment is the first step to determine not only the extent of inadequate nutrition but also the underlying cause of poor oral intake (if present). Common nutrition diagnoses that may necessitate alternate routes for nutrition interventions include the following: inadequate energy intake, inadequate oral intake, inadequate EN infusion, inadequate PN infusion, inadequate bioactive substance intake, increased nutrient needs, malnutrition, inadequate protein-energy intake, swallowing difficulty, altered gastrointestinal (GI) function, impaired nutrient utilization, unintended weight loss, suboptimal growth rate, and self-feeding difficulty.14 Nutrition support is a significant and extremely important component of nutrition interventions within the nutrition care process, and the nutrition practitioner will use its principles repeatedly in all areas of practice. Though interventions will be modified depending on the disease course

BOX 5.1

and the patient’s individual needs, each intervention begins with the foundational principles presented here. Ethical considerations impact decisions related to SNS, as discussed further in Box 5.2. Patients and their families should be involved in making these decisions. Furthermore, options for nutrition support therapy should be consistent with the level of medical care that the patient is receiving.15

5.2  ENTERAL NUTRITION Enteral nutrition (EN; from the Greek enteron, meaning “intestine”) refers to delivery of nutrients distal to (or beyond) the oral cavity of the GI tract via a tube, catheter, or stoma. The terms “enteral feeding” and “tube feeding” are used interchangeably in the clinical setting. Medical and nutritional research has increased understanding of the need for GI tract stimulation and the overall health benefits of continuing to provide nutrition via the GI tract, especially in the critically ill. The 2016 ASPEN/SCCM Critical Care guidelines recommend that: “…nutrition support therapy in the form of early EN be initiated within 24–48 hours in the critically ill patient who is unable to maintain volitional intake” (p. 165) and is at nutritional risk.12

Indications EN is indicated for adult patients who have a functioning GI tract and who present with inadequate oral intake for 7–14 days, or in whom inadequate oral intake is expected to continue over a 7- to 14-day period.16 The recommended criteria for use of EN in pediatrics include the following: unable to obtain >80% of caloric needs by mouth or requiring an extended time period to eat (>4 hours/day) and/or malnutrition or poor growth demonstrated by a decrease of two or more weight or height growth channels or persistent triceps skinfold (TSF) 80% of goal calories should be made in order to achieve the clinical benefit of EN over the first week of hospitalization” (p. 169).12 Overfeeding may lead to a condition called refeeding syndrome. This is discussed in more detail below. Overfeeding, on the other hand, may result in Chapter 5  Enteral and Parenteral Nutrition Support   107

Table 5.4 Electrolyte Requirements Dietary Reference Intake for Oral/ Enteral Feedings

Recommendations for Parenteral Intake

Potassium . 14 years

4700 mg

1–2 mEq/kg

14–50 years

1500 mg

1–2 mEq/kg

51–70 years

1300 mg

. 70 years

1200 mg

Sodium

Chloride 14–50 years

2300 mg

51–70 years

2000 mg

To maintain acid–base balance

. 70 years

1800 mg

Acetate

—

To maintain acid–base balance

14–18 years

1300 mg

10–15 mEq

19–50 years

1000 mg

. 51 years

1200 mg

Calcium

Magnesium Males

14–18 years

410 mg



19–30 years

400 mg



. 31 years

420 mg

Females 14–18 years

360 mg



19–30 years

310 mg



. 31 years

320 mg

8–20 mEq

8–20 mEq

Phosphorus 14–18 years

1250 mg

. 18 years

700 mg

20–40 mmol

Note: These are standard intake ranges for generally healthy people with essentially normal organ function who do not have abnormal needs or losses.

hyperglycemia, hypertriglyceridemia, and hepatic steatosis (fatty liver), but in reality this is most often associated with poorly monitored, home PN. While many clinicians prefer to feed hospitalized patients 25–30 kcal per kg, there are others who prefer to consider lower amounts (18–20 kcal/kg) for overweight patients. Current ASPEN guidelines state: “For all classes of obesity where BMI is >30, the goal of the EN regimen should not exceed 60%–70% of target energy requirements or 11–14 kcal/kg actual body weight per day for patients with BMI 30–50 (or 22–25 kcal/kg ideal body weight per day for patients with BMI>50” (p. 198).12

Hyperglycemia  During periods of physiological stress, such as that caused by severe illness or severe infection ­(sepsis), hyperglycemia can appear even in patients with no previous history of diabetes. The hyperglycemia associated with stress usually resolves as the stress response subsides, and nondiabetic patients do not experience long-term complications. Guidelines for the treatment of hyperglycemia during nutrition support vary between critically ill and noncritically 108  Part 2  The Nutrition Care Process

ill patients. Typically, insulin is initiated when blood glucose is greater than 180mg/dL, and it is recommended to have an established protocol for insulin management as well as prevention of hypoglycemia.43,44

Refeeding Syndrome  Refeeding syndrome is a term used to describe several common metabolic alterations that may occur during nutritional repletion of patients who are malnourished or in a state of starvation.45,46 This syndrome has been observed in the surviving victims of famine since the beginning of medical history. With the advent of PN, refeeding syndrome gained attention because of its often dramatic and sometimes fatal presentation. With starvation lasting more than a few days, liver gluconeogenesis slows, free fatty acids are used to produce energy in the form of ketones, and basal metabolic rate declines. The reintroduction of carbohydrate, whether in oral, enteral, or parenteral form, results in a shift from ketones to glucose as the primary energy source. Glucose metabolism requires large quantities of phosphorus. Magnesium, potassium, and thiamin requirements may also increase to meet anabolic needs. The result is a drop in serum levels of phosphorus, which, if severe, may result in hemolysis, impaired cardiac function, impaired respiratory function, and even death. Hypomagnesemia (low serum magnesium) may result in tremor, muscle twitching, cardiac arrhythmias, and even paralysis (see Chapter 7). Hypokalemia (low serum potassium) is also associated with cardiac abnormalities. Thiamin deficiency has been documented infrequently, but may result in Wernicke’s encephalopathy (see Chapter 16). Patients at risk for refeeding syndrome include those who present with malnutrition, those who have a history of long-term inadequate oral intake, and those who have had minimal intake for several days as a result of NPO status or poor appetite. It is critical to monitor serum levels of phosphorus, magnesium, and potassium and to provide supplementation as needed. Clinicians begin feedings slowly and avoid overfeeding as strategies to prevent refeeding syndrome. See Chapter 7 for additional information.

5.3  PARENTERAL NUTRITION The word parenteral means “alongside” or “outside” the GI tract and is now used to describe the administration of drugs or nutrients by vein (intravenously [IV]). ­Parenteral ­nutrition (PN) developed in the 1960s to sustain the lives of individuals with severe GI impairment and includes IV ­nutrients delivered through a peripheral vein (PPN) or a central vein (CPN). PN was previously referred to as central venous nutrition (CVN) or intravenous hyperalimentation (IVH), but PN is now used to encompass all IV delivery of nutrients. The term “hyperalimentation” originally described the practice of “hyperalimenting” or overfeeding patients. Although deliberately overfeeding or “hyperalimenting” patients is no longer common clinical practice, the term persists in many institutions. The distinguishing feature of PN is administration of concentrated macronutrients, vitamins, minerals, and electrolytes into a large central vein so that the volume of blood flow is sufficient to immediately dilute the concentrated parenteral solutions. The term peripheral parenteral nutrition (PPN) refers to the administration of large-volume, dilute solutions of

nutrients into a small vein in the arm or back of the hand. PPN is prescribed for short-term use and is most commonly used as a therapy to provide nutrients while awaiting placement of a central venous catheter (CVC) for CPN. The high osmolality of PPN may cause small veins to collapse, and peripheral access is difficult to maintain for more than a few

BOX 5.6

days. Therefore, the osmolarity of the PPN solution should be confirmed to be 10 days. A ­ ccording to ASPEN guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient,1 “in the patient at high nutritional risk exclusive parenteral nutrition (PN) should be initiated as soon as possible following ICU admission if early enteral n ­ utrition is not feasible.” In addition to identifying the need to initiate PN, ASPEN guidelines suggest withholding soybean-oil-based lipid e­ mulsions the first week of ICU admission. This patient meets the criteria for PN since he will be NPO and without EN for >10 days. Ht. 5’9”, Wt. 155#, UBW 165# (6 months ago).

Nutrition Diagnosis Predicted inadequate energy intake related to small bowel resection and diagnosis of Crohn’s disease as evidenced by prolonged post-op NPO status.

Determine the Parenteral Nutrition Prescription STEP 1: DETERMINE A “DOSING” WEIGHT A. Critical Thinking: The hospital bed has a built-in scale, so you can easily weigh the patient. Physical exam reveals no fluid retention. His current BMI of 22.9 is within the healthy weight range so his actual body weight is recommended for dosing weight in calculating energy requirements.

B. Calculations for the Nutrient Prescription: Convert the weight to kilograms by dividing weight in pounds by 2.2. 155 lbs ÷ 2.2 = 70.4 kg ABW

STEP 4: DETERMINE FLUID REQUIREMENTS (THIS PROVIDES A WORKING VOLUME FOR THE PARENTERAL SOLUTION) A. Calculations for the Nutrient ­Prescription: 1 mL/kcal = 2100 mL

STEP 2: DETERMINE A KCAL GOAL A. Critical Thinking: You could use several different methods to determine energy requirements. Research tells us that indirect calorimetry is the most accurate in acute care but this patient unit does not have access to the needed equipment. Many acute care settings and intensive care units use the American College of Chest Physicians recommendations for 25–35 kcal × weight (kg). The patient is within the range of ideal body weight but due to his post-op status and presence of infection, 25–30 kcal/kg is appropriate. B. Calculations for the Nutrient Prescription: Multiply the weight by the number of kcal/g selected. 70 kg × 25 kcal/kg = 1750 kcal 70 kg × 30 kcal/kg = 2100 kcal Range: 1750–2100 kcal C. More Critical Thinking: If indirect calorimetry is not available, use your estimated requirements of EER = 1750–2100 kcal

STEP 3: CALCULATE A PROTEIN GOAL A. Critical Thinking: There is minimal drainage from the surgical wound (100 mL over the last two shifts), which would not result in significant protein loss. To support postoperative wound healing, 1.5–1.8 g/kg of protein is appropriate. B. Calculations for the Nutrient ­Prescription: Multiply the protein requirement by the patient’s weight. 70 × 1.5–1.8 = 105–126 g protein/day

STEP 5: DETERMINE DEXTROSE AMOUNTS A. Critical Thinking: Guidelines recommend calculating the range of dextrose that the liver can metabolize, which is 3–5 mg/kg/min. 70 kg × 3 mg/kg/min × 1440 min/day ÷ 1000 mg/g = 302 g dextrose/day B. More Critical Thinking: When writing the first bag of PN, remember to start with 900 mOsm/L to allow delivery of 100% of the estimated nutrition requirements. The location of the catheter tip determines if a PPN or CPN solution can be infused. Therefore, prior to starting PN confirmation that the catheter tip is located in the vena cava adjacent to the right atrium is critical.47 VADs are available in single-, double-, or triple-lumen models. The lumen of the catheter refers to the interior of the tube through

Figure 5.11 Sites for Parenteral Access

IV solution Right subclavian vein Catheter Hub of catheter Filter

Internal jugular vein External jugular vein Left subclavian vein

Right superior vena cava

IV tubing

Left cephalic vein Left basilic vein

Catheter

Central venous catheter

Peripherally inserted central catheter

Source: S. Rolfes, K. Pinna and E. Whitney, Understanding Normal and Clinical Nutrition. 7th ed. Copyright © 2006, p. 677.

which the PN solution passes. The number of lumens should correspond to the number of therapies the patient is requiring. For example, medications, fluids, and nutrients can all be infused through these lumens. Figures 5.11 and 5.12 may be of assistance in visualizing the types and locations of VADs used for PN.

Figure 5.12 Types of Venous Access Devices Examples of venous access devices that are used for delivery of intravenous nutrients. From left to right: PICC line; tunneled catheter; implanted port that has been accessed; central venous catheter.

Short-Term VADs  The most common VAD is a ­central

venous catheter (CVC) or central line inserted ­percutaneously (through the skin) at the bedside while the patient is under local anesthesia. Central catheters are inserted into large veins such as the subclavian, jugular, or femoral veins. Ultimately, these catheters reside in the superior vena cava, or in the inferior vena cava, in the case of femoral placement. The use of a CVC placed in the femoral vein should be avoided for administration of PN solutions unless no other vein can be accessed due to the higher rate of infectious complications.47 CVCs are usually changed every few days to help decrease the risk of infection inherent with an opening from the skin into a large, central vein. These catheters are reserved for hospitalized patients and are not considered safe for long-term use. The peripherally inserted central catheter (PICC) is also frequently used. Unlike the CVC, which requires a ­b edside surgical procedure by a physician for insertion, the PICC can be inserted by specially trained nurses; this increases the availability of the procedure and decreases costs. PICC lines are inserted into the arm and threaded into the subclavian vein to the vena cava where the tip resides adjacent to the right atrium.47 These catheters can be used for both hospitalized and home PN patients.

Source: Courtesy of Kristen Roberts, PhD, RDN, LD.

Long-Term VAD  For long-term use, or for home PN, a cath-

eter is tunneled under the skin during a surgical procedure. Tunneled catheters (such as Hickman®, Broviac®, and Groshong®) most often enter the vein on the upper chest wall and Chapter 5  Enteral and Parenteral Nutrition Support   111

exit the body near the xyphoid process, axilla, or ­abdominal wall. They are considered permanent, and with proper care can be left in place for several years. If a tunneled catheter contains more than one lumen, it can accommodate infusions of medications, fluids, or blood products in a­ ddition to PN. Thus, it is useful for patients who receive IV medications in addition to PN. The number of lumens on the VAD is correlated with risk of developing a catheter line-associated bloodstream infection (CLABSI), and therefore it is critical to minimize the number of lumens on the VAD. Therefore, the pharmacist determines the compatibilty of medications with the PN prescription to inform the number of lumens required on the VAD. Implantable ports are similar to tunneled catheters in that they must be placed in the operating room by a surgeon. They are available with single or double ports and are suitable for long-term access. Unlike tunneled catheters, they lie completely under the skin and are more acceptable to patients with body image concerns. Because they are usually placed just below the clavicle on the chest wall, they may be difficult for the patient to access. Nursing intervention may be required to change needles used to gain access to these ports.

Solutions Unlike enteral formulas, which are most often purchased in a form appropriate for patient administration, parenteral formulas are mixed or “compounded” in the hospital pharmacy. The method the pharmacy uses to compound PN preparations is critical to development of PN prescriptions. In some institutions, a standardized approach includes not only standard ordering and monitoring but also standardized solutions. Advantages of this approach include improvements in efficiency and cost-effectiveness.48 The use of automated compounding equipment (see Figure 5.13) and bulk packaging of concentrated macronutrients allows for individualized

Figure 5.13 A Pharmacy Compounder Parenteral nutrition is compounded within the pharmacy under aseptic ­conditions. An automated compounder like the one shown here minimizes risks and errors in parenteral nutrition.

formulas that are adjusted daily to meet the rapidly changing needs of critically ill patients. An automated compounder is used to combine all nutrients needed for a 24-hour infusion into a single container. When an automated compounder is available, the PN prescription may include ingredients in as small as 1-mL increments. If an automated compounder is not available, formula changes and manufacture are more time consuming for the pharmacist. Automated compounders can be used to manufacture nutrient solutions that combine dextrose and amino acids (two-in-one formulas) or dextrose, amino acids, and lipids (three-in-one formulas). PN can be provided in either a two-in-one or three-in-one system, and each system has both advantages and disadvantages. Typically in the twoin-one, lipids are added separately based on the available container sizes (100 mL, 250 mL, or 500 mL). This system provides a greater degree of flexibility in the amounts of dextrose and amino acids that can be given since compatibility requirements with lipid emulsions are eliminated. Another advantage of the two-in-one system is that formulas containing only dextrose and amino acids are clear, and any precipitate can be observed. A disadvantage of the twoin-one system is the need for an additional administration set (IV tubing and other devices required for the delivery of PN) for the lipids. The three-in-one system requires a single ­administration set, which saves nursing time and reduces costs. On the other hand, the addition of lipids with the three-in-one ­system results in an opaque solution, which obscures precipitate and increases the risk of particulate being infused into the patient. Addition of lipid into the three-in-one solution ­limits the electrolytes and final concentration of amino acids in s­ olution, which minimizes the flexibility of dextrose and amino acids in the final solution. PN solutions are compounded from as many as 40 ­different items under the supervision of a licensed ­pharmacist. In order to maintain sterility, compounding is completed in a “clean room” under a laminar flow hood. Because PN is ­compounded from amino acid, dextrose, and lipid solutions, solubility is an important consideration ­affecting the ­maximum amount of both nutrients and fluid that can be incorporated. Precipitates may form in PN solutions if greater than recommended maximum amounts of electrolytes and minerals are added, especially when PN is subjected to changes in temperature or pH. Likewise, minimum ­volumes are impacted by the concentration of amino acids, dextrose, and lipid that are available for compounding.

PN Substrates Protein  Protein is included in PN in the form of individual

Source: Courtesy of Marcia Nelms.

112  Part 2  The Nutrition Care Process

amino acids in amounts consistent with the recommendations of the Food and Agriculture Organization and the World Health Organization. Modified products have been developed and marketed for renal failure, hepatic failure, and stress. Commercial amino acids are available from various manufacturers in concentrations of 3.5% (35 g/L) to 20% (200 g/L). Lower concentrations (3.5%–5.5%) are used for peripheral administration, while higher concentrations (8.5%, 10%, 11%, 15%, and 20%) are used for CPN administration. Details for

Table 5.5 Amino Acid Solutions Used in Parenteral Nutrition Brand Name/Manufacturer

Type/Indication

Stock Concentrations

Aminosyn II™/Hospira

Standard

3.5%, 5.2%, 7%, 8.5%, 10%

Travasol™/Baxter

Standard

10%

FreAmine® III/B. Braun

Standard

10%

™

Aminosyn II /Hospira

Standard/fluid restriction

15%

Clinisol™/Baxter

Standard/fluid restriction

15%

Plenamine/B. Braun

Standard/Fluid restrictions

15%

Prosol™/Baxter

Standard/fluid restrictions

20%

ProcalAmine /B. Braun

Metabolic stress

3%

HepatAmine™/B. Braun

Hepatic failure

8%

®

™

Aminosyn HBC /Hospira

Metabolic stress

7%

FreAmine HBC™/B. Braun

Metabolic stress

6.9%

Trophamine®. B. Braun

Pediatric

6%, 10%

Premasol™, Baxter

Pediatric

6%, 10%

Renal

5.4%

™

NephrAmine (essential amino acids plus histidine)/B. Braun

Source: www.bbraunusa.com, hospira.com, www.baxtermedicationdeliveryproducts.com

these products are available on Web sites of the major manufacturers and summarized in Table 5.5. PN is typically designed to provide individualized protein r­ equirements, which range from 0.8 g/kg for adults to 1.5–2.0 g/kg for patients with burns, trauma, or healing wounds.12 Factors that increase protein requirements above the DRI include diagnoses such as trauma, burns, sepsis, wounds, and bone marrow transplant. The lower range of protein (0.8 g/kg) may be needed for patients with acute kidney injury who are not receiving dialysis. It is important to ­remember, ­however, that without adequate energy from carbohydrate and lipid, the subsequent catabolism of lean body mass defeats the effort to control uremia in this manner.49

Carbohydrate  The primary function of parenteral

c­ arbohydrate is to serve as an energy source. In the United States, dextrose monohydrate is used as the c­ arbohydrate source for PN. This particular form of carbohydrate ­p rovides  3.4 kcal/g. The minimum carbohydrate intake ­s pecified by the DRI is 130 g/day, and it is known that ­approximately 100 g of carbohydrate is required daily to allow for protein sparing. The amount of 1 mg/kg/min is often used as the reference for the minimal amount of carbohydrate needed to spare protein. The maximum for glucose ­oxidation was originally studied in burn patients and found to be 7 g/ kg/day (5 mg/kg/minute). In practice, lower figures of 3–4 mg/kg/min have been recommended.12 Dextrose is commercially available in 5%, 10%, 50%, and 70% concentrations, but other concentrations may also be available. Excessive carbohydrate may contribute to hyperglycemia, hepatic steatosis, and excessive carbon dioxide production. The elevated carbon dioxide that occurs with overfeeding may jeopardize respiratory status and result in difficulty weaning from mechanical ventilation (see Chapter 21).

Lipid  The intravenous lipid emulsion (ILE) in most ­ arenteral solutions available in the United States since 1972 p is an emulsion of soybean oil. Other sources of lipid that contain fewer total omega-6 fatty acids and more omega-3

fatty acids have been developed but were unavailable in the United States until 2013, when the FDA granted approval for ­Clinolipid™. This ILE is a mixture of olive and soybean oils and is p ­ referred by some due to the classification of being inflammation neutral.50 Most recently, FDA approved SMOFlipid® for use in the United States, which is the first ILE approved that is characterized as anti-­inflammatory.50 (See Figure  5.14.) SMOFlipid ® incorporates soybean oil (30%), medium chain TGs (30%), olive oil (25%), and fish oil (15%). See ­Figure 5.14. Higher omega-3 solutions have been ­e valuated for their anti-inflammatory effects, whereas the omega-6 fatty acid profile is considered to be pro-inflammatory.50 The ILE provides essential fatty acids and vitamin K, as well as a concentrated source of energy—an avenue to meet energy needs if the patient is unable to tolerate a higher carbohydrate load. Available formulations contain 10% (1.1 kcal/mL), 20% (2 kcal/mL), or 30% (3 kcal/mL) lipids. Caloric values per gram depend on the energy provided by glycerol, so 10% ­solutions provide 11 kcal/g and the others provide 10 kcal/g. See Table 5.6 for nutrient profiles of representative ILEs. An estimated 2%–4% of energy from linoleic acid is recommended to prevent essential fatty acid deficiency (EFAD). Complications of ILEs, including hyperlipidemia and impaired immune response, support a more conservative ­prescription of lipids. The medication propofol, which is often administered to the critically ill, is lipid based and thus must be considered as a source of energy.12,49

Electrolytes  Using the standards established by the DRI as

the beginning benchmark, electrolyte requirements in PN are based on body weight, existing electrolyte deficiencies, ongoing electrolyte losses, and changes in organ function. Because electrolyte requirements are also inextricably linked with the amount of macronutrients provided in the PN, it is impossible to manage PN without a thorough understanding of these complex relationships (see Chapter 8). Recommendations for standard electrolyte intake are found in Table 5.4. Note, however, that in practice electrolytes are individualized according Chapter 5  Enteral and Parenteral Nutrition Support   113

Figure 5.14 SMOF Lipid

JIRATIKARN PENGJAIYA/Shutterstock.com / Iurii Kachkovskyi/Shutterstock.com / Alexander Raths/Shutterstock.com / Valentyn Volkov/Shutterstock.com

SMOF lipid emulsion recently received FDA approval for use in the United States as a lipid source with soybean oil, medium chain triglycerides, olive oil, and fish oil.

S oybean Oil (ω-6)

M CT

30%

30%

15% F ish Oil (ω-3)

25%

Medications  PN may be used to deliver

O live Oil (ω-9) Source: http://smoflipid.com

to patient needs and are often considered to be the most difficult component for new RDNs working with ­nutrition support.

Vitamins and Minerals  In 1979, the American Medical Association released recommendations for vitamin and mineral additives to PN. 51 These vitamin recommendations were used until 2003, when they were revised to include vitamin K.52 Rather than add individual amounts of vitamins to PN, most pharmacies purchase commercial multiple-vitamin infusion products that meet the recommendations. Because the vitamins are administered intravenously, there is no issue with absorption, and the amounts administered may differ from what is recommended for oral intake. ASPEN recently evaluated the currently available vitamin and mineral parenteral solutions and recommended that the levels of vitamin D, carnitine, choline, and trace elements be examined and revised. Until formulations are updated, ASPEN suggests individual supplementation may be necessary for some patients. 53 Due to the rapid development of nutrient deficiencies, all PN solutions should contain a multivitamin product. Table 5.7 lists daily adult parenteral vitamin requirements. 114  Part 2  The Nutrition Care Process

Trace Minerals Originally, zinc, copper, chromium, and manganese were added to PN. Based on reports of deficiencies, newer combination products have been introduced that contain the original trace minerals plus selenium. Trace element combination products are purchased commercially and contain four or five trace elements, while iodide, molybdenum, and iron can be purchased as individual injections as needed. In situations where reduced excretion or potential toxicities exist, trace elements are removed from the PN, and individual trace minerals are added according to need. As mentioned above, levels of PN trace minerals may need to be adjusted to better reflect current understanding of requirements for hospitalized patients.53 Trace element additions for adult PN are listed in Table 5.8.

medications. It is possible that albumin, aminophylline, metoclopramide, corticosteroids (i.e., methylprednisolone and hydrocortisone), histamine H2 receptor antagonists (i.e., cimetidine and famotidine, ranitidine), heparin, or regular insulin may be included in PN. Prior to recommending medications be added to PN, the clinician should gain a thorough understanding of the practice at his or her institution through observation and consultation with a pharmacist.

Table 5.6 Nutrient Content of Lipid Emulsions Used in Parenteral Nutrition Intralipid

Liposyn2

Omegaven

ClinoLipid/ ClinOleic SMOFlipid

Soybean oil, %

100

50

0

20

30

Safflower oil, %

0

50

0

0

0

Medium-chain triglycerides, %

0

0

0

0

30

Olive oil, %

0

0

0

80

25

Fish Oil, %

0

0

100

0

15

Glycerol, g/100 mL

2.25

2.5

2.5

2.25

2.5

Egg phospholipid, g/100 mL

1.2

1.2

1.2

1.2

1.2

Phytosterols, mg/100 mL

439 ± 5.7

38.3

3.66

274 ± 2.6

207

Vitamin E, mg/100 mL

3.8

0

15–30

3.2

16–23

LA, %

50

66

4.4

18.5

21.4

ALA, %

9

4.2

1.8

2

2.5

EPA, %

0

0

19.2

0

3

DHA, %

0

0

12.1

0

2

ARA, %

0

0

1–4

0

0.15–0.6

0

Present3

Component1

Vitamin K, mcg/dL

31–67

31–93

3

Present

1

Anez-Bustillos L, Dao DT, Baker MA, et al. Nutr Clin Prac. 2016; 31: 596–609.

2

Meisel JA, Le HD, Meijer VE, et al. J Ped Surg. 2011; 46: 666–73.

3

Noted on manufacturer website.

Table 5.7 Adult Daily Requirements for Parenteral Vitamins Vitamin

Requirement

Thiamin

6 mg

Riboflavin

3.6 mg

Niacinamide

40 mg

Folic acid

600 mcg

Pantothenic acid (dexpanthenol)

15 mg

Pyridoxine

6 mg

Cyanocobalamin

5 mcg

Biotin

60 mcg

Ascorbic acid

200 mg

Retinol

1 mg (3300 USP units)

Ergocalciferol

5 mcg (200 USP units)

dl-alpha

10 mg (10 USP units)

tocopheryl acetate

Phylloquinone

150 mcg

Source: Adapted from Journal of Parenteral and Enteral N ­ utrition by ­Mirtallo, Canada, Johnson, Kumpf, Petersen, Sacks, Seres, Guenter. ­Copyright 2004 by SAGE Publications Inc. Journals.

Table 5.8 Daily Trace Element Additions to Adult PN Formulations* Trace Element

Standard Intake

Chromium

10–15 mcg

Copper

0.3–0.5 mg

Iron

Not routinely added

Manganese

60–100 mcg†

Selenium

20–60 mcg

Zinc

2.5–5 mg‡

*Standard intake ranges based on generally healthy people with normal losses. †

The contamination level in various components of the PN formulation can significantly contribute to total intake. Serum concentrations should be monitored with long-term use.

‡

Add 12 mg/L of small bowel losses and 17 mcg/kg of stool or ileostomy losses.

Source: Adapted from Journal of Parenteral and Enteral N ­ utrition by ­Mirtallo, Canada, Johnson, Kumpf, Petersen, Sacks, Seres, Guenter. ­Copyright 2004 by SAGE Publications Inc. Journals.

Nutrition Assessment and Intervention: ­Determination of the PN Prescription The PN prescription will be based on the RDN’s nutrition assessment and the physician’s and pharmacist’s recommendations and is often communicated using a form (written or electronic) like that shown in Figure 5.15. Box 5.6 details the process of developing the PN prescription. The basic steps include the following: 1. Establish dosing weight and energy requirements. 2. Calculate a protein goal and start first PN solution with goal protein. 3. Distribute remaining kcal between carbohydrate and lipid. 4. Ensure first PN solution has 200 mg/dL should be corrected to 900 mOsm/L must be delivered via a central line with the tip of the catheter in the vena cava adjacent to the right atrium.

STEP 3: TOTAL THE MOSM/L. EXAMPLE: A 3-in-1 solution with 40 g/L amino acid, 150 g/L dextrose, 40 g/L lipid and Calcium 5 mEq/L, Magnesium 8 mEq/L, ­Potassium 35 mEq/L, Sodium 70 mEq/L

BOX 5.8

CLINICAL APPLICATIONS

Cycling PN 1-Hour Taper Down Main rate = total volume / (cycle hours − ½ hour) Taper rate = main rate / 2

2-Hour Taper Down Main rate = total volume / [(cycle hours − 2 hours) + 0.75] 1st hour taper rate = main rate / 2 2nd hour taper rate = 1st hour taper rate / 2

1-Hour Taper Up and 1-Hour Taper Down Main rate = total volume / (cycle hours − 1 hour) Taper rates = main rate / 2

1-Hour Taper Up and 2-Hour Taper Down Main rate = total volume / [(cycle hours − 2 hours) + 0.25] 1st hour taper up and 1st hour taper down rates = main rate / 2 2nd hour taper down rate = 1st hour taper rate / 2

The sample protocol for monitoring PN found in ­ igure 5.14 may serve as a guide, although most institutions F have protocols in place. Complications of PN feeding may be severe, and they are best prevented through patient monitoring by nutrition support experts. Many of the complications experienced with EN occur with PN as well. Patients receiving PN may experience electrolyte imbalance, underfeeding and/or overfeeding, hyperglycemia, and refeeding syndrome, just as patients receiving EN do. These conditions were described in detail earlier in the “Monitoring and Evaluation: Complications” subsection within the “Enteral Nutrition” section.

2-Hour Taper Up and 2-Hour Taper Down Main rate = total volume / [(cycle hours − 3 hours) + 0.50] 2nd hour taper up and 1st hour taper down rates = main rate / 2 1st hour taper up and 2nd hour taper down rates = 2nd hour taper rate / 2

EXAMPLE: HL is receiving 2 L of PN daily over 24 hours. He is metabolically stable without any blood glucose abnormalities. The NST decides to cycle his PN to a 12-hour infusion.

1-Hour Taper Down Main rate = total volume (2000mL)/ (12 − ½ hour) = 173.9 mL Taper rate = main rate (174mL / 2) = 86 mL Order: Start PN solution at 10 pm at 174 mL/h × 11 hours then decrease to 86 mL/h × 1 hour. Discontinue PN at 10 am.

GI complications of PN have been reported, primarily in those patients whose GI tract is at complete rest. These complications include cholestasis. Increased permeability to bacteria has been noted when atrophic intestinal cells result from lack of enteral stimulation. For this reason, many patients who require PN may receive trophic or “trickle” amounts of enteral feedings. If PN is administered continuously for several weeks, transient elevations in liver enzymes may be noted. These usually disappear after PN is discontinued but may respond to intermittent or cyclic feedings, adjustments in the lipid-to-dextrose ratio, and kcal reduction if overfeeding has occurred. Chapter 5  Enteral and Parenteral Nutrition Support   117

Patients receiving PN can develop serious infections, and they may have a higher infection rate overall than patients receiving oral or EN. Infections may be caused by improperly prepared PN solutions, and therefore most pharmacies institute rigorous monitoring to minimize this risk. Infection may be introduced into a patient’s bloodstream during the placement of the VAD or while performing a dressing change particularly when hand hygiene is poor. Another route for infection is the GI tract, which, according to the indications for PN, should be nonfunctioning. With disuse, a nonfunctioning GI tract may become permeable to intestinal bacteria, and infection may result. Finally, it has been noted that the infection rate may increase with higher amounts of energy provided by PN.58

5.4  SPECIAL CONSIDERATIONS Transitional Feedings Patients transitioning from one form of SNS to another require careful consideration to prevent overfeeding and hyperglycemia. Confirmation of adequate bowel function is necessary prior to transitioning off of PN. Selection of the appropriate diet and/or EN formula is essential to ease the transition off of PN. Discontinuation of PN should be considered once 50% of estimated nutritional needs are delivered via the GI tract. In those with malabsorption syndromes, special consideration is needed to ensure absorption of the EN prior to discontinuing the PN solution. Physician communication is essential to transition an insulin-dependent patient to EN in order to establish a protocol for glycemic control. For patients unable to meet 50%–65% of estimate nutritional needs on EN, supplemental PN can be considered until EN can be advanced and/or tolerated.

Home PN Beginning in the 1970s, home PN became readily available for the patient requiring PN that extends beyond the hospital stay. Providing this service in the home became possible with the use of home care infusion pharmacies and nursing services. A review of the Sustain™ registry indicates that the most common diagnoses for home PN include SBS, GI obstruction/fistula/motility disorder, non-SBS diarrhea/malabsorption, and intractable vomiting.59 Determining safety for home PN is assessed by a team of nutrition professionals including the RDN, registered nurse (RN), pharmacist, social worker, case manager, and nutrition support physician. Each of these professionals has a unique role that adds to the care of the home PN patient, which includes verification of insurance benefits, evaluation of cognitive, psychosocial, and safety concerns and determining proficiency with home PN procedures and protocols.60 Specifically, verification of insurance benefits requires documentation in the medical record clarifying intestinal failure (non-functioning GI tract) typically using Medicare criteria. Medicare criteria indicate the following situations to meet the requirements for home PN: • Massive small bowel resection with 18–55 y: 35 mL/kg

AI women, 19–70 years: 2.7 L

>55 y: >30 mL/ kg or minimum of 1.5 L/d (unless contraindicated)

Supplementation may assist wound healing that has been affected by vitamin A deficiency, radiation, chemotherapy, or ­diabetes mellitus.

RDA men: 900 RAE/~3000 IU

20,000–25,000 IU orally for 10 days if deficiency suspected or confirmed (low serum retinol and/or functional tests such as dark adaptation)

Supplementation rarely warranted in chronic kidney disease. Patients with fat malabsorption should receive water-soluble form.

Deficiency can delay wound healing.

RDA women: 75 mg

Up to 1–2 g/day for deficiency; during acute illness and injury for up to 3 months

Evaluation of serum ascorbic acid levels reflects dietary intake and not tissue levels. White blood cell ascorbic acid and ascorbic acid tissue saturation tests are better indices.

15–25 mg elemental zinc/day

Zinc intakes below RDA are commonly seen in older adults. Increased losses can occur from large skin wounds or urine (after trauma, closed head injury, etc.). Impaired absorption from GI tract can occur with high-volume diarrhea or fistula output.

Not applicable

Low hemoglobin concentration does not seem to impair wound healing, provided adequate tissue perfusion is maintained.

RDA women: 700 RAE/~2300 IU UL: 3000 RAE or 10,000 IU

RDA men: 90 mg Additional 35 mg/d for smokers UL: 2000 mg due to GI side effects (nausea, abdominal cramps, or diarrhea)

Zinc

Iron

Low serum zinc levels associated with impaired healing. Supplementation may enhance wound healing, but only in those who are zinc deficient.

RDA women: 8 mg

Routine supplementation not recommended for wound healing.

RDA women, 19–50 years (premenopausal): 18 mg

RDA men: 11 mg (Requirements may be up to 50% higher for vegans.) UL: 40mg

RDA women, 51+ years (postmenopausal): 8 mg RDA men: 8 mg

Provide additional fluid to maintain adequate hydration and compensate for additional losses from fever, draining wounds, etc. Additional fluid needed if fever is present.

UL: 45 mg (continued)

190  Part 3  Introduction to Pathophysiology

Nutrient/Factor

Function in Wound Healing

Dietary Reference Intake: RDA, AI, UL

Recommended Intake for Wound Healing

Additional Notes

Vitamin D

Role in innate immune response

Vitamin E

No clear role for vitamin E ­supplementation. Use may adversely affect healing of some types of wounds.

RDA: 15 mg alpha-tocopherol equivalents

Ensure 100% of DRI for all nutrients.

Large doses of vitamin E should be avoided before surgery unless deficiency is present. Topical vitamin E is often recommended to reduce scar formation and improve cosmetic appearance of scar tissue, but this benefit has not been documented by research.

Other vitamins, minerals, and trace elements

Thiamin, riboflavin, and pantothenic acid play a role in collagen production. Copper and manganese are required for tissue regeneration. Vitamin K is required for prothrombin and synthesis of other clotting factors.

Varies

Ensure 100% of DRI for all nutrients.

General multivitamin supplementation recommended if deficiency confirmed

Arginine

Supplementation may benefit wound healing by increasing collagen deposition, improving nitrogen balance, and enhancing several parameters of immune function. Most, but not all, research demonstrated enhanced nitrogen retention and immune function.

Not applicable

Oral dose of 17.0–24.8 g/day free arginine was used in previous human studies. The recommended dosage, and populations who may benefit most, are unknown at this time but it is suggested to supplement for a 30-day period and then reassess for effectiveness.

Supplementation may be contraindicated in patients with severe renal or hepatic failure.

Glutamine

Preferred fuel for enterocytes, lymphocytes, and macrophages. Precursor for nucleotides and glutathione.

Not applicable

Oral doses of 5–14 g/ day have been used in human studies with positive results for wound healing.

Supplementation may be contraindicated in patients with severe renal or hepatic failure. Effectiveness dependent on adequate energy and protein intake.

b-hydroxy b-methylbutyrate (HMB)

Metabolite of amino acid leucine.

Not applicable

3 g/day has been used in combination with other amino acids.

Limited research for wound healing—primary research documented in sarcopenia.

Sources: Gould L, Stuntz M, Giovannelli M, et al. Wound Health Society 2015 update on guidelines for pressure ulcers. Wound Repair Regen. 2016; 24: 145–162. Langer G, Fink A. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database of Syst Rev. 2014; 6: 1–85. CD003216. DOI: 10.1002/14651858.CD003216.pub2. Chow O, Barbul A. Immunonutrition: role in wound healing and tissue regeneration. Adv. Wound Care. 2014; 3: 46–53. Calder PC. Omega-3 fatty acids and inflammatory processes. Nutrients. 2010; 2: 355–374. Ekinci O, Yaik S, Terzioglu BB, et al. Effect of calcium b-hydroxy b-methylbutyrate, vitamin D and protein supplementation on postoperative immobilization in malnourished older adult patients with hip fracture: a randomized controlled study. Nutr Clin Pract. 2016; 31: 829–835.

unconnected tissues are abnormally joined together. This most often occurs after a surgical procedure, particularly after abdominal surgery.

Adaptive Immune Response  In the adaptive immune response (see Box 9.7), each B and T cell is programmed to attack one specific antigen, but these cells can interact with other antigens that are closely related or very similar. In rheumatic fever, for example, an immune response stimulated by antigens on a Group A Streptococcus can attack similar

antigens on the valves of the heart. The adaptive immune system takes time to respond initially, but it improves with additional exposures and responds more rapidly on subsequent encounters with the organism. Thus, it normally protects the human from reinfection. The response to a pathogen normally involves an initial contact with the innate immune system, which often is capable of eliminating the organism by itself. The innate immune response then stimulates the adaptive immune system to seek out and target any remaining pathogens.

Chapter 9  Cellular and Physiological Response to Injury: The Role of the Immune System   191

BOX 9.5

LIFE CYCLE PERSPECTIVES

Changes in Wound Healing Associated with Aging Colette LaSalle, PhD, RD, San Jose State University While the stages of healing after an injury are the same in adults of all ages (coagulation, inflammation, proliferation, and maturation), several age-related physiologic changes are known to impact wound healing. For example, morphological changes to the skin include structural changes with decreased vasculature, density of hair follicles, tissue mass, water content, and gland function, leading to dryness, impaired skin integrity, and reduced ability of skin cells to migrate toward wound closure. Furthermore, delays in macrophage and T-cell function, angiogenesis, and epithelialization has been noted as one ages. Progression through the highly coordinated process of healing can also be affected by chronic diseases such as diabetes and heart disease. These inflammatory conditions impair wound healing because they perpetuate the process of inflammation, increasing the risk that acute injuries will develop into what are known as “chronic wounds.” These wounds do not advance through the stages of healing as expected but instead remain in a state of inflammation. There are approximately 3–6 million people with nonhealing wounds in the United States; the majority (85%) of these wounds afflict people over the age of 65. Several other factors impact wound healing and immune function. Anemia, which is common in older adults, can ­impair wound healing when suboptimal levels of oxygen reach

BOX 9.6

­ amaged tissues, slowing the healing process. Other factors that d can impair wound healing are hormonal status (estrogen is associated with reduced inflammation), reduced blood flow related to chronic diseases, infections, medications (e.g., glucocorticoids), stress, and lifestyle factors such as obesity, smoking, and nutritional status. Achieving adequate intakes of energy, protein, and micronutrients is necessary to optimize wound healing, but intakes are often suboptimal or deficient in older adults. References 1. Cheung C. Older adults, falls and skin integrity. Adv Skin Wound Care. 2017; 30: 40–6. 2. Gould LJ, Fulton AT. Wound healing in older adults. RI Med J. 2016; 99: 34–6. 3. Gould L, Abadir P, Brem H, et al. Chronic wound repair and ­healing in older adults: current status and future research. Wound Repair ­Regen. 2015; 23: 1–13. 4. Marti GP, Liu L, Zhang X, et al. Wound healing in the elderly. In: ­Rosenthal RA, Zenilman ME, Katlic MR, eds. Principles and Practice of Geriatric Surgery. 2nd ed. New York: Springer; 2011: 107–27. 5. Posthauer, M. Nutrition: a critical component of wound healing. Adv Skin Wound Care. 2010; 23(12): 560–72. 6. Sgonc R, Gruber J. Age-related aspects of cutaneous wound healing: a mini-review. Gerontology. 2013; 59(2): 159–64. 7. Sherman AR, Barkley M. Nutrition and wound healing. J Wound Care. 2011; 20(8): 357–67. 8. Wild T. Basics in nutrition and wound healing. Nutrition. 2010; 26(9): 862–66.

CLINICAL APPLICATIONS

National Pressure Injury Advisory Panel Staging of Pressure Injury Stage 1 Pressure Injury: Non-blanchable erythema of intact skin Intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury. Further description: The area may be painful, firm, soft, warmer, or cooler as compared with adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk).

Stage 2 Pressure Injury: Partialthickness skin loss with exposed dermis Partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may also present as 192  Part 3  Introduction to Pathophysiology

an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough and eschar* are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. Further description: Presents as a shiny or dry shallow ulcer without slough or bruising.** This stage should not be used to describe moisture-associated skin damage (MASD) including incontinence-­ associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive-related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions).

Stage 3 Pressure Injury: Full-thickness skin loss Full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds.

Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

Stage 4 Pressure Injury: Full-thickness skin and tissue loss Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/ or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss, this is an Unstageable Pressure Injury.

Deep Tissue Pressure Injury: ­Persistent non-blanchable deep red, maroon, or purple discoloration Intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, purple discoloration, or epidermal separation revealing a dark wound bed or

National Pressure Injury Advisory Panel Staging of Pressure Injury (continued) blood-filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone–muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury, or

BOX 9.7

may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a fullthickness pressure injury (Unstageable, Stage 3 or Stage 4). Do not use DTPI to describe vascular, traumatic, neuropathic, or ­dermatologic conditions.

CLINICAL APPLICATIONS

Types of Immunity Specific immunity can be described as either active ­immunity, in which individuals synthesize their own ­antibodies or activate immune cells, or passive ­immunity, in which they receive antibodies or activated cells produced by another individual. Both active and passive immunity can be described as either natural (occurring without human ­intervention) or artificial (resulting from human ­intervention). Thus, the four types of immunity are as follows: • Active natural immunity: Mounting an immune response to an infectious organism. • Active artificial immunity: Mounting an immune response to vaccination. • Natural passive immunity: An antibody from the mother goes to the fetus across the placenta. Both regular breast milk and colostrum contain antibodies, but the ­concentration is higher in colostrum. • Passive artificial immunity: Transferring antibodies or immune cells produced in one organism to another organism to prevent the action of a virus or toxin before it does damage. Examples of clinically used a­ ntibodies include antirabies or hepatitis globulin, antivenom for snake bites, or antitoxin for tetanus or botulism. ­Commercially available intravenous immune ­globulins (Gamimune N, Gammagard, Gammar, Iveegam, Polygam, Sandoglobulin) contain gamma globulins from a number of individuals and are used to boost the body’s natural defense system against infection in persons with a weakened immune system.

In some cases, the adaptive immune system can eliminate the pathogen; in others, it merely tags or alters it in such a way that it becomes more susceptible to the cells of the innate immune system. The two systems thus work together and are interdependent. The Primary Response  The primary immune response (see Figure 9.9) normally begins with phagoc ytosis , which can be sufficient to block infection if virulence of the pathogens is low and/or the exposure is small. This

*Eschar means dead skin. **Bruising indicates suspected deep tissue injury. Source: Reprinted from National Pressure Ulcer Advisory Panel. Pressure Ulcer Stages; 2016. http://www.npuap.org/resources/educational-and-­ clinical-resources/npuap-pressure-injury-stages/ http://www.npuap.org/pr2.htm. Accessed: August 12, 2018.

process can remove about 90% of an antigen by the time the initial exposure has circulated through the body. Once a macrophage has engulfed a pathogen, its MHC proteins select and present antigens from that pathogen to the T cells. The phagocytic cells thus become APC for the helper T cells.7,8 Helper T-cell activation requires recognition of the MHC II and antigen presented by the APC and interactions between molecules on both the T cell and the APC. In ­addition to providing the MHC-antigen signal, the macrophages secrete cytokines that contribute to activation of helper T cells, B cells, WBCs, and NK cells. The activated helper T cell begins to divide and secretes cytokines that will activate other cells of the immune system. IL-2 made by T cells is the key cytokine involved in inducing proliferation and activating other T cells, B cells, monocytes, and NK cells. Cytokines induce proliferation of B cells that can react with antigens and trigger the B cells’ response. They, in turn, differentiate into a plasma cell or antibody-forming cell. Plasma cells are larger than B cells and packed full of endoplasmic reticulum to produce antibodies at a rate of 30,000 Ig/sec.7,8 The plasma cell will produce IgM for about 3 days before switching to the production of IgG. Some cells will switch to either IgE or IgA instead of IgG under the influence of cytokines. Since it takes time to produce sufficient antibodies and activated T cells, this response does not prevent disease but terminates an ongoing infection. The longevity of the antibody, which degrades over time, depends on a number of characteristics of the antigen and host.7,8 The Secondary Response   During the primary response to an antigen, some of the T and B cells that could react with the antigen are partially activated but do not participate in the immune response. These are called memory cells and are responsible for the secondary (or memory) immune response. The secondary response is more rapid than the primary response since it does not require activation of naive helper T cells by APC. IgM is not produced, and significantly more IgG is made. Memory cells are longlived and protect from reinfection for at least 20 years and sometimes for life. Thus, humans rarely become ill from the same organism twice unless the organism has mechanisms to evade the memory response, such as by changing its antigens.7,8

Chapter 9  Cellular and Physiological Response to Injury: The Role of the Immune System   193

Figure 9.9 Primary Immune Response: Interactions among Macrophages, B Cells, and Helper T Cells Invading bacteria

Macrophages secrete interleukin 1, which enhances B cell proliferation and antibody secretion Macrophages “process and present” bacterial antigen to B and T lymphocyte clones specific to the antigen

Macrophage

Interleukin 1

Helper T cell B cell Antibodies coat bacterial antigens and enhance their binding to macrophages

Activated helper T cell B cell growth factor and IL-2

Helper T cells secrete B cell growth factor that enhances B cell proliferation and antibody secretion

Plasma cell Plasma cells secrete antibodies that bind with the antigenic bacteria

Antibodies Source: Lauralee Sherwood, Human Physiology: From Cells to Systems, 5e, copyright © 2004, p. 434.

9.7  AUTOIMMUNITY Autoimmune disease occurs when a specific adaptive immune response is mounted against “self,” and is a consequence of the B and T cells that have the ability to recognize any pathogen. Since many antigens on human cells and pathogens are similar, immune cells targeted at pathogens can cross-react with human cells. This potential for cross-reaction cannot be eliminated, or there would be a limited response to pathogens. When an autoantibody is found in association with disease, the autoimmune response usually produces cellular damage, but in rare cases, such as the anticardiac antibody 194  Part 3  Introduction to Pathophysiology

found after myocardial infarction, tissue damage simulates an autoantibody. Autoimmune disease affects 5%–7% of adults in Europe and North America, with autoantibodies more common in older people. Autoimmune diseases have a strong ­tendency to run in families, with a 40% chance that a family with one affected adult will have another. Both genetic and ­epigenetic factors are involved with autoimmune diseases. Identical twins both develop a common autoimmune disease only 20%–40% of the time, so it is highly likely that environmental factors including dietary factors are also important.

Epigenetics is defined as the changes in the DNA transcription that may occur as a result of environmental factors. Transcription factors that may be involved in regulating cells of the immune system are thought to play a role in the pathogenesis of autoimmune diseases.30 Recent research has begun to examine the contribution of gut microbiota to the etiology of autoimmune disease. This research, in its early stages, proposes that there may be certain strains of bacteria that could be protective or could contribute to the development of the autoimmune response.31,32 Many clinically normal individuals have low titers of antibodies against some of their own tissues (e.g., against erythrocytes), and these increase with age. Babies can have autoimmune responses for a short time due to maternal antibodies. Most autoimmune diseases are more common in females. Estrogen and testosterone are thought to play a role because they activate cells to express different genes. In many autoimmune diseases, including RA, disease severity decreases during pregnancy but rapidly rebounds after birth.

Autoimmune diseases may be organ specific, with the thyroid, adrenal glands, stomach, and pancreas common targets, or nonorgan specific (see Table 9.6). Systemic lupus erythematosus involves all or almost all tissues in the body. Many autoimmune disorders have spontaneous exacerbations and remissions due to fluctuations between regulatory factors. An affected individual can have more than one autoimmune disorder (e.g., the RD cluster), and approximately 15% of all autoimmune patients have two disorders. Several mechanisms can cause damage associated with autoimmune disease. Antibodies can bind to cell membrane antigens, causing cell lysis (e.g., autoimmune hemolytic anemia), or bind and stimulate a response from the receptor (e.g., Graves’ disease). Autoantibodies can also bind to receptors and either block or damage the receptor (myasthenia gravis). Immune complex deposition in walls of small blood vessels in the kidney and joints is a key characteristic of systemic lupus erythematosus. In Sjogren’s syndrome, WBCs invade and destroy glands that produce moisture, resulting in dry

Table 9.6 Selected Autoimmune Diseases Disease

Organ

Mechanism

Hashimoto’s thyroiditis

Thyroid

Inflammation is linked to antibodies against thyroglobulin (TG) and t­ hyroid peroxidase (TPO); autoreactive cytotoxic T cells and natural killer cells destroy the thyroid gland.

Graves’ disease

Thyroid

The antibody to the thyroid-stimulating hormone receptor on thyroid cells reacts with the receptor and has the same effect as thyroid-­stimulating hormone, but it is not subject to feedback control, which results in ­overproduction of thyroid hormone.

Pernicious anemia

Red blood cells

An autoantibody reacts with intrinsic factor produced by parietal cells, resulting in decreased B12 absorption in the small intestine.

Autoimmune Addison’s disease

Adrenal

Antibodies attack and destroy the adrenal cortex cells that make Cortisol and aldosterone.

Immune-mediated infertility

Sperm

Antisperm antibodies bind to the sperm and impair motility, cause them to clump together, and interfere with fertilization of the egg.

Type 1 diabetes mellitus

Pancreas

Insulin-producing b cells are destroyed by cytotoxic T cells or antibodies.

Myasthenia gravis

Muscle

Antibodies attack the acetylcholine receptor, resulting in abnormal ­neuromuscular transmission.

Goodpasture’s syndrome

Kidney, lung

Autoantibodies are deposited in the membranes of the lung and kidneys, causing both inflammation in the kidney and bleeding in the lungs.

Autoimmune hemolytic anemia

Red blood cells, platelets

Antibodies bind to cell membrane antigens, causing red blood cell lysis.

Inflammatory bowel disease

Gastrointestinal tract

Cells from the immune system cause inflammation; the condition may also involve antibodies generated in response to an infection that cross-react with cellular antigens.

Sjogren’s syndrome

Secretory glands

The exact trigger and target are unknown, but WBC invade and destroy glands that produce moisture, resulting in dry mouth and dry eyes; also negatively affects joints, lungs, muscles, kidneys, nerves, thyroid gland, liver, pancreas, stomach, and brain.

Rheumatoid arthritis (RA)

Organ nonspecific (systemic)

The etiology is not fully understood; the presence of rheumatoid factor (an autoantibody, usually IgM, that reacts with IgG), cytokines, and cells of the immune system are indications of an autoimmune link to an acute or chronic inflammation of synovial joints that causes pain, damage, and loss of function.

Systemic lupus erythematosus (SLE)

Organ nonspecific (systemic)

Immune complexes containing antibodies to DNA, RNA, and nucleoproteins are deposited in the walls of small blood vessels in the kidney and joints.

Acute rheumatic fever

Heart

Antibodies generated in response to Group A Streptococcus cell wall ­antigens cross-react with cardiac muscle and heart valves, causing damage to the heart. Chapter 9  Cellular and Physiological Response to Injury: The Role of the Immune System   195

mouth and dry eyes. RA is characterized by acute and chronic inflammation of synovial joints, causing pain, damage, and loss of function. Etiology of RA is not fully understood but as described above its etiology involves multiple epigenetic factors.30 In Type 1 diabetes mellitus, insulin-producing beta cells are selectively destroyed by cytotoxic T cells or antibodies. In multiple sclerosis, immune cells attack and destroy the myelin sheath of neurons in the brain and spinal cord, resulting in a decrease in speed and efficiency when nerve ­messages are sent.

9.8  ATTACKING ALTERED AND FOREIGN CELLS: TUMORS AND TRANSPLANTS Research and development for the medical treatments used in cancer as well as for transplantation involves investigation of how our immune system reacts to different types of antigens. A tumor is a mass of cells that contains antigens normally found on the person’s cells as well as some new a­ ntigens that provoke an immune response such as viral or bacterial ­a ntigens. Similarly, a transplant is a mass of cells (i.e., an organ, tissue, or bone marrow) whose antigens are matched to some degree with those of the recipient. Thus, tumors and transplants appear the same to the immune system, and the mechanisms used by the immune system to attack tumors would also contribute to transplant rejection.

Tumor Immunology Cancer is caused by progressive, uncontrolled growth of a single transformed cell (see Chapter 23). Immune surveillance of these malignant cells is accomplished by the interaction of cytotoxic T cells, NK cells, macrophages, and interferon. Even though the immune system attacks cancer cells, some cells escape. Tumor cells are poor APC. Some, such as Hodgkin’s disease, suppress the immune system, while others cover themselves in molecules that block lymphocyte attachment (antigen masking).7,8

starts to function. However, rejection occurs in approximately 11–17 days and the tissue is infiltrated with macrophages, lymphocytes, and plasma cells. Second-set rejection occurs in cases involving a graft with the same MHC antigens as a previous graft. A memory response is mounted so the graft is sloughed off in 3–4 days. In contrast, it takes months to years for chronic rejection to occur. In well-matched grafts, chronic rejection is due to antibodies to minor histocompatibility antigens, immune complexes, or viruses that stimulate immune responses by placing new antigens on infected cells in the graft. The life spad of a kidney transplant is typically about 7–8 years.7,8 In graft-versus-host (GVH) rejection, which occurs in bone marrow transplants, immunocompetent cells are found within the graft, whereas the host is incompetent due to age, disease, or immunosuppression. Lymphocytes in the graft are sensitized to the recipient’s antigens and mount an immunological attack on multiple tissues and organs of the recipient. Acceptance or rejection is immunological, and r­ ejection is heavily dependent on T cells. T cells recognize donor-­ derived peptides in association with the donor’s MHC or HLA. In the first phase of rejection, the immune system must detect the presence of the graft. The graft releases soluble MHC antigens that initiate an immune response when they are presented by APC to helper T cells. Passenger cells, WBCs that were in the graft when it was taken from the donor, can migrate to lymph nodes and stimulate an immune response. Circulating T cells move through blood vessels in the graft, where they encounter foreign antigens, and then migrate to lymph nodes where they activate many cells. In the second phase, parts of the entire transplant are attacked by complement and antibodies specific for MHC I antigens, cytotoxic T cells, and NK cells.7,8

Matching  As mentioned earlier in this chapter, HLA

matching requires identifying similarities of HLA markers between the host and the donor (see Box 9.8). The closer the match of HLA markers, the more likely that the host will accept the donor transplant. Not only are HLA markers

Transplantation Immunology Transplants can normally occur between one part of a ­person’s body and another (autograft) or from an ­identical twin (isograft) without a problematic immune response. Most transplants, however, are between nontwin individuals (allografts), and immunological rejection is an important factor.7,8

Transplant Rejection  Host-versus-graft (HVG) rejection occurs when immunocompetent cells (those capable of mounting an immune response) in the host reject the graft. Acute rejection is caused by circulating antibodies that are either naturally occurring IgM or IgG against the graft, the result of multiple pregnancies or transfusions or improper blood type matching. The antibody reacts with antigens on the surface of cells, blocking establishment of good circulation, and the graft does not succeed. HVG rejection may be classified as first-set, second-set, or chronic depending on the onset of the rejection. When first-set rejection occurs, the graft at first appears healthy, with good vasculature and blood supply, and if it is an organ, 196  Part 3  Introduction to Pathophysiology

BOX 9.8

CLINICAL APPLICATIONS

Finding the Right Donor: MHC Matching In a cytotoxic assay, lymphocytes are mixed with antiserum (blood serum containing antibodies against specific antigens) to each MHC antigen in the presence of complement, and cell lysis due to an antigen–antibody reaction is detected by dyes such as trypan blue or Cr51 release. Unless a person inherited the same alleles from both parents, their lymphocytes will react with antisera to two of the A antigens, two of the B antigens, two of the C antigens, and at least two alpha and two beta chains each for DR, DP, and DQ. In mixed lymphocyte culture, lymphocytes from the donor and recipient are mixed in culture with the donor’s lymphocytes inactivated. If they are incompatible, proliferation (measured by increased DNA synthesis) is initiated. Absence of proliferation is a strong predictor of graft survival.

matched, but the patient’s blood is also tested for reactivity with the donor’s lymphocytes to determine if the recipient has antibodies to the donor’s cells and if hyperacute rejection is likely to occur. HLAs that test as the same serologically are not always exactly the same genetically. Family members are often considered as potential donors. Since the genes for MHC are inherited as a unit (haplotype), each individual will share at least one A, one B, and one C with each parent; ­hypothetically, with three-quarters of his or her siblings; and possibly with ­grandparents, aunts, uncles, and cousins.

Immunosuppression  Immunosuppression is required both at the time of the transplant and lifelong for the transplant recipient. Examples of the drugs used to accomplish immunosuppression include corticosteroids, cyclosporine, and tacrolimus. 33 These medications have numerous side effects, some of which can affect nutritional status. Table 9.7 summarizes the most common medications used as immunosuppressants. Transplantation of Specific Organs and Tissues  For

some sites and tissues, known as privileged sites, MHC matching is not required. Allograft tissue is protected from rejection in privileged sites such as the anterior chamber of the eye and the cornea because they are not vascularized. However, trauma at the site can lead to inflammation and

Table 9.7 Nutrition Side Effects of Selected ­Immunosuppressive Medications Used in Transplant and/or Treatment of ­Autoimmune Diseases Immunosuppressive Drug

Nutrition Side Effects

Azathioprine (Imuran)

Mouth ulcer, dyspepsia, vomiting, abdominal pain

Glucocorticoids

Increased appetite, weight gain, increased protein catabolism, hyperglycemia; may need additional supplementation with Ca, K+, vitamins D, A, and C, protein

Cyclophosphamide (Cytoxan)

Anorexia, weight loss, dry mouth, ­stomatitis, N/V, abdominal pain, diarrhea

Cyclosporine (Neoral, ­Sandimmune, Gengraf)

Anorexia, N/V, diarrhea, increased losses of Mg, hyperkalemia

Infliximab (Remicade)

Mouth ulcer, dyspepsia, vomiting, abdominal pain

Methotrexate (Trexall, Rheumatrex)

Stomatitis, altered taste, N/V, diarrhea

Mycophenolate mofetil; mycophenolic acid ­(Cellcept)

Stomatitis, dyspepsia, N/V, abdominal pain, diarrhea, constipation

Sirolimus/Everolimus (Rapamune)

Hyperlipidemia, constipation, diarrhea, abdominal pain

Tacrolimus (Prograf)

Stomatitis, dysphagia, dyspepsia, N/V, abdominal pain, gastritis, diarrhea, constipation; avoid St. John’s wort and grapefruit juice

Note: N/V, nausea and vomiting. Source: Adapted from Pronsky, et al. Food-Medication Interactions. 17th ed. Birchrunville, PA: Food-Medication Interactions; 2013.

then rejection. Privileged tissues such as bone, cartilage, heart valves, and blood vessels are usually not rejected no matter where they are transplanted, since they are more structural than cellular. A xenograft is when the donated organ or tissue is from an animal. Most xenografts, such as porcine heart valves in humans, are privileged tissues. The degree of MHC matching varies significantly according to the tissue, since tissues differ immunologically (e.g., expressing different levels of MHC II antigens). Matching is very important in hematopoietic stem cell (i.e., bone marrow) transplants, significant in kidney transplants, and desirable with heart transplants, but it appears to have no net beneficial effect in liver transplants. Outcomes for individuals receiving liver transplants are not improved by MHC matching. Corneal transplants are usually not matched, but if the recipient’s cornea has become vascularized, or if previous grafts have been rejected, MHC I matching may be warranted. Skin transplants are usually the patient’s own skin, so incompatibility and rejection are not typically an immunological issue. Kidneys for transplantation can come from donated organs or living donors. MHC matching currently emphasizes three loci—HLA-A, HLA-B, and HLA-DR—but the closer the overall match, the better the success rate. HLA-DR antigens have a powerful impact in heart transplantation, but heart size and availability often take precedence. Peripheral blood, bone marrow, and umbilical cord blood can all provide cells for hematopoietic stem cell transplants. Such transplants of healthy bone marrow are used to replace bone marrow that is nonfunctioning, has been damaged by high levels of chemotherapy or radiation, or has genetic defects. With autologous bone marrow transplants, the recipient is also the donor. Stem cells are harvested, stored, and returned to the individual after radiation or chemotherapy, and there is no risk of rejection. Both GVH and HVG rejection can occur in allogeneic bone marrow transplants, but GVH is normally the larger concern because the immunocompromised status of bone marrow recipients limits HVG rejection. Unrelated donor transplants using genetically matched marrow or stem cells from donors on national bone marrow registries are another source that can be used. The donor and recipient must share some HLA markers.

9.9  IMMUNIZATION Passive Immunity Passive immunization refers to the transfer of preformed antibodies. This occurs, for example, when antibodies are transferred from mother to fetus across the placenta or through breast milk. In other situations involving passive immunization, antibodies are administered to either prevent the disease or decrease the severity of the symptoms. Passive immunization vaccinations are commonly used to prevent or treat illness caused by viruses, including rabies, measles, hepatitis A and B, and chicken pox; bacterial toxins such as tetanus, diphtheria, and botulism; and bites from spiders and snakes. Immunity is fast acting but the antibodies are short lived, and no immunological memory is induced. The major risk is serum sickness.

Chapter 9  Cellular and Physiological Response to Injury: The Role of the Immune System   197

Active Immunization In active immunization, the individual is exposed to an antigen in a harmless form and produces antibodies as well as activated T and B cells and memory cells. The memory immune response, initiated upon exposure to the pathogen or a booster, prevents infection and provides additional antibodies and memory cells. In some cases, such as influenza, the residual antibodies are more important than the memory response due to the short incubation period of the disease, and more frequent vaccinations are often required to maintain the antibody level.

Types of Vaccines Thanks to scientific progress in producing vaccines, it is now often possible to acquire immunity to a disease without actually contracting it. Most vaccines are whole-organism vaccines (see Table 9.8). Live natural vaccines immunize with an organism similar to the one that is being vaccinated against. Killed vaccines are inactivated using heat and/or chemicals that may alter the antigens. They are safe but not as effective as attenuated vaccines since they produce primarily IgG and often require more frequent boosters. Attenuated vaccines are live mutants that have lost their pathogenicity while retaining immunogenicity and provide more natural protection. Attenuated vaccines prolong the immune system’s exposure to antigens and often can be given by the portal of entry used by the pathogen, resulting in mucosal immunity from IgA in addition to IgG in the blood and tissue. The increased immunogenicity can result in activation of cytotoxic T cells and a stronger memory response and thus requires fewer booster vaccinations. The chief drawback of attenuated vaccines is reversion to the pathogenic form. The Sabin vaccine (attenuated) has been a powerful weapon in the control of polio, but the Salk vaccine (inactivated) is now used in the United States because wild-type polio has been eradicated, and all reported cases were caused by vaccine reversions. Sabin vaccine is used where the virus is still endemic and to control potential epidemics. Other examples

of vaccines include influenza, meningococcal, human papillomavirus (HPV), and herpes zoster to name a few.

9.10  IMMUNODEFICIENCY Throughout the world, malnutrition is a major contributor to immunodeficiency and poor growth.34 UNICEF data in 2018 indicate that one in four children are malnourished and inadequate nutrition contributed to more than 50% of all deaths for children under 5 years.35,36 Other sources of immunodeficiency results from genetic disorders, infectious disease (HIV), or immunosuppressive therapy for other medical conditions. Infants experience transient immunodeficiency since the antibodies provided via the placenta and in colostrum wane before the infant is able to achieve normal levels. Low levels of “natural” IgM antibodies, derived from neonatal lymphocytes and formed without direct immunization with foreign antigens, are found circulating in the umbilical cord and the neonate. Adult levels of IgM are found at 2 years of age, but mucosal secretory IgA antibodies do not reach adult levels until age 6–8 years. The subclasses of IgG attain adult levels at from 1 to 5 years of age.7

Malnutrition and Immunodeficiency A combination of factors including insufficient protein, energy, and micronutrients, and not just an insufficient amount of food, are involved in the relationship between ­malnutrition and adequate immune function. Thus, undernutrition can result from personal choices such as adherence to fad diets with limited food choices as well as socioeconomic factors resulting in food insecurity. An individual’s need for proper nutrition for optimal immune function begins in utero with maternal nutrition and continues throughout life. M ­ aternal nutritional deficiencies—both large-scale deficiencies due to lack of access to sufficient food and ­specific nutrient deficiencies due to dietary choice—impair fetal development. Maternal nutrition can impact immune functioning throughout life, not just in the fetal and neonatal stages. For example, adolescents who were prenatally

Table 9.8 Common Vaccines Disease

Preparation

Disease

Preparation

Chickenpox (varicella)

Attenuated virus

Anthrax

Extract of attenuated bacteria

Measles

Attenuated virus

Haemophilus influenzae, type b (HIB)

Capsular polysaccharide conjugated to protein

Mumps

Attenuated virus

Hepatitis B

HBsAg surface protein

Polio Sabin

Attenuated virus

Influenza

Hemagglutinins

Rubella

Attenuated virus

Meningococcal disease

Polysaccharides

Smallpox

Attenuated virus

Pertussis

Purified components (acellular pertussis 5 “aP”)

Tuberculosis

Attenuated bacteria (BCG)

Pneumococcus

Capsular polysaccharides

Yellow fever

Attenuated virus

Staphylococcus

Two capsular polysaccharides conjugated to protein

Hepatitis A

Inactivated virus

Diphtheria

Toxoid

Hepatitis B

Inactivated virus

Polio Salk

Inactivated virus

Tetanus

Toxoid

Rabies

Inactivated virus

198  Part 3  Introduction to Pathophysiology

undernourished and continue to be so may produce a significantly lower a­ ntibody response to vaccination.37 In a series of vicious cycles, infants with w ­ eakened immune function may benefit less from vaccines and are more susceptible to ­infections such as infectious diarrhea, which can in turn result in a continued impaired nutrition status. Nutritional deficiencies in older adults can exacerbate the decline in immune responses associated with aging. Protein-energy malnutrition in infancy and early ­c hildhood has adverse effects on the thymus, including a ­s ignificant reduction in thymic weight, lowered thymic ­hormone levels, and fewer maturing T cells. It can also cause alterations in the thymic microenvironment and peripheral T-cell function. Lowered helper T-cell function will have a negative impact on both innate and acquired immunity. Short-term provision of a high-protein, high-calorie diet later can increase levels of serum IgG and IgM and improve the functioning of the cellular immune system, but cell-mediated immune responses diminish within a year of such treatment. Nutrients critical to the development and effective functioning of the immune system include vitamins A, C, B6, and E, essential fatty acids, beta-carotene, and the minerals manganese, selenium, zinc, copper, iron, sulfur, and magnesium.4,10,38,39 Zinc deficiency promotes apoptosis in B and T lymphocytes (especially helper T cells), hinders the function of the macrophage, alters the production and potency of several cytokines, and is linked to poor thymic development in infants. Low maternal selenium is associated with lowered numbers of cytotoxic and helper T cells, B cells, and NK cells in neonates, while neutrophils and helper T cells are affected by selenium deficits later in life.40 Vitamin B6 is a cofactor for many enzymes involved in protein metabolism and is important for cellular growth and maintenance of the thymus, spleen, and lymph nodes. Vitamin A deficiency hinders normal regeneration of mucosal barriers; decreases the function of neutrophils, macrophages, and NK cells; negatively impacts the development of helper T cells and B cells; and diminishes antibody-mediated responses. The essential omega-3 and omega-6 fatty acids are needed for the production and maintenance of immune cells. Vitamin C supports phagocyte oxidative burst activity as well as B- and T-cell function.10

Inherited Immunodeficiencies Most congenital/inherited immunodeficiencies are detected in young children because they experience recurrent and/ or overwhelming infections, often from opportunistic infections. Males are more apt to have immunodeficiencies because many such deficiencies involve recessive genes, often on the X chromosome. Some immunodeficiencies involve just one part of the immune response. In X-linked agammaglobulinemia, individuals have few or no B cells and produce no IgA, IgM, or IgE and small amounts of IgG. They suffer from numerous staphylococcal and streptococcal infections but can be treated with passive antibodies. Some individuals are deficient in a single antibody class, with IgA being the most common. Individuals with deficiencies in phagocytic cells have difficulties in killing intracellular and ingested extracellular bacteria.10 Other disorders impact more than one part of the immune response. In DiGeorge syndrome, the thymus

epithelium fails to develop, so T cells cannot mature, affecting the production of cell-mediated immunity and T-dependent antibodies. In Wiskott–Aldrich syndrome, a defect in a gene on the X chromosome coding for Wiskott–Aldrich syndrome protein affects B and T lymphocytes and platelets, which results in overwhelming opportunistic infections. There are several types of severe combined immune deficiencies (SCIDs), which are characterized by extreme susceptibility to infection due to the absence of T- and B-lymphocyte function and often NK cells. Some forms are treated with bone marrow transplants, and gene therapy is proposed for others.

Acquired Immunodeficiencies Some immunodeficiencies are acquired in later life. The immune system can be suppressed by many cancer drugs; by infectious agents, including HIV (see Chapter 22); or in clinical situations such as burns where there is a severe loss of immunoglobulins through wound output. Anergy is the term used to refer to a situation when a lymphocyte fails to respond when stimulated by its antigen-specific receptor.

9.11  HYPERSENSITIVITY (ALLERGY) Overview of Hypersensitivity Definition Hypersensitivity  (allergy) occurs when the body’s immune system reacts inappropriately to a normally harmless substance within the environment. Epidemiology  Over 50 million Americans have allergic diseases, making allergies a leading cause of chronic disease. Allergies are the sixth leading cause of chronic illness in the United States. The prevalence of allergy has continued to rise consistently over the past 50 years but as statistics for the diagnoses are difficult, the true prevalence is not known.40–43 Atopy is the tendency to develop allergic diseases. Many individuals are predisposed to the development of multiple allergies. For example, children who are diagnosed with eczema within the first 6 months of life are more likely to develop food allergies.44 Etiology: Classifications of Allergic Reactions  ­Allergic reactions are categorized as either immediate or delayed hypersensitivity (see Table 9.9). The differences in timing are related to the type of immune response that is elicited. ­Immediate hypersensitivity reactions involve B lymphocytes and their pathology results from the antibodies produced when these WBCs are exposed to the allergen. Delayed hypersensitivity involves T lymphocytes, which react more slowly; thus, the symptoms for this type of reaction may not appear for hours to days. Sensitization is the production of IgE antibodies after exposure to an allergen. Sensitization can occur via the skin exposure or through the GI tract.43,45 These antibodies can be detected through either blood or skin testing. It is estimated that IgE antibodies are present in up to 40% of the population. Sensitization, however, does not equate to an allergic response: Individuals can be sensitized but not exhibit a clinically measurable allergic response.45,46 This is important to remember as we discuss the types of tests used to diagnose allergies.

Chapter 9  Cellular and Physiological Response to Injury: The Role of the Immune System   199

Table 9.9 Characteristics of Immediate versus Delayed ­Hypersensitivity (Allergic) Responses Characteristic

Immediate

Delayed

Time to onset of symptoms

20–30 min

24–72 hrs

Name

Anaphylactic

Delayed

Immunoglobulin

IgE

None (T cells)

Antigens involved

Heterologous

Autologous or heterologous

Cellular involvement

Mast cells and basophils

Host tissue cells

Pathophysiology  Common IgE-mediated allergies involve

reactions to pollen, bee stings, penicillin, molds, dust, feathers, animal dander, and certain foods. Upon first exposure to these allergens (i.e., sensitization), IgE antibodies attach themselves to mast cells and basophils. After attachment, the mast cells or basophils rupture, releasing histamine and other chemical mediators. If the mediators are within the respiratory system, symptoms will include sneezing, watery red eyes, a runny nose, and respiratory distress. IgE-mediated food allergy involves the failure of the GI tract to digest a particular food component and subsequent absorption of the intact food component across the GI mucosa.45,46 APCs initiate the immune response, which results in the production of antigen-specific IgE antibodies. IgE antibodies activate mast cells, which can cause oral inflammation, canker sores, cramps, nausea, diarrhea, gas, hives (urticaria), and sometimes, respiratory distress. Hives occur when histamine, released from skin cells due to an allergic reaction, causes blood vessels to dilate, leak fluid, and produce swelling, which in turn irritates nerve endings and results in itching. Food allergy will be discussed in further detail later in this section and is covered in Box 9.9 (p. 205). The most severe reaction, anaphylactic shock or ­a naphylaxis, is potentially fatal. Risk of anaphylaxis is ­greatest when the allergen is injected directly into circulation so that it activates cells all over the body, as occurs with insect stings and IV drugs. Diagnosis of anaphylaxis is made when ­significant signs and symptoms occur rapidly and involve respiratory compromise, reduced blood pressure, involvement in the skin or GI tract.47,48

Medical Diagnosis and Treatment  The National

I­ nstitute of Allergy and Infectious Diseases (NIAID) 2011 guidelines recommend the following as the basis for diagnosis of allergy: in-depth physician analysis that includes the clinical history of reactions, a skin prick test, an allergen-specific serum IgE test, and an oral food challenge for suspected food allergies.49 An additional crucial component of diagnosis is reproducibility.45 The skin prick test involves either placing a small amount of a suspected allergen on the skin and then pricking the area or injecting the allergen under the surface of the skin. A positive reaction to the allergen is defined as a “wheal at least 3 mm greater than the negative control.”49 This swelling and redness occur within about 20 minutes at the site of the substance(s) to which the person is allergic. Commercial inhalant allergens are available for use in diagnosing 200  Part 3  Introduction to Pathophysiology

respiratory allergies, but the stability of the extracts of food allergens makes testing for food allergies a greater challenge. Serum IgE testing quantifies the amount of serum IgE associated with a specific antigen. As mentioned previously, the level of serum IgE does not necessarily diagnose an allergy; it needs to be correlated with clinical symptoms. The “cut-off ” value for the IgE levels defines the amount of IgE that is 90% predictive of a clinical reaction. For example, the cut-off value for peanut IgE in a child T indicates that there is a SNP at nucleotide number 677 in one allele of the Single-Nucleotide Polymorphisms  Understandmethylenetetrahydrofolate (MTHFR) reductase gene characing monogenic disorders such as those described earlier terized by a thymine in place of the more common cytosine. helps lay the groundwork for comprehending the complexSince each individual inherits one copy of the gene from each ities of polygenic diseases such as obesity, diabetes, cancer, parent, genotype can further identify them as MTHFR 677CC, and CVD. The study of gene–nutrient interactions that are 677 CT, or 677TT to indicate the nucleotides in place at posidependent upon gene variance (nutrigenetics) is focused prition 677 in both copies of the gene. The MTHFR 677C>T marily on single-nucleotide polymorphisms (SNPs; proSNP results in an amino acid change in that position from the nounced “snips”).3 SNPs are defined as those genetic variants typical alanine to the less typical valine. This particular SNP or polymorphisms in which a single nucleotide is present in has implications for folate metabolism and cancer risk, as displace of another. For example, in place of the more common cussed later in this chapter. SNPs may also be defined by the codon UGU, the codon UGC is found. Because both encode amino acid change; for instance, PPARA-Leul62Val indicates the amino acid cytosine, this particular SNP does not result the 162nd amino acid in the protein sequence for peroxisome in any difference in function. However, if UGA is present in proliferator activated receptor-α is a valine (Val) when the place of UGU, that is a potential problem, because UGA is a typical amino acid in this position is a leucine (Leu). Other nonsense or stop codon (see example of a SNP in Figure 10.5). similar variations may be seen in the literature as well. Note Depending on the location of the polymorphism within a that symbols for genes are commonly italicized, whereas refgene, there could be deleterious effects. If the affected codon erences to their protein products are not, although alternative is near the end of a coding sequence, it is possible that the nomenclature for genes is prevalent in the literature. Identification of SNPs has been a primary focus of genomics research Figure 10.5 DNA Sequence Variation in a Gene since completion of the Human Specific codons direct the cell’s protein-synthesizing machinery to add specific amino acids. Genome Project in 2003. The human For example, the base sequence ATG codes for the amino acid methionine. Since three genome has approximately 10 million bases code for one amino acid, the protein coded by an average-sized gene (3000 bp) polymorphisms, meaning that any will contain 1000 amino acids. The DNA code is thus a series of codons that specify which amino acids are required to make up specific proteins. Some variations in a person’s genetic two unrelated humans have millions code will have no effect on the protein that is produced; others can lead to disease or an of genetic differences.20 These polyincreased susceptibility to disease. morphisms are not all independent of each other. Rather, when a specific DNA Sequence Variation in a Gene Can Change gene variant is present on a chromothe Protein Produced by the Genetic Code some, it is associated with other particular gene variants on that same GCA AGA GAT AAT TGT ... Protein Products chromosome. This group of gene Gene A from variants that associate together is Arg Asp Asn Cys ... Ala Person 1 referred to as a haplotype, and these 1 2 3 4 5 variants may work in concert to produce a specific phenotype. One focus Gene A from GCG AGA GAT AAT TGT ... in genomics research now is to deterPerson 2 Codon change made no mine which of these millions of polyAla Arg Asp Asn Cys ... difference in amino acid morphisms is likely to be functionally sequence 1 2 3 4 5 important, and to continue to identify how each might relate to each other and to environment and health.21 Gene A from GCA AAA GAT AAT TGT ... fathers will not inherit the disorder because only a Y chromosome is inherited from the father. However, female offspring of affected fathers are carriers (heterozygotes), and male children born to them have a 50% chance of having the disorder, depending wholly on which copy of the maternal X chromosome is passed on. X-linked dominant traits are relatively rare. Y-linked disorders are extremely rare, occurring only in males as a result of the inheritance of mutations in the Y chromosome from the father. Y-linked disorders are not considered dominant or recessive because only one copy of the affected chromosome can exist in an individual.

Person 3 Codon change resulted in a difference in amino acid at position 2

OR Ala

Lys

Asp

Asn

1

2

3

4

Cys ... 5

Source: U.S. Department of Energy Human Genome Program, http://genomics.energy.gov.

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Other Polymorphisms  Other

types of polymorphisms include inser tion or deletion p oly morphisms, in which a number of nucleotide base pairs are either added to or deleted from a gene. For example,

the angiotensin-converting enzyme (ACE) gene has an insertion/deletion polymorphism characterized by the presence or absence of a 287–base pair fragment in one of its introns, which is linked to alterations in circulating levels of ACE and risk of renal complications related to type 2 diabetes.22 Frameshift mutations can occur when the reading frame of a gene is altered by inserting or deleting a single nucleotide or series of nucleotides. These tend to have less impact if the insertion is in the form of a triplet but can be devastating when only one or two nucleotides are inserted. For example, see what happens when the reading frame for the following sequence is shifted by an insertion of a single nucleotide (adenine, shown in red): ... CUU Leu

AUG Met

UUA Leu

CGU Arg

... CUU Leu

AAU Asn

GUU Val

ACG Thr

AAG ... Lys

UAA STOP

G...

Other syndromes can occur as a result of inheriting extra copies of chromosomes, as in Down syndrome, or deletions of sections of chromosomes, which is one cause of the neurological disorder Angelman syndrome.

Epigenetic Regulation Epigenetics relates not to the genome sequence itself but to the inherited pattern of gene expression regulated by modifications to DNA.15 Gene expression is regulated in many ways, including DNA methylation; histone methylation, acetylation, or phosphorylation; and transcription factors.15 More recently, noncoding RNAs, such as the miRNAs described earlier in the chapter, have been identified as playing a regulatory role as well.17,23 All these regulatory mechanisms can be influenced by early programming in response to nutrition and other environmental factors in fetal life or infancy as well as throughout the life span. For example, monozygotic (identical) twins have an identical genotype but have been found to have differing epigenetic patterns as they got older.24,25 This was especially true of those who spent more of their lifetime apart and had the greatest lifestyle differences. This could explain differences in disease risk in twin pairs and indicates that modifying the epigenome to activate or suppress genes through diet has potential to modify risk of chronic disease and cancer. Epigenetic patterns may also be passed from one generation to the next;26 thus, individual patterns may reflect environmental exposures of previous generations.

DNA Methylation  Although humans have the full complement of genetic material in all nucleated cells, not all genes are expressed in all cells, and the actual level of expression varies based on DNA methylation patterns. Each tissue type in the body has a distinctive methylation pattern that results in the tissue-specific gene expression,15 such as the expression of the gene for insulin only in the beta cells of the pancreas. Approximately 2%–5% of cytosines in mammalian DNA are methylated, primarily in CpG dinucleotides present in the promoter regions of genes, and the pattern of methylation is inherited, though it also changes with aging and is influenced

by environmental factors.15 This methylation (a CH3 group is donated by S-adenosylmethionine or SAM) provides tight control over genes by keeping chromatin (DNA plus the histone proteins with which it is associated) condensed and thereby suppressing gene expression, or keeping the genes “silenced.”15 For most genes, both maternal and paternal alleles contribute to production of the protein product, but for others, genomic imprinting takes place. In other words, for specific genes, only the maternal or paternal allele is expressed. For example, the gene encoding insulin-like growth factor 2 (IGF2) is expressed only from the paternal allele, while the maternal allele in mammals is silenced.27 In humans, it is predicted that there are a few hundred imprinted genes.28 Imprinting errors can result in devastating outcomes in offspring, including the neurological disorders Angelman syndrome and Prader–Willi syndrome.27 It is proposed that imprinted genes (as opposed to gene sequence) hold the most promise for rapid evolutionary adaptation to changes in the nutritional environment and may therefore be implicated in the current epidemic of obesity, metabolic syndrome, and type 2 diabetes mellitus.29 Methyl groups are derived from dietar y sources including folate, choline, methionine, and vitamin B 12. 30 As shown in Figure 10.6, MTHFR catalyzes conversion of 5,10-­methylenetetrahydrofolate to 5-methyl-­tetrahydrofolate, which then donates its methyl group to vitamin B12. Vitamin B12, thus activated, then methylates homocysteine in order to form methionine. Alternatively, choline can be converted to betaine, which can also methylate homocysteine to form methionine. Methionine adenosyl transferase then unites methionine with adenosine to form SAM, which m ­ ethylates DNA via the action of DNA methyltransferases.30 Thus, dietary adequacy plays a role in maintaining appropriate DNA methylation.30 A deficiency of methyl groups related to lack of the previously listed nutrients means that as cells divide, methylation may be reduced, and some of that transcriptional regulation is lost. Impaired methylation of DNA is related strongly to impaired fetal development and cancer.30,31 For example, hypomethylation of DNA is related to chromosomal instability, including gain or loss of entire chromosomes or increased gene mutation rates during mitosis, both of which can contribute to cancer.30 Research also suggests that hypomethylation of DNA coupled with genetic risk factors contributes to greater susceptibility to autoimmune diseases such as type 1 diabetes mellitus.32

Histone Modification  Like DNA methylation, histone

modification is a form of epigenetic regulation.33 Histones are small proteins around which DNA is wrapped. The histone tail can be modified by methylation, acetylation, phosphorylation, ubiquitination, biotinylation, and so forth, which helps to regulate transcription, DNA repair, apoptosis (programmed cell death), mitosis, and meiosis. This pattern is often referred to as the histone code. Histone modifications work in concert with DNA methylation to determine shape and accessibility of chromatin for transcription (see Figure 10.7). For example, enzymes called histone acetyltransferases attach acetyl groups to histones, and this acetylation is associated with unfolding and accessibility of chromatin for transcription, whereas histone deacetylases, which remove acetyl groups, promote folding of chromatin and block gene transcription. Several dietary factors—including sulforaphane in cruciferous vegetables, Chapter 10 Nutritional Genomics  219

Figure 10.6 The Resynthesis of Methionine from Homocysteine, Showing the Roles of Folate and Vitamin B12 5-methyl THF

Cobalamin (Vitamin B12)

Methionine ATP Methionine adenosyl transferase Pi 1 PPi

MTHFR

DMG S-adenosyl methionine (SAM) Methionine synthase

5,10-methylene THF

Serine hydroxymethyltransferase

DNA DNMTs DNA-CH3

S-adenosyl homocysteine (SAH)

Glycine

Betaine H2O

Serine

Adenosine

THF

Methylcobalamin

Roles of folate

BHMT

Choline

Homocysteine

Roles of vitamin B12

DMG, dimethylglycine BHMT, betaine homocysteine methyltransferase MTHFR, methylene tetrahydrofolate reductase DNMTs, DNA methyltransferases Source: J. Smith, J. Groff, and S. Gropper, Advanced Nutrition and Human Metabolism, 4e, copyright © 2005, p. 305.

diallyl disulfide in garlic, and butyric acid derived from fermentable fibers—have been identified as inhibitors of histone deacetylase.33

Figure 10.7 Histone Modification Modifications to histones, such as acetylation or methylation, determine accessibility of genes for transcription. Promoter

Nucleosomes Promoter not accessible for transcription

Gene

Histone modification exposes promoter

The Epigenotype  Because the epigenotype (an individual’s unique pattern of DNA methylation and histone modification) displays greater variability than the genotype, it may be more responsive to environmental influences. Several reviews on the topic have been published.29,34–36 The roles of dietary folic acid, vitamin B12, choline, and methionine are of particular interest in this regard, since these are primary sources of methyl groups, and dietary adequacy may influence DNA methylation patterns and thus genomic stability and gene expression. Methionine deficiency is unlikely, but folic acid, vitamin B12, and choline adequacy are of concern. Research is only at the early stages of elucidating how dietary modifications may manipulate the epigenome. The LIPOGAIN clinical trial, for example, has shown that diet interventions high in both polyunsaturated fatty acid (PUFA) and saturated fat increased DNA methylation in adipose tissue, with differing effects of each.37 To date, an optimal epigenotype and nutrient intake levels necessary to achieve it have not been defined. Developmental Origins of Adult Disease  Epigenetic

Promoter now accessible for transcription Gene 220  Part 3  Introduction to Pathophysiology

variation has been implicated in obesity and related comorbidities. This stems back to the “developmental (or fetal) origins of adult disease” or “thrifty phenotype” paradigm, which relates metabolic status and fetal adaptation in the womb to disease risk in later life.33,38,39 Fetal adaptation likely involves innumerable histone modifications and DNA methylation patterns determined by the maternal diet. Beyond maternal and fetal genome sequence and interaction with the immediate

the insulin-like-growth factor 2 (IGF2) gene (which is expressed environment, nutrient availability during fetal life is predictive only from the paternal allele), which, besides identifying an earof future growth trajectory and disease. For example, nutrilier time point, also suggests there is a role for both maternal ent deprivation in utero has the outcome of low birth weight and paternal obesity that transcends gene sequence.47 but also leads to fetal adaptation to a deprived environment by an increased efficiency in use of nutrients. This has been termed a “predictive adaptive response” in which the fetus 10.4  GENOMICS AND TECHNOLOGY predicts the postnatal environment based on fetal nutritional conditions and adapts in order to maximize ability to survive Individual SNPs may not be the best measure of genotype. postnatal life.38 This adaptation is epigenetically regulated and Rather, looking at the totality of a gene, including all SNPs is referred to as metabolic imprinting or metabolic programin coding, noncoding, and regulatory regions, may be more ming.40 It may manifest itself through alterations in appeappropriate as a measure of gene function in combination tite regulation, decreased physical activity, altered adipocyte with epigenetic modifications.27,48 Additionally, regardless of 29 metabolism, and altered mitochondrial function. individual genotypes, environmental factors play a large role As a consequence of the previously listed adaptations, in regulating epigenetics and, therefore, gene expression. In nutritional deprivation in both the fetal environment and early other words, diet, activity, smoking, and so forth can turn childhood has been linked to a predisposition for metabolic specific genes on or off and thus determine the quantity of syndrome, obesity, diabetes, and CVD in later life.35,38,39,41,42 specific protein products produced as well as the activity of For example, dietary protein restriction in pregnant rats has related metabolic pathways. Thus, it is important to underbeen shown to alter methylation and expression of genes stand when and where a gene is expressed as well as the cirinvolved in glucose and lipid metabolism and to alter glucose cumstances that influence its expression level. metabolism in offspring. The same parameters were even In recent years, the advent of microarray technology altered in grand-offspring who experienced nutritional ade(outlined in Figure 10.8) and other high throughput technoloquacy in their own fetal environment, indicating the environgies permit large-scale identification of SNPs and exploration ment of the grandmother during pregnancy may influence of the effects of diet on the expression of thousands of genes disease risk in grandchildren related to epigenetic programsimultaneously.49 While the entire complement of DNA is 43,44 This has been termed the “transgenerational effect.” ming. present in all nucleated cells, and genotyping can be done on In another study examining the role of epigenetic programany sample containing such cells, the sample used in determing in obesity, it was shown that Agouti mice whose mothers mining gene expression must come from the tissue of interest were fed a diet high in methyl groups during pregnancy were because not all genes are expressed in all tissues. For example, less likely to be obese than mice whose mothers were fed a determining the effects of diet on expression of lipogenic genes low-methyl diet.45 In humans, researchers have recently been (those involved in synthesizing fat in the body, such as fatty able to describe genome-wide methylation patterns in children Figure 10.8 Microarray Technology exposed to maternal diabetes Microarray technology is used to study the expression of many genes at once. It involves placing in utero, and this has enabled thousands of gene sequences in known locations on a glass slide called a gene chip. A sample identification of new areas in containing DNA or RNA is placed in contact with the gene chip. Complementary base pairing which to explore the connecbetween the sample and the gene sequences on the chip produces light that is measured. Areas on the chip producing light identify genes that are expressed in the sample. tion between maternal diabetes, epigenetic changes, and cardiometabolic risk in offspring.46 Adaptive responses such as this provide excellent examples of phenotypic changes that can occur without regard to genotype (specific gene sequence) and profoundly impact health risk. In fact, it has been hypothesized that the fetal environment is the most critical determining factor in the development of type 2 diabetes.39 Interestingly, research suggests that not only the transgenerational impact from grandmother to mother to child plays a role, but that an even earlier time point may affect methylation patterns in newborns. Soubry et al. found that paternal obesity was associated with hypomethylation of Source: Darryl Leja, National Human Genome Research Institute. Chapter 10 Nutritional Genomics  221

acid synthase) would be best accomplished by analyzing liver tissue or white adipose tissue because this is where lipogenesis occurs. Because tissue biopsy is not always realistic in human research, much of the gene expression information is derived from animal and cell research following exposure to various experimental diets. mRNA is isolated from tissue samples, and the quantity of mRNA for a specific gene provides information about how highly that gene is being expressed at the time the sample was collected. Each spot on the microarray gene chip represents a single gene, and the color intensity of each spot corresponds to the level of expression of that particular gene. Animals on different experimental diets often show differing expression levels of multiple genes.49 Further analysis is required to follow up and confirm altered expression of specific genes of interest once identified via microarray.50 This technology is invaluable in determining specific impacts of dietary components or dietary patterns on largescale gene activity. SNP microarrays and a number of other high-throughput DNA sequencing methods that can be used to conduct genome-wide association studies to pinpoint gene variants linked with specific diseases have been developed.51 These technologies allow simultaneous screening of thousands of genes and analysis of entire genomes. More recent technological advances allow study of genome-wide epigenetic modifications such as DNA methylation patterns and are being used to explore epigenetics in disease pathology including the potential role of locus-specific DNA methylation in obesity.52–54 In cancer biology, the Food and Drug Administration (FDA) recently approved two new next-generation sequencing (NGS) panels that assay 468 and 324 genes, respectively, to characterize the genetics of a tumor and individualize the treatment based on findings.55

10.5  NUTRITIONAL GENOMICS IN DISEASE Completion of the Human Genome Project and advances in exploration of the epigenome and role of microRNAs have thrust the interactions between the genome and environment into the limelight. Efforts to identify genes and gene variants linked to disease have escalated, as have efforts to identify environmental factors that can modulate gene function, interact with genotype, and modify epigenotype for optimization of health. Nonetheless, for the purposes of nutrition practice, high-quality evidence supporting specific nutrition interventions based on the individual genome, availability of quality testing in the marketplace, and educational resources to assure accurate and optimal application of available knowledge by health care providers are areas of need.13 While in most cases it is premature to base medical nutrition therapy on specific gene variants or epigenomic differences, this discussion provides a glimpse into the future by examining the current state of research and practice as well as challenges that lie ahead. See Chapters 12, 13, 17, and 23 for current medical nutrition therapy guidelines for obesity, CVD, diabetes, and cancer.

Cancer From Single-Gene Inherited Cancers to Gene–Nutrient Interactions  Several well-defined and relatively rare cancers have a clearly established genetic inheritance based on mutations

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in a single gene. An inherited mutation in the adenomatous polyposis coli (APC) tumor suppressor gene, for example, carries a 100% risk of developing the disease familial adenomatous polyposis (FAP).56 The APC mutation causes FAP because it encodes a truncated, or shortened, and therefore dysfunctional, protein product that is unable to act as a tumor suppressor. FAP is characterized by development of thousands of tumors, primarily in the gastrointestinal tract, and requires intensive treatment.56 Remarkably, this well-defined path to intestinal tumorigenesis can be thwarted to some extent by dietary means—an illustration of nutrigenetics. For example, mice bearing an inherited APC mutation develop 50% fewer tumors when consuming a diet supplemented with the long-chain omega-3 polyunsaturated fats stearidonic acid (SDA, 18:3 n-3) or eicosapentaenoic acid (EPA, 20:5 n-3).57 Fortunately, strictly inherited mutations are rare, although they are devastating to those affected. Until recently, other “noninherited” cancers have been attributed primarily to environmental exposures including diet, physical activity, alcohol intake, and tobacco use.58 These links between cancer and environmental exposure have formed the basis for public health initiatives and education (e.g., World Cancer Research Fund/American Institute for Cancer Research and American Cancer Society), although it has not been completely clear who will benefit the most from the broad recommendations presented in these initiatives and educational efforts. At this time, though, there is not a strong base of human research establishing clear diet interventions based on cancer genetics,59 so the broader dietary recommendations apply. Predicting benefit is difficult because people do not all respond in the same way to environmental exposures.60 Individuals have consequently been classified as responders or nonresponders to a specific treatment. For example, not all who smoke develop lung cancer. Not all who eat red and processed meat, which has long been associated with higher rates of colon cancer in epidemiological studies, develop cancer. One important variant has been the lack of knowledge as to each individual’s genetic background and how that may interact with nutrients or nonnutritive substances in food.60 Nutrients have the potential to alter carcinogen metabolism, hormonal status, cell signaling, apoptosis, cell-cycle control, angiogenesis, or a combination thereof. Therefore, current research strives to identify less penetrating polymorphisms or groups of polymorphisms in a single metabolic pathway that may interact with environmental variables such as diet to increase or decrease risk of various disease states, including cancer.60 While genotyping itself is a straightforward undertaking, linking individual foods, nutrients, or other bioactive components in foods to an interaction with each common genetic variant and with the epigenome and other complex biological variables remains a daunting task.59

Variations in Xenobiotic Metabolism Influence Risk A study published by Le Marchand et al. illustrates the early complexities identified with regard to gene–environment interactions.61 Both N-acetyl transferase 2 (NAT2) and cytochrome P450 1a2 (CYP1A2) enzymes in the liver are involved in biotransformation of incoming xenobiotics into harmless substances for excretion. Individuals exhibiting different

phenotypes of these enzymes metabolize xenobiotics at different rates and are thus often classified as slow, intermediate, or rapid acetylators.60,61 This phenotypic variation has potential implications for cancer risk because such enzymes transform some xenobiotics into genotoxic substances. For example, both NAT2 and CYP1A2 are integral to the biotransformation of heterocyclic amines from cooked meat into genotoxic substances, which by definition have the potential to cause cancer. Furthermore, smoking is known to induce CYP1A2—that is, it increases production of the CYP1A2 enzyme. Epidemiological research has long linked cooked meats to increased risk of colon cancer, and the authors in this study examined how that risk is modified by phenotypic variation in these two enzymes. The only group members experiencing a statistically higher risk were those with a rapid NAT2 phenotype combined with an above-average CYP1A2 phenotype who were also smokers and consumed their red meat well done. More recently, Fu et al. took the same concept to the next level by examining combinations of 16 different gene variants involving 10 key enzymes in heterocyclic amine (HCA) metabolism, including variants of CYP1A2 and NAT2, to determine an overall HCA-metabolizing score.62 Those with a high HCA-metabolizing score had a greater risk of developing colorectal polyps, especially more advanced or multiple adenomas. Another study examined the potential role of red meats in modulating colorectal cancer risk according to genotypes of different sets of genes than those described before—genes encoding various DNA repair enzymes. Findings indicate that components in red meats may interact with DNA repair mechanisms to result in higher colorectal cancer risk in individuals with specific genotypes.63 Thus, the findings of these three studies together clearly illustrate the oversimplification associated with stating that “eating red meat increases colon cancer risk” when that appears to depend at least in part on individual genetics and other environmental variables. It further illustrates that it is important to look beyond dietary modifications based on a single gene polymorphism when a number of genes involved in the same or different metabolic pathways may work together to modify the relationship between dietary factors and other environmental variables and disease outcomes. It also illustrates the importance in the future of looking toward individualization of dietary recommendations based on specific genomic and environmental variables as research findings begin to more clearly establish such relationships.

MTHFR and ADH Polymorphisms Interact with Dietary Folate and Alcohol  Cancer is characterized by

altered DNA methylation patterns, an epigenetic modification. Regulatory genes, that is, those that would normally suppress tumor formation, are frequently hypermethylated or “silenced.” Alternatively, cancer can also result from genomewide hypomethylation due to inappropriate gene activation and chromosomal instability. Histone methylation patterns are thought to play a role as well. 33 Low intakes of folate have a long association with cancer risk, including cancer of the colon, and this risk appears to escalate in the presence of high alcohol intake. However, results are not always consistent, suggesting individual effects may vary based on genomic

characteristics. Polymorphisms in the MTHFR reductase gene, primarily C677T, which causes an amino acid change from alanine to valine, can reduce MTHFR activity. 27 As mentioned previously, MTHFR plays a critical role in metabolizing 5,10-methylenetetrahydrofolate (5,10-methylene THF) to 5-methyl-tetrahydrofolate (5-methyl THF), which is necessary for remethylation of homocysteine to methionine, formation of SAM, and, therefore, DNA methylation. Because 5,10-methylene THF itself is also necessary for production of thymine, both forms of folate are needed in adequate quantities for genome health. Folate deficiency and reduced activity of MTHFR can thus contribute to both compromised genome integrity and the risk of acquiring genetic damage and cancer.27,30 But it is possible high folate intake and consequent hypermethylation of tumor suppressors could increase cancer risk as well. Examples of both are present in the research literature. The interaction between folate status and MTHFR polymorphisms in carcinogenesis is illustrated by findings from the Health Professional Follow-Up Study.64 That study showed that individuals homozygous for the TT mutation at nucleotide 677 (thus encoding valine from both copies of the gene) tend to accumulate 5,10-methyl THF intracellularly. They appear to be hyperresponders to folate status, meaning they are at low risk for colon cancer if following a low-risk diet (high in folate, low in alcohol), presumably due to accumulation of 5,10-methyl THF and optimal chromosomal stability, but may be at higher risk for developing colon cancer if consuming a low-folate, high-alcohol diet. Folate intakes were relatively high among the study population, and it is possible that more dramatic effects would have been observed with respect to the relationship of folate intake to risk had there been a wider spread in consumption levels. That will likely be difficult to see in U.S.-based studies due to the folate fortification of the food supply in place since 1998. The interaction of folate status and MTHFR genotype with alcohol appears to be a critical point. The same researchers also examined the alcohol dehydrogenase (ADH) genotype of this cohort and found those with a slow metabolizing genotype had significantly higher risk of developing colon cancer with an alcohol intake ≥20 g/day combined with folate intakes A has also been associated with a lower baseline body weight (234 vs. 251 lbs among obese subjects enrolled in the study) and the researchers’ findings further suggest that this SNP confers resistance to weight loss while following a reduced-kilocalorie diet for 1 year.96 A more recent study of 234 obese children participating in a 20-week weight loss intervention examined the relationship between PLIN genotype and weight loss success.97 Children with the PLIN6 14995A>T variant were the most successful weight losers, further suggesting perilipin gene polymorphisms are related to weight loss success. Recent work has attempted to identify ways to capitalize on findings that PLIN1 expression shows substantial circadian variation, thus suggesting meal timing could play a role in weight loss success of those with PLIN1 SNPs associated with obesity.98 The researchers found that PLIN1 SNPs predicted magnitude of weight loss and that with the PLIN1 14995A>T SNP lost significantly more weight if they were early versus late lunch eaters. Findings with regard to perilipins have not all been consistent, with one discovery being the regulation of PLIN4 by miRNA influencing obesity phenotype as reported in a review on perilipins.99 Such findings require further confirmation with larger samples but have important implications if specific genotypes are definitively proven predictive of weight loss success. In all, the polygenic nature of obesity paired with its complex environmental interactions will require large studies with thousands of subjects to accurately identify the role and ­contributions of various gene polymorphisms to obesity. Chapter 10 Nutritional Genomics  225

Beyond characterizing genetic contributions to obesity, characterizing phenotypes may be most critical to implementing precision prevention and treatment of obesity.100 Phenotypes may include many factors that vary from individual to individual including composition of the gut microbiota, epigenetic modifications influencing gene regulation, and psychological and behavioral factors relating to response to food and physical activity that reach beyond genetic variation alone.100

Diabetes Hundreds of genes have been examined for potential roles in the development of type 2 diabetes, including those that may play a role in pancreatic beta cell function, insulin signaling, and so forth, in order to identify targets for precision nutrition intervention. However, like obesity, type 2 diabetes is a complex polygenic disease process and dietary patterns and individual dietary components may not only interact with numerous SNPs but also influence gene expression, modify metabolic pathways, and alter composition of the gut microbiota, which can itself alter glycemic control.101 Considering genetic variation alone, over 100 susceptibility loci to date have been identified for development of type 2 diabetes.102 Many of the gene variants (SNPs) are common, are present across various ethnicities, and have modest effects.102 These commonalities have made it difficult to identify prevention and treatment approaches based on differing genetics alone and suggest it is most practical to maintain focus on current lifestyle intervention recommendations for diabetes.101 Nonetheless, ongoing research integrating the role of lifestyle factors with genetics, epigenetics, composition of the microbiota, biochemical data, health history, and so forth, has potential in time to impact diabetes prevention and treatment in many ways.101,103 These could include predicting the impact of lifestyle factors on individual diabetes risk (prevention), identifying optimal timing for and impact of lifestyle intervention, and determining most efficacious lifestyle interventions for those who already have diabetes (treatment).103 However, it is well acknowledged that this work is in the very early stages and cannot yet advance clinical practice beyond current recommendations for prevention and management of type 2 diabetes.101,103 It is possible, though, to explore current research to see how future diabetes prevention and treatment efforts may evolve. Because type 2 diabetes risk is influenced by such a large number of gene variants representing different mechanisms and pathways, it has become common to combine multiple variants into a genetic risk score (GRS). Genetic risk scoring uses a grouping of susceptibility SNPs to predict polygenic disease.104 For example, Huang et al. examined how weight loss diets differing in macronutrient composition differentially impacted improvements in insulin resistance based on a GRS calculated from a combination of 31 SNPs in the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial.105 They found that overweight and obese adults with a high GRS for development of type 2 diabetes had greater improvement in insulin resistance with a high-protein weight loss diet, whereas those with a low GRS fared better with a lower protein weight loss diet.105 In contrast, no interaction was observed between a 48-SNP GRS and a diet risk score in determining likelihood of developing 226  Part 3  Introduction to Pathophysiology

type 2 diabetes in more than 25,000 individuals participating in the Mälmo Diet and Cancer cohort.106 The 6% of the cohort with the highest genetic risk and highest diet risk score had the greatest likelihood of developing diabetes during the follow-up, but the effects were independent of each other. Thus there is not a clear mandate for genetically based diet modification for prevention of type 2 diabetes at this time and standard lifestyle recommendations for prevention still apply. One complicating factor in linking gene polymorphisms and multi-SNP GRSs to type 2 diabetes that must be considered as research moves forward is that obesity is strongly associated with type 2 diabetes risk. Some gene variants appear associated with diabetes only in the presence of obesity, so the gene and obesity interaction may be the main one at play. Other gene variants are associated with type 2 diabetes risk only in nonobese individuals.107 Of the more than 100 loci associated with diabetes risk in a recent large GWAS, diabetes risk did not differ significantly for most genes when BMI was considered.102 However, considering presence or absence of obesity modified the relationship of four genes with diabetes risk: FTO (previously discussed with regard to obesity), MC4R, SLC30A8, and TCF7L2.102 Transcription Factor 7-Like 2 (TCF7L2) is involved in regulating insulin secretion from pancreatic beta cells and TCF7L2-rs7903146 has been described as the SNP having the strongest association with type 2 diabetes risk.107,108 Findings from the PREDIMED trial indicate the TT polymorphism of TCF7L2 is associated with higher type 2 diabetes risk only in nonobese individuals.107 Failing to consider body weight when including TCF7L2 in a GRS to predict diabetes risk could thereby obscure results, especially if other SNPs are included that have the opposite association with body weight. Accordingly, researchers have proposed stratification by weight and use of obesity-specific and non-obesity-specific GRS scoring, which should more accurately predict diabetes risk.107 Such stratification will likely be important as future research efforts work toward identifying gene–diet interactions that lead to optimal lifestyle interventions for prevention. Epigenetic contributions to development of diabetes have also been examined to identify potential means of modifying regulation of gene expression to prevent or treat diabetes, as described in two recent reviews.109,110 Epigenetic modifications, among other roles, are key to normal differentiation and maintenance of pancreatic beta cell function. Several genes that are normally very highly expressed in beta cells have been shown to have low levels of DNA methylation and histone modifications consistent with promoting gene expression. If this normal epigenetic regulation is altered, beta cell function can become impaired. This can occur through several means, including repressed expression of genes involved in insulin secretion or expression of genes that are normally silenced. For example, a transcription factor involved in differentiation of pancreatic alpha cells is normally silenced in beta cells via DNA hypermethylation. Studies in mice have shown that reducing this DNA methylation causes beta cells to produce glucagon and results in hyperglycemia, illustrating a role for epigenetics in diabetes. While the roots of epigenetic dysregulation lie in the period before birth—influenced by parental obesity and an adverse fetal environment as described in the section on Epigenetic Regulation—there

is opportunity to influence the epigenome at time points in later life as well. Hence, the epigenome is a current target of lifestyle and drug intervention research for prevention and treatment of diabetes. Diabetes is a complex polygenic disease that has been heavily targeted with regard to research in genetics, epigenetics, and the microbiome in efforts to develop more personalized, targeted nutrition interventions. While this may be more possible in the future as technology and research evolves, at this time it continues to be most prudent to focus on currently recommended lifestyle strategies for prevention and management of diabetes.

Cardiovascular Disease Examples of interactions of dietary components with the genome in modulation of lipid metabolism, inflammation, and development of CVD are many. Early studies examined relatively simple relationships between individual SNPs and single nutrients.111 However, like cancer, obesity, and diabetes, CVDs are largely polygenic in origin and diets are more complex than single nutrients. Many genes involved in CVDs have now been identified through GWAS and combined into genetic risk scores, but a role for environmental factors such as diet and physical activity has often been left out of the equation in identifying associations between GRS and cardiovascular outcomes.112 This must be further explored in order to develop personalized diets for CVD risk reduction. 112 Additionally, the complex nature of dietary patterns and the consideration of aspects including epigenomics, microbiota composition, smoking, medications, and sleep patterns—both individual and possible synergistic effects—make it difficult to know how to best proceed with precision nutrition intervention. Disentangling the parts will require much research, integration through bioinformatics approaches, and time.111 A recent review by Corella et al. describes the complexity of dietary patterns, specifically the Mediterranean diet pattern, which includes many foods representing potentially thousands of nutrients, phytochemicals, and so forth, with individual and synergistic effects, and that can interact with individual factors (i.e., genomics) for differential effects throughout the population.111 Much of the research in this area has been observational in design, though many recent findings have come from the PREDIMED trial. The PREDIMED trial is a Mediterranean diet intervention study in which participants followed a control diet, Mediterranean diet with extra virgin olive oil, or Mediterranean diet with nuts. Through this trial, several gene SNPs have been identified that may interact with the Mediterranean diet pattern in determining CVD outcomes, including a polymorphism in the CLOCK gene.113 The CLOCK gene encodes a transcription factor that is involved in circadian regulation and SNPs in humans have been associated with obesity and type 2 diabetes risk.113 In the PREDIMED trial, researchers have shown that the CLOCK-rs4580704 SNP is associated with type 2 diabetes incidence and that this relationship was modifiable by diet. Furthermore, among study participants who developed type 2 diabetes, there was a significantly greater risk of stroke. Of those with type 2 diabetes and on the Mediterranean diet with extra virgin olive oil, G carriers (CG + GG)

had a significantly lower stroke risk compared to those homozygous for the C allele in CLOCK-rs4580704.113 The same research group in another study also showed that methylation of the CLOCK gene is associated with dietary intake of monounsaturated fatty acids (MUFA) and PUFA,114 suggesting that effects of the Mediterranean diet may be mediated in part by epigenetic mechanisms. In a separate analysis, these researchers also investigated potential interactions of the Mediterranean diet with variants of MLXIPL, which encodes a transcription factor called carbohydrate response element binding protein.115 SNPs in this gene have been associated with serum triglyceride levels and risk of myocardial infarction. Results from PREDIMED showed not only that MLXIPL-rs3812316 G-carriers compared to CC homozygotes had lower triglycerides and that those on the Mediterranean diet had lower triglycerides compared with those on the control diet, but that genotype interacted with the Mediterranean diet. In short, G-carriers with high Mediterranean diet adherence had a greater triglyceride reduction and lower risk of myocardial infarction compared to CC homozygotes with high adherence. Conversely, G-carriers with low Mediterranean diet adherence had less cardiovascular benefit. In yet another analysis, Corella et al. investigated the role of a DNA repair gene polymorphism OGG1-rs1052133, for which they also found a significant association with triglycerides and CVD mortality.116 While there was not a significant OGG1 gene interaction with the Mediterranean diet in predicting CVD mortality, they did observe that high vegetable intake as a component of the Mediterranean diet reduced CVD mortality in cys326cys homozygotes compared to serine carriers. These examples clearly illustrate a relationship between dietary pattern and individual genetics in determining CVD risk and help begin to explain, at least in part, differential responses to diet intervention. Potential effects of diet on CVD risk likely go beyond gene polymorphisms alone, however. The Mediterranean diet has been shown to downregulate genes involved in inflammation, a contributor to CVD risk, regardless of genotype.117 DNA methylation patterns are associated with expression of inflammatory markers including cytokines and high-sensitivity C-reactive protein,118 which could explain downregulation of inflammatory genes with the Mediterranean diet pattern. DNA methylation patterns have also associated with circulating lipid levels in several studies.118 While studies have investigated effects of the Mediterranean diet and its components on DNA methylation and on noncoding RNAs (mainly miRNAs), findings so far are limited.111 It is known that aging, dietary fat, smoking, and other environmental factors affect methylation patterns.37,118 To further complicate matters, it has been shown that SNPs themselves affect DNA methylation, which could in turn influence the nature of any gene–diet interactions, though intervention studies are needed in order to establish a base of evidence.118 Polymorphisms in miRNAs themselves and in binding sites for miRNAs may affect gene regulation as well. Histone modification has not yet been studied with regard to Mediterranean diet effects.111 As the Mediterranean diet is also associated with composition of the gut microbiota119 and the gut microbiota has been shown to play a role in metabolism and CVD risk,120 there is yet another dimension to the puzzle of implementing Chapter 10 Nutritional Genomics  227

precision or personalized nutrition for CVD prevention and treatment. As noted in current reviews, 111,118 numerous investigations are exploring individual aspects of –omics, but in order to fully integrate the vast amounts of information being generated, a more advanced approach at the systems biology level is required than what is currently in place.

10.6  NUTRITIONAL GENOMICS AND THE PRACTICE OF NUTRITION AND DIETETICS Grasping the intricate interactions between the genome and innumerable dietary factors, in conjunction with an understanding of phenotypic characteristics, lifestyle factors, behavior, and so forth, that influence human health is critical to the future of nutrition and dietetics practice. As evidenced by the examples in this chapter and the many others that might have been mentioned (but were beyond its scope), this is a complex issue. In most cases, barring monogenic diseases and disorders (e.g., phenylketonuria and cystic fibrosis), appropriate intervention is not simply a matter of genotyping an individual and matching each polymorphism to a specific dietary change as has been the focus of directto-consumer (DTC) marketing. Depending on the outcome sought—decreased risk of colon cancer, breast cancer, or pancreatic cancer; lower triglyceride levels; increased HDL cholesterol—the interventions may end up contradicting each other. The fact is that much remains unknown about the interactions of genes with each other. Even less is known of nutrient interactions with genotype to define an individualized diet that achieves the best outcome based on the genotypes of 20,000-plus genes.121 Furthermore, the developing understanding of epigenetics and discovery that much of the human DNA formerly classified as “junk DNA” now appears to play a critical regulatory role in gene expression suggests that much remains unknown.16 The recommendation of one diet intervention in response to one polymorphism is too simplistic, and as research evolves, practice will in time evolve as well. In addition to the genome sequence itself, the role of epigenetics, the microbiome, modulation of gene expression by dietary factors, and overall phenotype must also be considered in the overall scope of genome–nutrient interactions. At this time, therefore, it is premature to routinely apply nutritional genomics principles to complex chronic disease conditions, such as diabetes and CVD, in everyday dietetics practice.3

Individual Genomic Testing in Practice Despite the fact that few deem nutritional genomics research to be ready for general clinical application even today, some practitioners began offering genetic testing and an individualized diet during the years following completion of the Human Genome Project.122,123 DTC genetic testing also took hold as the Human Genome Project unfolded, but the services of DTC purveyors were heavily curtailed as they came under fire from consumer watchdog groups and the FDA (see Box 10.1).124,125 Today, the prominence of DTC companies has dwindled to 23andMe and few others, whose health risk information provided to consumers is currently limited.126,127 228  Part 3  Introduction to Pathophysiology

Nonetheless, some DTC testing remains available and more extensive genomic testing is available through some health care providers. A primary question that nutrition and dietetics practitioners need to consider is whether health outcomes are actually better when consumers have knowledge of their own genomics, whether through DTC or through a health care provider, and experience personalized nutrition intervention based on genomic results. Findings thus far are limited and mixed.128 In a 2014 double-blind, randomized controlled trial, researchers found that healthy young men and women who received personalized dietary advice based on a risk version of the ACE genotype significantly reduced their sodium intake compared to participants who received general dietary guidance without genetic information.129 While the study participants may not mirror those whom RDNs would typically be targeting for sodium intake reduction, findings do suggest potential for DNA-based personalized nutrition intervention to result in dietary change. The same researchers in the Impact of Personal Genomics (PGen) Study surveyed 1002 DTC consumers to evaluate changes in fruit and vegetable intake and physical activity after receiving genetic test results compared to before130 and found small but significant positive changes in health behavior. However, these changes did not correspond with genetic results, rather indicating that changes occurred regardless of genetic findings. Perhaps the largest trial investigating response to gene-based diet intervention, though, is the Food4Me European randomized controlled trial.131 In this study, participants were randomized to one of four intervention levels: control, diet, diet + phenotype, or diet + phenotype + genotype. Those in the control group received nonpersonalized guidance on diet and physical activity. Those in the diet group received guidance personalized based on current dietary intake, physical activity, and body weight. Those in the diet + phenotype group received guidance further personalized based on biochemical data, waist circumference, and other phenotypic characteristics. Finally, those in the diet + phenotype + genotype group received guidance further personalized based on genotyping. For example, those with the FTO risk allele received guidance based on diet and phenotype plus information that they would benefit from reducing body weight and waist circumference due to genetic risk. Those in this last intervention group who did not carry the risk allele were made aware of their nonrisk status. Findings at 6 months showed that although FTO risk carriers whose personalized intervention included genetic information had more weight loss and greater reduction in waist circumference than controls, results did not differ from those receiving personalized intervention without the genetic component. Thus providing genetic information on obesity risk may not result in additional benefit beyond personalized intervention based on factors such as diet and physical activity history and lab results. The Food4Me investigators similarly explored whether knowledge of APOE risk genotype (E4+), associated with risk of both CVD and Alzheimer’s disease, resulted in greater changes in fat, particularly saturated fat, intake.132 Among carriers of the risk allele (E4+), saturated fat intake decreased at 6 months compared to controls but did not differ from personalized intervention based on factors such as diet and

physical activity history and lab results. Among noncarriers (E4–), those at the diet + phenotype intervention level demonstrated the greatest reduction in saturated fat intake— significantly more than those who were advised of their nonrisk status. This raises some concern that knowledge of genetic nonrisk may reduce intervention effectiveness. As in the examination of FTO, it remains unclear whether information on genetic risk provides additional impetus to promote healthful behavioral change beyond a personalized intervention based on baseline characteristics, including phenotype. Thus, while the evidence base for SNP-based nutrition interventions remains limited and much more evidence is needed to support efficacy of genotype-based personalized nutrition interventions, RDNs may best promote healthful change through personalized behavioral nutrition interventions based on baseline diet and physical activity and phenotypic characteristics.128 The Evaluation of Genomic Applications in Practice and Prevention (EGAPP) initiative was developed by the Office of Public Health Genomics (OPHG) of the Centers for Disease Control and Prevention (CDC) to address such issues as described before.133 The goal of EGAPP is to establish a coordinated evidence-based process for evaluating genetic tests and translating genomic applications that are in transition, such as those predictive for common diseases, from research to both clinical and public health applications. Information derived from the EGAPP initiative will help to ensure that available tests are safe, effective, and used appropriately.134 Most recently, for example, EGAPP issued a recommendation statement citing insufficient evidence for genetic testing to determine risk of type 2 diabetes in the general population because it is not proven to add predictive value beyond that of traditional risk factors such as BMI.134 Furthermore, they found no direct evidence that genetic testing for type 2 diabetes risk effects management changes to prevent development of type 2 diabetes or improve outcomes.134 The CDC provides a tiered listing of genomic tests based on levels of evidence, which is updated regularly and designed to provide guidance to health care providers, public health programs, and researchers.135 RDNs engaged in nutritional genomics practice at this time may encounter ethical dilemmas beyond those expected in complying with Health Insurance Portability and Accountability Act (HIPAA) regulations. For example, in treating a child with an autosomal recessive disease, the dietitian may discover that the male parent does not carry the expected mutation. What is the role of the RDN when he or she unexpectedly discovers nonpaternity? In another example, an individual may be identified with a gene variant placing him or her at high risk for CVD. What is the responsibility of the RDN to siblings or children of that individual who may likewise be at risk? In another example, the APOE gene has been the target of nutritional genomics intervention to modulate CVD risk. However, the same gene variant placing an individual at risk for CVD is also associated with high risk of Alzheimer’s disease. Is the registered dietitian as counselor prepared adequately to discuss the risk of this devastating illness as well as diet modification? Additionally, dietitian nutritionists incorporating nutritional genomics into practice must consider from an ethical perspective whether research

on the link of the gene to disease and diet is adequately robust to warrant intervention and how that information fits in overall with information on other genotypes, phenotype, overall health history, and individual preferences to determine the role of precision nutrition. The dietitian should also be aware of testing lab certification and privacy policy and have a clear written policy of his or her own in place detailing how sensitive private information will be managed. Furthermore, he or she must be familiar with state and federal laws governing his or her actions regarding handling of genetic information.123,136–138

Evolving Knowledge and Practice Requirements for Dietitians Clearly, registered dietitians must be knowledgeable in general genetics and genomics concepts. They must also be able to understand the role of diet in interactions with the genome, knowledgably read and interpret the current research literature, and place the role of nutritional genomics in context with phenotypic characteristics. The Dietitians in Integrative and Functional Medicine (DIFM) dietetic practice group of the AND have published standards of practice for the RDN that include use of nutritional genomics and other emerging technologies as a component of the nutrition assessment in practice.139 As the research base in this area continues to expand, as practice evolves, and as gene sequencing to determine disease risk is incorporated into health care over time, RDN with a solid grasp of genomics and diet will perhaps be among the health professionals best equipped to provide precision nutrition intervention, with or without genomic data, to optimize health. Such growth in the field of nutrition and dietetics will require a substantial expansion of the knowledge base to include pathophysiology of disease at the genomic level as well as at the biochemical, metabolic, and dietary manipulation levels. Practitioners will also need to effectively communicate with consumers not only about diet but also about the intricacies of genomics and, specifically, how the dietary interventions exert their beneficial effects. With regard to implementation of genomics into the practice of dietetics, it is important for practitioners to remember that nutritional genomics “is not an end in itself.” Rather, integrated as part of the nutrition care process, it provides an additional component to the nutritional assessment for arrival at an appropriate nutrition diagnosis and implementation of appropriate personalized nutrition intervention approach. Nutritional genomics research is a key to closing gaps in the evidence base and strengthening evidence-based nutrition practice—but practitioners must be up to the task. In the meantime, however, much of the practical application awaits rigorous evidence, and it is simply premature to base dietary advice on nutrigenetic testing as a part of routine practice.3

10.7 CONCLUSION Beyond evolution in clinical practice, there will be other changes as well. Research will continue to identify bioactive food components and examine how they interact with specific genes and specific genotypes and genetic risk scores, and how they influence epigenotype and gene expression to yield Chapter 10 Nutritional Genomics  229

changes in health risk.139 Dietary guidelines will be informed by genomics research and focus on disease prevention. Food scientists will measure bioactive components in foods and develop new functional foods to meet the demand.140 Clinical trials will examine how functional foods and dietary supplements prevent or slow progression of disease. Medical nutrition therapy will be more individualized and public health interventions will be better targeted to meet the needs of a genetically diverse population. RDNs have the opportunity to be involved every step along the way, from development of functional food products to serving as clinical trial coordinators or principal investigators. The new knowledge base is expanding rapidly, and dietitians will be called upon

to translate new research findings into something consumers can understand and apply. It is also important that RDNs be involved in developing nutrition policies that reflect this new knowledge and find effective ways to communicate to the public dietary recommendations that may contain individualized guidance based on gene polymorphisms and epigenetic profiles. The merit of dietitian involvement is further underscored by the AND’s development of a position paper on nutritional genomics.3 Many opportunities unique to the intersection of nutrition with genomics will arise in the future and, if the nutrition and dietetics profession is prepared, nutrition and dietetics practice will undergo an exciting metamorphosis that will shape the future of health care.

CHAPTER REVIEW QUESTIONS 1. What is a genome? How does knowledge of its content possibly affect dietary recommendations for individuals? 2. What are the differences among genotype, haplotype, epigenotype, and phenotype? 3. Define the following terms: autosomal dominant; autosomal recessive; X-linked dominant; X-linked recessive; Y-linked; heterozygous alleles; and homozygous alleles. Name one autosomal recessive disorder, one

autosomal dominant disorder, and an X-linked recessive disorder. 4. What is the difference between a monogenic disorder and a polygenic disorder? 5. Define single-nucleotide polymorphisms. How are they identified? Give an example of one and explain what it means. 6. What is meant by epigenetic regulation? How could the nutrients

folate, choline, methionine, and vitamin B12 affect gene expression? 7. For each of the following disorders, list at least one gene that is linked to its occurrence: ­obesity, type 2 diabetes, and colon cancer. For each gene listed, describe its ­possible role in the development of the disorder. 8. Describe an example of “developmental origins of adult disease.”

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40. Waterland RA, Garza C. Potential mechanisms of metabolic imprinting that lead to chronic disease. Am J Clin Nutr. 1999; 69:179–97. 41. Barker DJP, Osmond C, Forsén TJ, Kajantie E, Eriksson JG. Trajectories of growth among children who have coronary events as adults. N Engl J Med. 2005; 353:1802–809. 42. Syddall HE, Sayer AA, Simmonds SJ, et al. Birth weight, infant weight gain, and cause-specific mortality: The Hertfordshire Cohort Study. Am J Epidemiol. 2005; 161:1074–80. 43. Benyshek DC, Johnston CS, Martin JF. Glucose metabolism is altered in the adequately-­ nourished grand-offspring (F3 generation) of rats malnourished during gestation and perinatal life. Diabetologia. 2006; 49:1117–19. 44. Burdge GC, Slater-Jefferies J, Torrens C, Phillips ES, Hanson MA, Lillycrop KA. Dietary protein restriction of pregnant rats in the F0 generation induces altered methylation of hepatic gene promoters in the adult male offspring in the F1 and F2 generations. Br J Nutr. 2007; 97:435–39. 45. Jirtle, RL, Skinner MK. Environmental epigenomics and disease susceptibility. Nat Rev Genet. 2007; 8:253–62. 46. West NA, Kechris K, Dabelea D. Exposure to maternal diabetes in utero and DNA methylation patterns in the offspring. Immunometabolism. 2013; 1:1–9. 47. Soubry A, Schildkraut JM, Murtha A, et al. Paternal obesity is associated with IGF2 hypo-methylation in newborns: results from a Newborn Epigenetics Study (NEST) cohort. BMC Med. 2013; 11:29. 48. Syvanen AC. Toward genome-wide SNP genotyping. Nat Genet. 2005; 37:S5–S10. 49. Davis CD, Milner J. Frontiers in nutrigenomics, proteomics, metabolomics and cancer prevention. Mutat Res. 2004; 551:51–64. 50. Chuaqui RF, Bonner RF, Best CJM, et al. Post-analysis follow-up and validation of microarray experiments. Nat Genet. 2002; 32:509–14. 51. Walker EJ, Siminovitch KA. Primer: Genomic and proteomic tools for the molecular dissection of disease. Nat Clin Pract Rheumatol. 2007; 3:580–89. 52. Shen L, Kondo Y, Guo Y, et al. Genome-wide profiling of DNA methylation reveals a class of normally methylated CpG island promoters. PLoS Genet. 2007; 3:2023–36. 53. Waterland RA. Epigenetic epidemiology of obesity: Application of epigenomic technology. Nutr Rev. 2008; 66:521–23. 54. Angarica VE, Del Sol A. Bioinformatics tools for genome-wide epigenetics research. Adv Exp Med Biol. 2017; 978:489–512. 55. Allegretti M, Fabi A, Buglioni S, et al. Tearing down the walls: FDA approves next generation sequencing (NGS) assays for actionable cancer genomic aberrations. J Exp Clin Cancer Res. 2018; 37:47. 56. Ficari F, Cama A, Valanzano R, et al. APC gene mutations and colorectal adenomatosis in familial adenomatous polyposis. Br J Cancer. 2000; 82:348–53. 57. Hansen Petrik MB, McEntee MF, Johnson BT, Obukowicz MG, Whelan J. Highly unsaturated (n-3) fatty acids, but not α-linolenic, conjugated linoleic or γ-linolenic acids, reduce

tumorigenesis in ApcMin/+ mice. J Nutr. 2000; 130:2434–43. 58. Le Marchand L. The predominance of the environment over genes in cancer causation: Implications for genetic epidemiology. Cancer Epidemiol Biomarkers Prev. 2005; 14:1037–39. 59. Theodoratou E, Timofeeva M, Li X, Meng X, Ioannidis JPA. Nature, nurture, and cancer risks: genetic and nutritional contributions to cancer. Annu Rev Nutr. 2017; 37:293–320. 60. Nowell SA, Ahn J, Ambrosone CB. Gene-­ nutrient interactions in cancer etiology. Nutr Rev. 2004; 62:427–38. 61. Le Marchand L, Hankin JH, Wilkens LR, et al. Combined effects of well-done red meat, smoking and rapid N-acetyltransferase 2 and CYP1A2 phenotypes in increasing colorectal cancer risk. Cancer Epidemiol Biomarkers Prev. 2001; 10:1259–66. 62. Fu Z, Shrubsole MJ, Li G, et al. Using gene-environment interaction analyses to clarify the role of well-done meat and heterocyclic amine exposure in the etiology of colorectal polyps. Am J Clin Nutr. 2012; 96:1119–28. 63. Joshi AD, Corral R, Siegmund KD, et al. Red meat and poultry intake, polymorphisms in the nucleotide excision repair and mismatch repair pathways and colorectal cancer risk. Carcinogenesis. 2009; 30:472–79. 64. Giovannucci E, Chen J, Smith-Warner SA, et al. Methylenetetrahydrofolate reductase, alcohol dehydrogenase, diet, and risk of colorectal adenomas. Cancer Epidemiol Biomarkers Prev. 2003; 12:970–79. 65. Hines LM, Stampfer M, Ma J, et al. Genetic variation in alcohol dehydrogenase and the beneficial effect of moderate alcohol consumption on myocardial infarction. N Engl J Med. 2001; 344:549–55. 66. Ericson U, Sonestedt E, Ivarsson MI, et al. Folate intake, methylenetetrahydrofolate reductase polymorphisms, and breast cancer risk in women from the Malmö Diet and Cancer cohort. Cancer Epidemiol Biomarkers Prev. 2009; 18:1101–10. 67. Teegarden D, Romieu I, LeLiévre SA. Redefining the impact of nutrition on breast cancer incidence: Is epigenetics involved? Nutr Res Rev. 2012; 25:68–95. 68. McCullough ML, Robertson AS, Chao A, et al. A prospective study of whole grains, fruits, vegetables and colon cancer risk. Cancer Causes Control. 2003; 14:959–70. 69. Fung T, Hu FB, Fuchs C, et al Major dietary patterns and the risk of colorectal cancer in women. Arch Int Med. 2003; 163:309–14. 70. World Cancer Research Fund International/ American Institute for Cancer Research. Continuous Update Project Report: Diet, Nutrition, Physical Activity and Colorectal Cancer. 2017. wcrf.org/ colorectal-cancer-2017. 71. van Breda SGJ, van Agen E, van Sanden S, et al. Vegetables affect the expression of genes involved in anticarcinogenic processes in the colonic mucosa of C57B1/6 female mice. J Nutr. 2005; 135:1879–88. 72. van Breda SGJ, van Agen E, Engels LGJB, Moonen EJC, Kleinjans JCS, van Delft JHM. Altered vegetable intake affects pivotal carcinogenesis pathways in colon mucosa from adenoma patients and controls. Carcinogenesis. 2004; 25:2207–16.

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73. van Breda SGJ, Wilms LC, Gaj S, et al. The exposome concept in a human nutrigenomics study: evaluating the impact of exposure to a complex mixture of phytochemicals using transcriptomics signatures. Mutagenesis. 2015; 30(6):723–31. 74. Seow A, Yuan J-M, Sun C-L, Van Den Berg D, Lee H-P, Yu MC. Dietary isothiocyanates, glutathione S-transferase polymorphisms and colorectal cancer risk in the Singapore Chinese Health Study. Carcinogenesis. 2002; 23:2055–61. 75. Yang G, Gao YT, Shu XO, et al. Isothiocyanate exposure, glutathione S-transferase polymorphisms, and colorectal cancer risk. Am J Clin Nutr. 2010; 91(3):704–11. 76. Martin SL, Kala R, Tollefsbol TO. Mechanisms for inhibition of colon cancer cells by sulforaphane through epigenetic modulation and hTERT down-regulation. Curr Cancer Drug Targets. 2018; 18(1):97–106. 77. Ambrosone CB, Freudenheim JL, Thompson PA, et al. Manganese superoxide dismutase (MnSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. Cancer Res. 1999; 59:602–06. 78. Cai Q, Shu XO, Wen W, et al. Genetic polymorphism in the manganese superoxide dismutase gene, antioxidant intake, and breast cancer risk: results from the Shanghai Breast Cancer Study. Breast Cancer Res. 2004; 6(6):R647–R55. 79. Bouchard C. Gene-environment interactions in the etiology of obesity: defining the fundamentals. Obesity. 2008; 16:S5–S10. 80. Kaur Y, de Souza RJ, Gibson WT, Meyre D. A systematic review of genetic syndromes with obesity. Obes Rev. 2017; 18(6):603–34. 81. Day FR, Loos RJF. Developments in obesity genetics in the era of genome-wide association studies. J Nutrigenet Nutrigenomics. 2011; 4:222–38. 82. Ferguson LR, De Caterina R, Görman U, et al. Guide and position of the International Society of Nutrigenetics/Nutrigenomics on personalized nutrition: part 1—fields of precision nutrition. J Nutrigenet Nutrigenomics. 2016; 9(1):12–27. 83. Wang T, Jia W, Hu C. Advancement in genetic variants conferring obesity susceptibility from genome-wide association studies. Front Med. 2015; 9(2):146–61. 84. Dong S-S, Zhang Y-J, Chen Y-X, et al. Comprehensive review and annotation of susceptibility SNPs associated with obesity-related traits. Obes Rev. 2018; 19(7):917–30. 85. Frayling TM, Timpson NJ, Weedon MN, et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 2007; 316:889–94. 86. Sonestedt E, Roos C, Gullberg B, Ericson U, Wirfält E, Orho-Melander M. Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity. Am J Clin Nutr. 2009; 90:1418–25. 87. Livingstone KM, Celis-Morales C, Lara J, et al. Associations between FTO genotype and total energy and macronutrient intake in adults: a systematic review and meta-analysis. Obes Rev. 2015; 16:666–78. 88. Cecil JE, Tavendale R, Watt P, Hetherington MM, Palmer CAN. An obesity-associated FTO

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gene variant and increased energy intake in children. New Engl J Med. 2008; 359:2558–66. 89. Xiang L, Wu H, Pan A, et al. FTO genotype and weight loss in diet and lifestyle interventions: a systematic review and meta-analysis. Am J Clin Nutr. 2016; 103:1162–70. 90. Castellini G, Franzago M, Bagnoli S, et al. Fat mass and obesity-associated gene (FTO) is associated to eating disorders susceptibility and moderates the expression of psycho-pathological traits. PLoS ONE. 2017; 12(3):e0173560. 91. De Groot C, Felius A, Trompet S, et al. Association of the fat mass and obesity-associated gene risk allele rs9939609A, and reward-related brain structures. Obesity. 2015; 23(10):2118–22. 92. Mottagui-Tabar S, Rydén M, Löfgren P, et al. Evidence for an important role of perilipin in the regulation of human adipocyte lipolysis. Diabetologia. 2003; 46:789–97. 93. Tansey JT, Sztalryd C, Gruia-Gray J, et al. Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity. Proc Natl Acad Sci USA. 2001; 98:6494–99. 94. Kern PA, Di Gregorio G, Lu T, Rassouli N, Ranganathan G. Perilipin expression in human adipose tissue is elevated with obesity. J Clin Endocrinol Metab. 2004; 89:1352–58. 95. Qi L, Shen H, Larson I, et al. Gender-specific association of a perilipin gene haplotype with obesity risk in a white population. Obesity Res. 2004; 12:1758–65. 96. Corella D, Qi L, Sorli JV, et al. Obese subjects carrying the 11482G>A polymorphism at the perilipin locus are resistant to weight loss after dietary energy restriction. J Clin Endocrinol Metab. 2005; 90:5121–26. 97. Deram S, Nicolau CY, Perez-Martinez P, et al. Effects of perilipin (PLIN) gene variation on metabolic syndrome risk and weight loss in obese children and adolescents. J Clin Endocrinol Metab. 2008; 93:4933–40. 98. Garaulet M, Vera B, Bonnet-Rubio G, et al. Lunch eating predicts weight-loss effectiveness in carriers of the common allele at PERILIPIN1: the ONTIME (Obesity, Nutrigenetics, Timing, Mediterranean) study. Am J Clin Nutr. 2016; 104:1160–66. 99. Smith CE, Ordovás JM. Update on perilipin polymorphisms and obesity. Nutr Rev. 2012; 70:611–21. 100. Yanovski SZ, Yanovski JA. Toward precision approaches for the prevention and treatment of obesity. JAMA. 2018; 319(3):223–24. 101. Wang DD, Hu FB. Precision nutrition for prevention and management of type 2 diabetes. Lancet Diabetes Endocrinol. 2018; 6:416–26. 102. Scott RA, Scott LJ, Mägi R, et al. An expanded genome-wide association study of type 2 diabetes in Europeans. Diabetes. 2017; 66(11):2888–2902. 103. Franks PW, Poveda A. Lifestyle and precision diabetes medicine: will genomics help optimise the prediction, prevention and treatment of type 2 diabetes through lifestyle therapy? Diabetologia. 2017; 60(5):784–92. 104. Smith JA, Ware EB, Middha P, Beacher L, Kardia SL. Current applications of genetic risk scores to cardiovascular outcomes and subclinical phenotypes. Curr Epidemiol Rep. 2015; 2(3):180–90.

105. Huang T, Ley SH, Zheng Y, et al. Genetic susceptibility to diabetes and long-term improvement of insulin resistance and β cell function during weight loss: the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial. Am J Clin Nutr. 2016; 104(1):198–204. 106. Ericson U, Hindy G, Drake I, et al. Dietary and genetic risk scores and incidence of type 2 diabetes. Genes Nutr. 2018; 13:13. 107. Corella D, Coltell O, Sorlí JV, et al. Polymorphism of the transcription factor 7-like 2 gene (TCF7L2) interacts with obesity on type-2 diabetes in the PREDIMED study emphasizing the heterogeneity of genetic variants in type-2 diabetes risk prediction: time for obesity-specific genetic risk scores. Nutrients. 2016; 8:793. 108. Facchinello N, Tarifeño-Saldivia E, Grisan E, et al. Tcf7l2 plays pleiotropic roles in the control of glucose homeostasis, pancreas morphology, vascularization and regeneration. Sci Rep. 2017; 7(1):9605. 109. Dayeh T, Ling C. Does epigenetic dysregulation of pancreatic islets contribute to impaired insulin secretion and type 2 diabetes? Biochem Cell Biol. 2015; 93(5):511–21. 110. Nilsson E, Ling C. DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes. Clin Epigenetics. 2017; 9:105. 111. Corella D, Coltell O, Macian F, Ordovás JM. Advances in understanding the molecular basis of the Mediterranean diet effect. Annu Rev Food Sci Technol. 2018; 9:227–49. 112. Corella D, Coltell O, Mattingley G, Sorlí JV, Ordovas JM. Utilizing nutritional genomics to tailor diets for the prevention of cardiovascular disease; a guide for upcoming studies and implementations. Expert Rev Mol Diagn. 2017; 17(5):495–513. 113. Corella D, Asensio EM, Coltell, et al. CLOCK gene variation is associated with incidence of type-2 diabetes and cardiovascular diseases in type-2 diabetic subjects: dietary modulation in the PREDIMED randomized trial. Cardiovasc Diabetol. 2016; 15:4. 114. Milagro FI, Gómez-Abellán P, Campión J, et al. CLOCK, PER2 and BMAL1 DNA methylation: association with obesity and metabolic syndrome characteristics and monounsaturated fat intake. Chronobiol Int. 2012; 29:1180–94. 115. Ortega-Azorín C, Sorlí JC, Estruch R, et al. Amino acid change in the carbohydrate response element binding protein is associated with lower triglycerides and myocardial infarction incidence depending on level of adherence to the Mediterranean diet in the PREDIMED trial. Circ Cardiovasc Genet. 2014; 7:49–58. 116. Corella D, Ramírez-Sabio JB, Coltell, et al. Effects of the Ser326Cys polymorphism in the DNA repair OGG1 gene on cancer, cardiovascular, and all-cause mortality in the PREDIMED study: modulation by diet. J Acad Nutr Diet. 2018; 118(4):589–605. 117. Herrera-Marcos LV, Lou-Bonafonte JM, Arnal C, Navarro MA, Osada J. Transcriptomics and the Mediterranean diet: a systematic review. Nutrients. 2017; 9:e472. 118. Ma Y, Ordovas JM. The integration of epigenetics and genetics in nutrition research for CVD risk factors. Proc Nutr Soc. 2017; 76:333–46.

119. De Fillipis F, Pellegrini N, Vannini L, et al. High-level adherence to a Mediterranean diet beneficially impacts the gut microbiota and associate metabolome. Gut. 2016; 65(11):1812–21.

127. Wynn J, Chung WK. 23andMe paves the way for direct-to-consumer genetic health risk tests of limited clinical utility. Ann Intern Med. 2017; 167(2):125–26.

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128. O’Donovan CB, Walsh MC, Gibney MJ, Brennan L, Gibney ER. Knowing your genes: Does this impact behaviour change? Proc Nutr Soc. 2017; 76:182–91.

121. Corella D, Tucker K, Lahoz C, et al. Alcohol drinking determines the effect of the APOE locus on LDL-cholesterol concentrations in men: the Framingham Offspring Study. Am J Clin Nutr. 2001; 73:736–45. 122. Bergmann MM, Gorman U, Mathers JC. Bioethical considerations for human nutrigenomics. Annu Rev Nutr. 2008; 28:447–67. 123. Kraft P, Hunter DJ. Genetic risk prediction— are we there yet? N Engl J Med. 2009; 360:1701–03. 124. U.S. Food and Drug Administration. Inspections, Compliance, Enforcement, and Criminal Investigations. 23andMe, Inc. 11/22/13. Silver Spring, MD: U.S. Food and Drug Administration; 2013. http://www.fda.gov/ICECI/EnforcementActions/WarningLetters/2013/ucm376296.htm. 125. Sinha G. News feature: Designer diets. Nat Med. 2005; 11:701–02. 126. Alysse MA, Robinson DH, Ferber MJ, Sharp RR. Direct-to-consumer testing 2.0: Emerging models of direct-to-consumer genetic testing. Mayo Clin Proc. 2018; 93(1):113–20.

129. Nielsen DE, El-Sohemy A. Disclosure of genetic information and change in dietary intake: a randomized controlled trial. PLoS ONE. 2014; 9(11):e112665. 130. Nielsen DE, Carere DA, Wang C, Roberts JS, Green RC. Diet and exercise changes following direct-to-consumer personal genomic testing. BMC Med Genomics. 2017; 10(1):24.

134. Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group. Recommendations from the EGAPP Working Group: does genomic profiling to assess type 2 diabetes risk improve health outcomes? Genet Med. 2013; 15(8):612–17. 135. Centers for Disease Control and Prevention. Public Health Genomics Knowledge Base (v4.0). Tier Table Database. https://phgkb.cdc.gov/ PHGKB/topicFinder.action?Mysubmit=init& query=all. Accessed June 28, 2018. 136. Reilly PR, DeBusk RM. Ethical and legal issues in nutritional genomics. J Am Diet Assoc. 2008; 108:36–40. 137. Castle D, DeBusk R. The electronic health record, genetic information, and patient privacy. J Am Diet Assoc. 2008; 108:1372–74.

131. Celis-Morales C, Marsaux CFM, Livingstone KM, et al. Can genetic-based advice help you lose weight? Findings from the Food4Me European randomized controlled trial. Am J Clin Nutr. 2017; 105:1204–13.

138. Castle D, Ries NM. Ethical, legal and social issues in nutrigenomics: the challenges of regulating service delivery and building health professional capacity. Mutat Res. 2007; 622:138–43.

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CHAPTER 11

Source: Gorodenkoff/Shutterstock.com

Pharmacology Marcia Nahikian Nelms, PhD, RDN, LD, FAND The Ohio State University

LEA RNING O B JECTIV ES LO 11.1  Differentiate between pharmacology and pharmacotherapy. LO 11.2  Discuss the role of nutrition therapy in pharmacotherapy. LO 11.3  Describe the common mechanisms for drug action. LO 11.4  Identify the various administrative routes of drugs. LO 11.5  Explain the processes involved in the absorption of drugs and the movement of drugs throughout the body to its target sites.

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LO 11.6  Understand factors that impact the metabolism of drugs and how they are eliminated from the body.

LO 11.10  Identify which populations are at an increased risk of improper or inadequate pharmacokinetics.

LO 11.7  Identify potential alterations in each pharmacokinetic phase.

LO 11.11  Recognize the importance of nutrition assessment as a tool for evaluating patients who might be at risk for drug-nutrient interactions.

LO 11.8  Discuss the role of nutrition on drug action from dissolution to excretion.

LO 11.12  Identify what factors practitioners should examine and evaluate during the assessment.

LO 11.9  Understand the role of drugs on nutrient ingestion, absorption, metabolism and excretion.

LO 11.13  Identify various folk remedies, vitamin and mineral supplements, and their common use and potential side effects.

G LOSSARY biotransformation—modification of a drug through metabolism buccal—refers to placement of a drug in the cheek complementary health approaches—a ­collective term for: • complementary medicine—the use of a nonmainstream health practice that is used together with conventional ­medicine • alternative medicine—unconventional health practices used in place of conventional medicine • Integrative health care—systems that bring both conventional and complementary health practices together in a coordinated way. creatinine clearance—rate at which creatinine is filtered through the kidney; often used as a measure of kidney function cyclosporine—immunosuppressant medication that is often prescribed after organ transplant CYP 3A4—a specific cytochrome enzyme involved in drug metabolism cytochrome P450 mixed-function ­oxidases—a system of enzymes responsible for drug metabolism digoxin—cardiac glycoside that is prescribed to alter the contractions of the heart

dissolution—dissolving of a medication epidural—refers to placement of a drug into the spinal fluid excipients—those substances added to formulations of medications, such as color or coating agents gentamycin—an antibiotic H2 blockers—medications that interrupt the production of acid in the stomach inhalation—introduction of a substance into the respiratory system through breathing; can refer to placement of a drug so that it is breathed in intradermal (ID)—refers to injection under the outermost layer of skin intramuscular (IM)—refers to injection into the muscle intraperitoneal (IP)—refers to injection into the body’s peritoneal cavity intrathecal—refers to injection of a drug into the membrane surrounding the central ­nervous system intravenous (IV)—refers to injection directly into a vein ionization—process of producing negatively or positively charged ions monoamine oxidase inhibitors (MAOIs)— group of medications that block the enzyme system that inactivates some neurotransmitters

11.1  INTRODUCTION TO PHARMACOLOGY The use of drugs has been a significant component of medical care since ancient times. Historically, drugs were available without a prescription, and alcohol, cocaine, marijuana, and opium were common components of drugs. The Pure Food and Drug Act of 1906, along with the subsequent Food, Drug, and Cosmetic (FD&C) Act, enacted in 1938, began government regulation for drugs in the United States through the Food and Drug Administration (FDA).1 As medical care has advanced, so has the development of pharmacotherapy. Today, more than 75% of all physician visits include a written prescription with over three million drugs ordered in 2016. Approximately, 50% of individuals in the United States were prescribed at least one medication within a 30-day period and with almost 25% of individuals using three or more prescriptions.2 The magnitude of medication use is reflected in its impact on health care costs. Spending on prescription drugs is approximately 10% of all national health expenditures approximating almost $320 billion dollars.3 Pharmacotherapy is defined as the use of drugs for treatment of disease and health maintenance. A medical drug (or medicine) is defined as a chemical used for the diagnosis, prevention, treatment of symptoms, or cure of diseases. Drugs can be classified by structure or pharmacological

omeprazole—a type of proton pump inhibitor used to treat GERD and peptic ulcer disease ophthalmic—refers to placement of a drug into the eye otic—refers to placement of a drug into the ear parenteral—refers to injection into the body’s circulatory system through a blood vessel pharmacokinetics—study of drug absorption, distribution, metabolism, and excretion pharmacology—study of drugs, their properties, and their effects pharmacotherapy—use of drugs for treatment of disease and health maintenance pressor agents—substances that cause blood pressure to increase prokinetics—medications that increase peristalsis proton pump inhibitors—drugs that reduce acid secretion in the stomach statin—a type of medication that is used to treat hyperlipidemias subcutaneous (SC)—refers to injection into the body under the skin sublingual—refers to placement of a drug under the tongue topical—refers to placement of a drug on the skin

action. Many drugs require a physician’s prescription, while others are classified as over-the-counter (OTC) medications (not requiring a prescription). Complementary health approaches is the term that the National Center for Complementary and Integrative Health recommends to describe the use of nonmainstream health practices. Some of these may include the use of nonvitamins, nonmineral dietary supplements such as herbs and botanicals. These substances may have pharmacological properties as well (Box 11.1). In 2012, approximately 17% of adults and 6% of children, who participated in the National Health Interview Survey, reported using complementary health approaches.4 Those most commonly used are listed in Table 11.1. Pharmacology is the study of drugs, their properties, and their effects; pharmacokinetics is the study of drug absorption, distribution, metabolism, and excretion. This chapter focuses on the basic principles of pharmacology, with an emphasis on the interaction of medications with nutrition. An understanding of the basic principles of pharmacology is especially valuable for registered dietitian nutritionists (RDNs) as they work toward coordination and integration of nutrition therapy with pharmacotherapy. Lifestyle, behavior changes, and complementary and alternative therapies (which include nutrition therapy) are important elements in treatment for many conditions, but use of medications remains a cornerstone of most medical management. An understanding Chapter 11 Pharmacology  235

BOX 11.1

CLINICAL APPLICATIONS

Complementary and Integrative Health Practices The use of complementary health practices [previously referred to as complementary and alternative medicine (CAM)] has continued to increase in their use in the United States. The terms “complementary and alternative medicine” have previously been used to describe these practices, but the NIH National Center for Complementary and Integrative Health (NCCIH) includes the following definitions that are recommended for use: • “If a non-mainstream practice is used together with conventional medicine, it’s considered ‘complementary.’ • If a non-mainstream practice is used in place of conventional medicine, it’s considered ‘alternative.’”1 Data from the 2012 National Health Interview Survey (NHIS) reported that nearly 30% of adults and 12% of children use some type of complementary health practice. The top five practices identified in this survey include the use of natural products, deep breathing, yoga, tai chi or qi gong, chiropractic manipulation, and meditation. The NCCIH defines natural products as nonvitamin, nonmineral supplements that are usually herbs and botanicals. The 2012 NHIS estimated that approximately 18% of the general population had used natural products in the past 12 months.2 This same survey estimates that consumer spending on complementary health practices was estimated to be >$30 billion dollars per year.3 Individuals choose these products with the desire to maintain health, prevent disease, treat pain, lose weight, reduce stress, induce sleep, and improve strength, stamina, speed, and mental acuity. They are taken as whole foods, teas, cold beverages and beverage supplements, nutritional bars, injections, tablets, capsules, powders, and suppositories. According to data from the NHIS report, fish oil/omega-3 fatty acids, pro/prebiotics, melatonin were the supplements consumed most often. There were decreases in the use of glucosamine/chondroitin, echinacea, garlic, ginseng, ginko biloba, methylsulfonylmethane (MSM), and saw palmetto.2 In addition to single remedies, blends of botanicals (and sometimes other substances) are promoted for a variety of

236  Part 3  Introduction to Pathophysiology

ailments. Although many natural products have demonstrated anecdotal effectiveness for certain conditions, research has questioned or refuted many of the claims made for these products. Beyond questions of efficacy, there are several potential problems with natural product consumption. Quality and content can vary from the label information, and in some cases the supplement does not even contain the product.4 Some substances can cause toxicity due to heavy metal contamination, and contraindications should be checked before a product is used.5,6 More serious reactions can result from interactions with prescription drugs or with other natural products. For example, therapeutic doses of garlic may act synergistically with fish oil to inhibit blood platelet aggregation; valerian may decrease the breakdown of certain drugs in the liver since it affects cytochrome P450 3A4; and black cohosh may alter the response of cells to chemotherapy in patients under treatment for breast cancer.5 St. John’s wort has been shown to cause multiple drug interactions resulting in increased metabolism of those drugs, with decreased concentration and clinical effect.5 Green tea may have an additive effect for antiplatelet medications.7 As stated earlier, natural products can be adulterated with pesticides and/or heavy metals (such as mercury).5,6 Natural products are regulated by the 1994 Dietary Supplement and Health Education Act. The act defines dietary supplements as neither foods nor drugs but in a separate category, and thus not subject to federal monitoring by the Food and Drug Administration (FDA). Safety evaluation, efficacy testing, and quality control are left up to manufacturers. The FDA does take action for false claims made about the efficacy and use of supplements. In 2017, one company was cited for false claims for products purported for use in asthma, arthritis, cold, flu, and inflammation.8 Many in the industry have adopted uniform manufacturing standards; however, variation in potency is still common. For example, in August 2017 the FDA took action against several products that were found to be produced in facilities not consistent with safe manufacturing.8

The American Herbal Products Association has developed a numerical rating system for botanical safety: (1) safe when consumed appropriately, (2) restricted for certain uses, (3) use only under supervision of an expert qualified in the appropriate use of this product, and (4) insufficient data to make a safety claim. Interactions are scored as (A) no clinical relevant interactions, (B) potential for clinical interaction, or (C) clinically relevant interactions are known to occur. (These ratings are available in the 2013 Botanical Safety Handbook from the American Herbal Products Association.) The NCCIH also provides guidance on current safety of some products.9 The FDA has the authority to protect the public from harmful natural products, but the government has the burden of proving a product is unsafe. Manufacturers may make statements regarding a product’s general effects on structure and function within the body, but no claims regarding its use to prevent or cure specific illnesses and conditions. One resource that provides evidence-based research regarding efficacy and safety is the independent testing organization—Consumer Lab.10 Ultimately though, it is up to the consumer to make informed choices regarding natural product selection and use.

Vitamin/Mineral Supplements and Megavitamin Therapy The Academy of Nutrition and Dietetics’ position paper on nutrient supplementation states that supplements can be useful when there is an identified inadequacy in an individual’s dietary intake. It is crucial for individuals to understand that if adequate intake is achieved by food that an additional supplement will not necessarily provide added health benefits.11 Despite this, there is the practice of megavitamin therapy. There is no consistent definition for the term “megavitamin therapy,” but it usually encompasses mineral as well as vitamin intake, often in amounts of over 10 times the Recommended Dietary Allowances. It is sometimes also called orthomolecular medicine, a system that uses vitamin, mineral, and enzyme supplements to address the individual biochemical differences and needs of each client.

Complementary and Integrative Health Practices (continued) Most practitioners of orthomolecular medicine are medical doctors (MDs) who typically prescribe a regimen of injections followed by tablets taken several times daily. However, many megavitamin consumers self-diagnose or rely on the advice of supplement salespeople in health food and other stores. Over-the-counter megavitamin therapy is used frequently for minor complaints. For instance, vitamin C or zinc is taken for colds and chromium picolinate to lower fasting blood sugars and improve insulin sensitivity. Megavitamin therapy, unfortunately, has been recommended for the treatment of cancer, heart disease, schizophrenia, attention-deficit/hyperactivity disorder, and autism without adequate evidence. Though any vitamin(s) may be recommended to prevent or delay the onset of disease, multivitamins, B vitamins, vitamin D, and vitamin C are most often used. Proponents argue that megavitamins can remedy nutrient deficiencies that damage DNA, improve enzyme-to-coenzyme binding in numerous genetic disorders and in certain diseases, and reduce oxidant leakage from decaying mitochondria, thus slowing aging. Advocates believe that megavitamin therapy is relatively inexpensive and safe. Little research on long-term use of megavitamin therapy has been conducted.12,13 Excess intake of zinc resulting in copper deficiencies have been reported.14 Hepatotoxicity and carcinogenicity from beta-carotene intake in smokers and drinkers suggest that even supplements presumed safe in the

majority population may be dangerous for some clients.15 Furthermore, megadose side effects are not uncommon. Headaches, insomnia, nausea, constipation or diarrhea, anorexia, mood changes, kidney stones, and allergic reactions (from dermatitis to anaphylactic shock) are possible. Vitamin and mineral supplements can also suffer from poor manufacturing practices. No governmental agency routinely assesses the ingredient claims on these products. One recent survey identified that 46% of the 35 most popular vitamin and mineral supplements did not contain the amount of ingredients as listed on their label.10 References 1. National Center for Complementary and Integrative Health (NCCIH). U.S. Department of Health and Human Services, National Institutes of Health. Complementary, alternative, or integrative health: what’s in a name? https://nccih.nih.gov/health/integrative-health#cvsa. Updated September 2017. Accessed August 21, 2018. 2. Clarke TC, Black L, Stussman BJ, et al. Trends in the use of complementary health practices among adults: United States, 2002–2012. National Health Statistics Reports: no 79. Hyattsville, MD: National Center for Health Statistics; 2015. 3. Nahin RL, Barnes PM, Stussman BJ. Expenditures on complementary health approaches: United States, 2012. National Health Statistics Reports. Hyattsville, MD: National Center for Health Statistics; 2016. 4. Newmaster SG, Grguric M, Shanmughanandhan D, Ramalingam S, Ragupathy S. DNA barcoding detects contamination and substitution in North American herbal products. BMC Med. 2013; 11: 222. 5. Harris ES, Cao S, Littlefield BA, et al. Heavy metal and pesticide content in commonly prescribed individual raw Chinese Herbal

of all aspects of medical care, including pharmacotherapy, among practitioners should result in improved patient outcomes, maximized nutritional status, and decreased complications or risks of the prescribed medical care. The organization that accredits medical facilities, The Joint Commission, requires monitoring, documentation, and patient education for food–drug interactions. Ensuring that this requirement is met necessitates the coordinated efforts of all health care practitioners.

11.2  ROLE OF NUTRITION THERAPY IN PHARMACOTHERAPY Consider the situation of a 52-year-old male currently being treated for hypertension and hyperlipidemia. His physician has prescribed 40 mg Inderal twice daily (BID) to control his blood pressure; 20 mg of Zocor each day; and Niacor 500 mg

Medicines. Sci Total Environ. 2011; 409(20): 4297–305. 6. Bolan S, Kunhikrishnan A, Balaji S, et al. Sources, distribution, bioavailability, and risk assessment of heavy metal(loid)s in complementary medicine. Environ Int. 2017; 108: 103–18. 7. Alsanad SM, Howard RL, Williamson EM. An assessment of the impact of herb-drug combinations used by cancer patients. BMC Complement Altern Med. 2016; 16: 393–403. 8. Food and Drug Administration. Inspections, Compliance, Enforcement, and Criminal Investigations. https://www.fda.gov/ICECI/­ EnforcementActions/WarningLetters/2017/ ucm572479.htm. Accessed August 21, 2018. 9. National Center for Complementary and Integrative Health. How safe is this practice or product? https://nccih.nih.gov/health/ safety/topics.htm. Accessed August 21, 2018. 10. Consumer Lab. https://www.consumerlab .com. Accessed August 21, 2018. 11. Academy of Nutrition and Dietetics. Position of the American Dietetic Association: nutrient supplementation. J Am Diet Assoc. 2009; 109: 2073–85. 12. Bjelakovic G, Nikolova D, Gluud LL, ­Simonetti RG, Gluud C. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA. 2007; 297(8): 842–57. 13. Neuhouser ML, Wassertheil-Smoller S, Thomson C, et al. Multivitamin use and risk of cancer and cardiovascular disease in the ­Women’s Health Initiative cohorts. Arch Intern Med. 2009; 169(3): 294–304. 14. Poujois A, Djebrani-Oussedik N, Ory-Magne F, et al. Neurological presentations revealing acquired copper deficiencies: diagnosis features, etiologies and evolution in seven patients. Intern Med J. 2018; 48: 535–40. 15. Lawson KA, Wright ME, Subar A, et al. Multivitamin use and risk of prostate cancer in the National Institutes of Health–AARP Diet and Health Study. J Natl Cancer Inst. 2007; 99: 754–64.

three times per day (TID) to treat his hyperlipidemia. What is the role of nutritional care within this typical patient situation? Though nutrition’s role in pharmacotherapy can be approached from several perspectives, it has traditionally been discussed within the context of the effect of nutrition on the action of the prescribed medication or the effect of the medication on an aspect of nutrition. Food–medication interactions are defined as “undesirable/harmful interaction(s) between food and OTC medications, prescribed medications, herbals, botanicals, and/or dietary supplements that diminishes, enhances, or alters effect of nutrients and/or medications.”5 The Academy of Nutrition and Dietetics (AND) emphasizes a collaborative model of health care that allows maximum benefit from the use of both pharmacotherapy and nutrition therapy.6 In the patient scenario just presented, the well-trained RDN would first recognize that a therapeutically important Chapter 11 Pharmacology  237

Table 11.1 Top-Selling Herbal and Nonvitamin, Nonmineral Products Used in Complementary Health Practices 2007 Age-Adjusted ­Percent2 (Standard Error)

Number (in Thousands)

Age-Adjusted Percent2 (­Standard Error)

p Value

Fish oil ................................................................................

10,923

4.8 (0.17)

18,848

7.8 (0.22)

†

Glucosamine or chondroitin.................................................

7,236

3.2 (0.14)

6,450

2.6 (0.11)

†

Probiotics or prebiotics.........................................................

865

0.4 (0.05)

3,857

1.6 (0.09)

†

Melatonin............................................................................

1,296

0.6 (0.06)

3,065

1.3 (0.08)

†

Coenzyme Q–10 (CoQ10)....................................................

2,691

1.2 (0.08)

3,265

1.3 (0.08)

††

Echinacea............................................................................

4,848

2.2 (0.12)

2,261

0.9 (0.06)

†

Cranberry (pills or capsules).................................................

1,560

0.7 (0.06)

1,934

0.8 (0.06)

††

Garlic supplements..............................................................

3,278

1.4 (0.09)

1,927

0.8 (0.06)

†

Ginseng...............................................................................

3,345

1.5 (0.10)

1,752

0.7 (0.06)

†

Dietary Supplements1 3

†

2012

Number (in Thousands)

Ginkgo biloba......................................................................

2,977

1.3 (0.10)

1,619

0.7 (0.06)

†

Green tea pills (not brewed tea) or EGCG (pills)4..................

1,528

0.7 (0.06)

1,503

0.6 (0.05)

††

Combination herb pill..........................................................

3,446

1.5 (0.10)

1,463

0.6 (0.05)

†

MSM (methylsulfonylmethane)............................................

1,312

0.6 (0.05)

1,051

0.4 (0.04)

†

Milk thistle (silymarin)..........................................................

1,001

0.4 (0.05)

988

0.4 (0.04)

††

Saw palmetto......................................................................

1,682

0.7 (0.07)

988

0.4 (0.04)

†

Valerian...............................................................................

877

0.4 (0.05)

801

0.3 (0.04)

††

p < 0.05.

††

Difference is not statistically significant.

1

Respondents may have used more than one nonvitamin, nonmineral dietary supplement.

2

The denominator used in the calculation of percentages was all sample adults.

3

In 2007, fish oil was described as fish oil or omega-3 or DHA fatty acid. In 2012, fish oil was described as fish oil or omega-3 or DHA or EPA fatty acid.

4

EGCG is epigallocatechin gallate.

Notes: Estimates were age adjusted using the projected 2000 U.S. population as the standard population and using four age groups: 18–24, 25–44, 45–64, and 65 and over. Estimates are based on household interviews of a sample of the civilian noninstitutionalized population. Source: CDC/NCHS, National Health interview Survey, 2007 and 2012.

drug–nutrient interaction could occur between Zocor and grapefruit.7 Furanocoumarins found within grapefruit block the metabolism of Zocor and could significantly change availability of this medication. Next, it is important to note that consuming food with propranolol (Inderal) decreases its breakdown in the liver (i.e., it decreases “first-pass” hepatic metabolism), which results in increased bioavailability of the drug. It is not necessary to take propranolol either with or without food, but it should be consistently taken either with food or not with food each day. Though important, preventing interactions is only one goal of understanding nutrition’s contribution to pharmacotherapy. Current recommendations for treatment of hyperlipidemia include nutrition therapy as a component of treatment for cardiac disease, hyperlipidemia, and hypertension.8 Weight loss, if the patient were overweight, could lower his blood pressure, reducing the required dosage of Inderal, and improve his lipid profile so that his other medications could be reduced or eliminated. Incorporating principles of the Dietary Approaches to Stop Hypertension (DASH) diet with his weight-loss program may result in a further decrease in his blood pressure (see Chapter 13). Complete counseling for this patient would encompass the following recommendations: avoid grapefruits, grapefruit and other fruit juices,8 take Inderal on an empty stomach, and follow a low-kcal, low-saturated fat, 238  Part 3  Introduction to Pathophysiology

and low-sodium diet that is rich in fruits and vegetables and fat-free or low-fat dairy products. The complete care of this patient requires communication with all health care team members including the RDN, the pharmacist and the physician. Over time, successful nutrition therapy could impact his health care costs. 9,10 Hence, intervention by the RDN provides clinical and economic benefits while also meeting all legal responsibilities. This chapter addresses the complex relationship between nutrition therapy and pharmacotherapy in detail, focusing on information the RDN will need to successfully integrate the two.

11.3  DRUG MECHANISMS The most common mechanisms for drug action involve binding of the drug to specific receptors on the cell membrane, which initiates changes in specific enzyme reactions. Drugs react with a cellular receptor site due to their three-­ dimensional shape—as a lock and key might fit together (see Figure 11.1). When this occurs, physiological functions are altered. Most drugs can interact with more than one cell receptor, which may account for various side effects of medication use. Some drug effects are independent of cellular receptors and are called nonspecific cellular responses. Ethanol and osmotic diuretics act by this type of mechanism.

11.4  ADMINISTRATION OF DRUGS

Figure 11.1 Cellular Receptor Site The drug had no effect because it was not recognized by the cell receptors

Drug Cell receptor

Biological response since the cell receptor recognized the drug

Drug Cell receptor

Medications cause alterations in enzyme systems either by stimulating (induction) or inhibiting them (see the section “Pharmacokinetics: Metabolism of Drugs”). An example of enzyme system inhibition is the action of the class of medications called angiotensin-converting enzyme (ACE) inhibitors, illustrated in Figure 11.2. In normal control of blood pressure, ACE stimulates conversion of angiotensin I to angiotensin II. The function of angiotensin II is to constrict blood vessels and resulting in an increase in blood pressure (see Chapters 7 and 13 for more detail). If this enzyme system is inhibited, it causes a decrease in blood pressure. Of course, other physiological functions can change as a result of drug action. These nonspecific responses can either be therapeutic or result in side effects and drug interactions.

Drugs can be administered in multiple ways. The administrative route depends on the chemical properties of the drug, the type of effect desired, and, of course, patient characteristics that affect how the medication could be administered. The oral route of administration requires that the patient be able to swallow medication and that the slower rate of absorption of this administration method is acceptable. Sublingual or buccal administration means the drug is placed under the tongue or in the cheek, respectively. It dissolves there, so it is quickly absorbed across mucous membranes into the circulatory system. When an individual takes nitroglycerin for angina, it is usually via a sublingual route. Some medication can also be administered as a suppository via the rectum (to be absorbed in the lower gastrointestinal [GI] tract) or the vagina. Routes of administration can also be parenteral, ­topical via skin and mucous membranes, or through inhalation. ­Parenteral administration requires an injection into the body through routes that are either subcutaneous (SC), intradermal (ID), intramuscular (IM), intraperitoneal (IP), or intravenous (IV). Topical medications may be applied for their direct effects on the skin but can also be absorbed via skin or mucous membranes; for example, Estraderm is an estrogen patch worn to increase circulating levels of estrogen. Drugs that are inhaled may act locally within the respiratory system or have a systemic effect. Inhaled anesthesia works systemically, whereas the medication Combivent uses two different types of bronchodilators, which act locally to treat asthma and other respiratory conditions. Medications can also be placed directly into target tissues such as the eye (ophthalmic), ear (otic), or spinal canal (epidural or intrathecal).

(a) Normal action of ACE; (b) Inhibition of ACE through medication causes blood pressure to drop. Angiotensin— converting enzyme (ACE)

Angiotensin II

Vasoconstriction— blood pressure increases

Inhibited conversion to angiotensin II

Vasodilation— blood pressure decreases

(a) Angiotensin— converting enzyme (ACE)

ACE inhibitor

Angiotensin I (b)

®

11.5 PHARMACOKINETICS Absorption of Drugs

Figure 11.2 Inhibition of an Enzyme System

Angiotensin I

®

Absorption of the drug/medication involves several steps as the substance is transferred from the administrative site (e.g., oral, sublingual, and intravenous) to the circulatory or lymphatic system. Absorptive mechanisms for drugs encompass the same basic processes as those for nutrients (see Chapters 14 and 15). Collectively, these processes include passive diffusion, facilitated diffusion, and active transport. The rate and effectiveness of absorption for drugs is dependent on several key factors. First, solubility of the medication determines where in the GI tract the medication will dissolve and thus be absorbed. Dissolution or dissolving of the medication has to occur before absorption is successful. Excipients are those substances added to formulations of medications that affect dissolution. Binders, lubricants, and coating agents decrease dissolution, whereas disintegrants (ingredients that dissolve readily in water) increase dissolution. Coloring and flavoring agents have varying effects on dissolution. Tablet formulation is also a factor; hard, round, and large tablets dissolve more slowly. Dissolution rates of generic equivalents to the original medication may also vary.11–13 Chapter 11 Pharmacology  239

The amount of time a medication is present in a specific portion of the GI tract, the pH of that portion of the GI tract, and the surface area of the GI tract also affect absorption capability. The largest surface areas for drug absorption are located in the small intestine and lungs. Other factors that affect absorption include the chemical properties of the drug, the integrity of the GI tract and other tissues, and the circulation and blood supply. Anatomical regions with the highest blood flow, including the small intestine, lungs, muscle, and buccal and nasal cavities, have efficient rates of absorption and distribution. The most important chemical properties of medications related to drug absorption include the solubility of the drug in lipid or water and the ionization of the medication. Lipid-based drugs will be absorbed across cell membranes quickly, since cell membranes are primarily lipid based. Drugs that are not ionized will also be absorbed much more readily. If the drug is ionized, absorption will be dependent on the pH of the solution where it will be absorbed. For example, if a medication is mildly acidic, absorption will be enhanced in solutions that are also acidic, such as gastric juices.14 Aspirin is a good example of a medication that is absorbed in the stomach but can also damage the gastric mucosa.

Distribution of Drugs After absorption, distribution of the drug occurs. Distribution is defined as the movement of the drug throughout the body to the target sites where it can act. Distribution is variable and is affected by the circulation, the binding of the drug to proteins within the circulation (e.g., albumin and 1-acid glycoprotein), capillary permeability, the drug’s solubility in water, and the binding of the drug to other tissues within the body. Overall, the greater the amount of the drug that binds to another substance, the smaller the amount of active or free drug within circulatory or storage tissues. Physiological or anatomical features also affect distribution of the drug. For example, some drugs cannot cross the placenta or enter the central nervous system, whereas others, mostly lipid soluble or with neutral pH, are readily distributed to those sites. The blood–brain barrier of juxtaposed cells (cells that form a tight junction) usually inhibits the passage of polar or ionized drugs. Drug distribution can vary from person to person. For example, more fat-soluble drugs may be stored in the adipose tissue of obese individuals than in those with less adiposity.

enzyme system called the cytochrome P450 mixed-­function oxidases system, but there are numerous enzyme systems that are responsible for the extensive reactions that metabolize drugs within the GI tract and liver.14 The interaction between substrate and the enzyme systems may be further described simplistically as an inhibitor or inducer. An inhibitor reacts with a specific enzyme by competing for its receptor site. An inducer works to stimulate synthesis of the enzymes, increasing action potential. Inhibitors decrease metabolism and generally lead to increased drug effect, whereas inducers will increase metabolism and generally lead to decreased drug effect. Phenobarbital and theophylline are examples of inducers of the P450 enzymes. Examples of drugs known to be inhibitors include chloramphenicol, cimetidine, valproic acid, allopurinol, and erythromycin. A drug’s delivery method can affect its metabolism. Drugs delivered directly into the bloodstream (sublingual and parenteral routes) may differ in their onset of peak plasma concentration and duration of action as compared to drugs delivered enterally. Drug dosages must be adjusted to accommodate metabolism of each medication. Blood levels are measured in order to establish the most effective dose for each person (see Figure 11.3). The dosage range with therapeutic efficacy is referred to as the “therapeutic window.” Levels below this window may not be effective, and those above may result in toxicity.14

Excretion of Drugs Generally, after drugs are metabolized, the remaining compounds are eliminated from the body. There are exceptions; some drugs can be excreted before they are metabolized. Most drugs are removed by either urinary or biliary excretion, but some can be excreted via the lungs or feces, depending on the chemical structure of the metabolite. It is important to be aware that some drugs can be excreted in breast milk, which means that a nursing infant will be exposed to them. In addition, patients who are taking drugs excreted via the salivary glands may complain of taste changes.

Figure 11.3 Therapeutic Levels of Drugs Dose-response curves: efficacy vs. safety

Metabolism of Drugs

240  Part 3  Introduction to Pathophysiology

Clinical efficacy Therapeutic response

A metabolized drug has been chemically altered (undergone biotransformation). Drug metabolism is typically discussed in the context of phase 1 reactions (oxidation, reduction, etc.) and phase 2 where a second molecule is conjugated with the substrate from Phase 1.14 The resulting substance (metabolites) may be similarly active, inactive (and ready for excretion via urine or bile), or differently active in terms of therapeutic activity or toxicity. The GI tract and liver are the major sites for biotransformation, including oxidation, reduction, and hydrolysis. The GI tract serves as the first site of metabolism for orally administered drugs. Absorbed drugs are then delivered to the liver via the portal vein. Most drug biotransformation in the liver is accomplished by the hepatic microsomal

Therapeutic window

Toxicity

Dose Source: Bottorll MD, Evans WE. Drug concentration monitoring. In: Progress in Clinical Biochemistry and Medicine. 1988.

Urinary excretion of drugs can occur in all three stages of urinary filtration and concentration within the nephron, the functional unit of the kidney (see Chapter 18). Each of the over 1 million nephrons consists of a glomerulus and tubule. Each tubule is divided into several sections, depending on the type of epithelial cells it contains. Sections are referred to as the proximal tubule, Loop of Henle, distal tubule, and the collecting duct. (See Figure 18.2 in Chapter 18.) All collecting ducts drain into the ureter and ultimately into the bladder. Most drugs of low molecular weight are filtered out of the blood in the glomerulus unless they are bound to large molecules such as proteins or to erythrocytes. Drugs can be reabsorbed within the tubules. Reabsorption depends on the pH of the urine and the solubility of the drug. Since the acidity of the urine is quite variable, there is a significant variation in drug reabsorption.

Alterations in Drug Pharmacokinetics No two people will react in the same way to any given medication. Age; gender; cardiovascular, hepatic, and renal function; presence of disease or infection; diet; and genetic differences will affect how an individual will respond to a drug dosage. One of the fastest growing fields is pharmacogenetics. The following sections describe potential alterations in each pharmacokinetic phase.

Altered GI Absorption  Altered health conditions, dis-

ease, and treatment modalities can interrupt the normal GI absorption processes. However, a more common factor that may change the effectiveness of absorption is consumption of food simultaneously with the medication.15–17 The presence of food stimulates normal digestion and absorption mechanisms, such as changes in rate of gastric emptying and the release of enzymes and hydrochloric acid. All these normal mechanisms may alter the GI environment so that it is not suitable for absorption of the medication. The presence of food also increases the chance of the drug binding to a food component, possibly affecting absorption. A classic example of this situation is the effect of calcium on the antibiotic tetracycline. Tetracycline binds to calcium, resulting in decreased efficacy of the medication. 17 Directions for a medication should indicate whether the drug should be taken with or without food. Vomiting and diarrhea can influence drug absorption by reducing the time available for solubility and dissolution. Diseases or health conditions that interrupt normal transit time or surface area will decrease drug absorption. For example, Crohn’s disease or other malabsorptive diagnoses will alter the GI tract’s capacity to absorb a drug across the membrane of the enterocyte. Drugs, nutrients, and other substances may also compete for the carriers needed for active transport across a cell membrane. For example, Levodopa, a standard medication for treatment of Parkinson’s disease, is transported using the same pathways as neutral amino acids such as leucine and isoleucine. This medication should be taken on an empty stomach so that adequate absorption can be ensured.17 As mentioned previously, the pH at the absorption site can alter ionization of the drug, which may change the speed and effectiveness of absorption. For example, Ketoconazole,

an antifungal agent, must be in an acidic environment for appropriate dissolution and absorption. Lastly, decreased blood circulation to and from the GI tract could also reduce the effectiveness of absorption from the small intestine to the rest of the body.

Altered Distribution  Major factors that change distribution of a drug include variations in circulation, body size and body composition, and protein binding of the medication. Factors that could alter circulation include age and disease. For example, the drugs propranolol and dextropropoxyphene increase blood flow to the liver, and thus increase circulation or distribution of other medications. Any factor that causes vasodilation would theoretically increase distribution of the drug; for example, physical activity and increased body temperature increase vasodilation and thus drug distribution. Body size and body composition can alter drug distribution. Older adults may have decreased muscle mass requiring an adjustment for drug dosing.18 Large amounts of body fat may slow down the distribution of a medication. Many medications are bound to a protein carrier—most often, albumin. Any situation that could alter albumin concentrations, such as liver or kidney disease or malnutrition, would increase the amount of unbound medication, multiplying the amount of active drug within the body. Altered Metabolism  Age is also a major factor in how drugs are metabolized. Neonates, infants, and young children have vastly different levels of liver function and enzyme systems than adults do, which affects their reactions to different medications. On the other end of the spectrum, older adults may also have a decreased ability to metabolize drugs because of the normal physiological changes of aging. For instance, circulation within the liver decreases by approximately 35% by age 70 years with concurrent decreases in liver mass. Drug metabolism alterations may surface as either decreased effectiveness of some medications or as toxicity symptoms. Appropriate metabolism of drugs requires adequate function of organs—especially the liver. When disease and injury interrupt organ functioning, drug metabolism may change as well. The types of drugs or alternative regimens will need to be considered when concurrent drug treatment interferes with metabolism. Genetic factors may also play a major role. Hereditary differences are often attributed to differences in genetic coding of metabolic enzyme systems.8,19 For example, differences in metabolism for proton pump inhibitors (e.g., omeprazole) can affect treatment effectiveness for Helicobacter pylori infections. 20 In 2007, the FDA announced the addition of genetic information to the label for warfarin, an anticoagulant drug. Individuals who have the phenotype(s) for vitamin Κ epoxide reductase may not be able to metabolize warfarin, or may metabolize it more slowly, resulting in a greater tendency to bleed and a need to lower the dosage.21 Five common enzyme variants associated with warfarin sensitivity have been described.22 Gender differences are also apparent in metabolism for some drugs.23 One of the most common mechanisms for alteration of drug metabolism is concurrent use of other medications, which may interrupt enzyme systems and prevent clearance of metabolites. Numerous drug–drug interactions have Chapter 11 Pharmacology  241

been identified that, unless monitored closely, can cause significant adverse symptoms.

Altered Urinary Excretion  Urinary excretion of drugs can change as a result of numerous mechanisms. As stated earlier, the pH of the urine has a direct effect on the type of drugs easily excreted. Nutritionally, different foods can affect the pH of the urine, though these effects are difficult to predict due to variations in digestion and metabolism.24 Excretion can also be changed by the presence of a competitor for active transport across the renal tubule. Finally, urinary excretion can be altered by changes in urinary flow rates or kidney function, which may result from another medication, a disease or injury, or the aging process. Changes in creatinine clearance significantly alter the effectiveness of medications. If an individual has renal insufficiency from any etiology, drug levels must be adjusted to ensure therapeutic levels. Digoxin, cyclosporine, and gentamycin are examples of medications affected by changes in kidney function. Other medications such as ampicillin or cephalosporins are nephrotoxic and could themselves change kidney function.25

How Foods and Drugs Interact Food–medication interactions can be organized by examining the effect of nutrition on the action of the prescribed medication, the effect of the medication on nutritional status, or the role of nutrition therapy in maximizing the prescribed effect of pharmacotherapy and/or minimizing the side effects.5

Effect of Nutrition on Drug Action This section discusses the effects of food and nutritional status on dissolution, absorption, metabolism, and excretion of medications. Since it is virtually impossible to have a working knowledge of all potential reactions, health professionals in specialty areas become very familiar with medications of their typical patient population. Throughout this textbook, there are highlights of specific drug–nutrient interactions for each diagnosis. Heightened awareness of potential interactions makes the integration of nutrition and pharmacotherapy a routine component of patient care.

Effect of Nutrition on Drug Dissolution  In order for oral drugs to be absorbed, dissolution of the medication is necessary. The pH of the stomach and the gastric emptying rate are two of the most important nutrition-related factors impacting drug dissolution. Medications may require an acidic environment for dissolution. Achlorhydria, which is decreased production of hydrochloric acid, occurs in aging as well as with the use of medications that could affect gastric acidity. These include H2 blockers (cimetidine, famotidine), proton pump inhibitors (PPIs) (omeprazole, lansoprazole), and antacids (TUMS, Rolaids) (see Chapter 14). Gastric emptying rate influences the amount of time in which dissolution can occur; medications that affect gastric emptying time include prokinetics, such as metoclopramide. Any disease, injury, or surgery that affects oral intake or gastric function can affect dissolution of medications. For example, vomiting and diarrhea would certainly decrease dissolution. Gastric surgical resections or a diagnosis of 242  Part 3  Introduction to Pathophysiology

gastroparesis can dramatically change the rate of gastric emptying as well as the amount of gastric secretions (see ­C hapter 14 for a discussion of these surgical procedures). Any client who presents with this medical history will need adjustments in the form of the medication to ensure appropriate dissolution. Medications in liquid form are more easily dissolved than those in capsule or tablet form.

Effect of Nutrition on Drug Absorption  The pres-

ence of food, alcohol, or dietary supplements can interact with drugs in several important ways that interfere with drug action. If interactions with food increase absorption of medications, they increase the amount of available drug; in contrast, if absorption of a medication is decreased by food, therapeutic levels may not be achieved. The presence of food in the stomach will increase gastric emptying time (i.e., slow emptying rate), especially when a high-fat or high-fiber meal is consumed, and this could potentially affect absorption. For example, the presence of food dramatically reduces absorption of Fosamax, a medication used to treat osteoporosis. Another example is the oral diabetic drug metformin that should not be taken with foods containing guar gum, a fiber used for thickening foods, since it reduces the absorption of the drug. On the other hand, it is recommended that some medications be taken with food in order to decrease the gastric distress associated with them. Examples include amoxicillin, ketoconazole, and erythromycin. Chelation is another mechanism that affects absorption. Chelation, the binding of a nutrient or food component with a drug, makes the drug unabsorbable. For example, consumption of calcium with the antibiotic tetracycline causes chelation of the drug, which decreases absorption. Patient education should include specific guidelines for consuming a medication with or without food, if applicable.

Effect of Nutrition on Drug Metabolism  Some of the

most important nutrient–drug interactions fall into the category of metabolism changes. Research has identified several mechanisms; a summary of these findings is that, in general, some nutrients act either as an inducer or as an inhibitor for metabolic enzyme systems. These actions can change drug effectiveness as well as produce toxic side effects, which increase the potential for morbidity and mortality.15,26–28 Nutrients can also compete for carrier systems involved in normal drug metabolism. For example, a study found that St. John’s wort, an herbal supplement used to treat depression, significantly induced activity of CYP 3A4, a member of the liver’s P450 mixed-function oxidase system. Long-term use of St. John’s wort may result in diminished clinical effectiveness or increased dosage requirements for at least 50% of all marketed medications.27 These types of interactions appear to pose a much more common and serious risk than was previously recognized. The potential for nutrient–drug interactions with anticoagulation therapy, a standard component of clinical care in prevention of stroke and heart attack, provides an important illustration of how foods interrupt drug metabolism. ­Vitamin Κ improves blood clotting. When foods high in vitamin Κ or vitamin Κ supplements are ingested during the same time period as warfarin (Coumadin), a vitamin Κ antagonist, the amount of warfarin needed is increased. Vitamin Κ intake

should therefore be consistent in order to maintain the levels of warfarin within a therapeutic level. Additionally, the dietary supplements feverfew, garlic, ginkgo biloba, ginger, cayenne, and omega-3 fatty acids can also affect blood coagulation. A change in the dosage of anticoagulation drugs may be required in order to compensate for a patient’s dietary intake of these foods and supplements. This is a perfect example to highlight the importance of team communication. The pharmacist and the RDN together can optimize the patient care and minimize any risk.6 A classic example of a food–medication interaction resulting in harmful side effects is the interaction between pressor agents in foods (tyramine, dopamine, histamine, phenylethylamine) and monoamine oxidase inhibitors (MAOIs) (e.g., Nardil). This interaction can result in sudden increases in blood pressure with resulting complications.6 Box 11.2 outlines the specifics for this drug–nutrient interaction. As previously mentioned in this chapter, the interaction of drugs with grapefruit and grapefruit and other fruit juices is a common food–medication interaction. 8

BOX 11.2

Numerous drugs subject to such metabolic interactions— including statin medications used to treat hyperlipidemia, several medications used in cardiac care (talinol, nifedipine), and cyclosporines (which are immunosuppressants)— have been identified and are a targeted patient education issue for clinicians.6,7 See Table 11.2 for a summary of these interactions.

Effect of Nutrition on Drug Excretion  The pH of the urine can vary widely and is one of the most important concerns related to maintenance of consistent drug excretion. Variable urine pH can alter reabsorption of the drug, resulting in fluctuating therapeutic levels. Dietary intake, kidney and respiratory function, acid–base balance, hydration status, and the presence of disease or infection can alter urinary pH and necessitate evaluation of drug dosage. Some nutrients may compete for absorption by the renal tubules. Lithium, a drug that is used to treat bipolar disorder, is absorbed in the same site as sodium in the kidney. Excess sodium intake results in excess lithium excretion, lowering lithium blood levels below its therapeutic range.29,30

CLINICAL APPLICATIONS

Monoamine Oxidase Inhibitors and Nutrient Interactions Monoamine oxidase (MAO) is an intricate enzyme system distributed predominantly in nervous tissue, the liver, and the lungs. This enzyme system is responsible for inactivating the neurotransmitters dopamine, norepinephrine, and serotonin once they have played their part in sending messages to the brain. Monoamine oxidase inhibitors (MAOIs) are drugs that block this activity. When the excess neurotransmitters are not destroyed, they can accumulate in the brain. In addition to inactivating these neurotransmitters, MAO breaks down another amine called tyramine. When MAO is blocked by an MAOI, levels of tyramine also rise. Excess ­tyramine can cause sudden, sometimes fatal, increases in blood pressure. To avoid this life-threatening side effect, those taking MAOIs must avoid or limit foods that contain high levels of ­tyramine and other pressor agents. Tyramine occurs naturally in foods, but it is difficult to quantify the exact amounts present. Tyramine content among different brands of certain foods may vary based on processing, storage, and preparation methods. It is also formed from bacterial breakdown of protein in foods as they age. MAOIs are most often prescribed for depression and ­Parkinson’s disease. Class Antidepressants

Generic Name

Trade Names

Isocarboxazid

Marplan

Phenelzine

Nardil

Tranylcypromine

Parnate

Selegiline

Eldepryl

Rasagiline

Azilect

Foods high in tyramine that should be avoided include the following: • • • •

• •

• • • •

Fermented vegetables: such as kim chi and sauerkraut Fava beans Aged cheeses such as blue cheese, cheddar, and gorgonzola Fermented or aged meats such as chorizo, imported pepperoni, salami, corned beef, caviar, pickled herring, anchovy, meat extract, meat tenderizers, beef or chicken livers, and pate Soybeans or soy products Soy sauce, teriyaki sauce, soybean paste, fermented bean curd (fermented tofu), miso soup, tamari, natto, shoyu, and tempeh Yeast extract including Brewer’s yeast in large quantities— Marmite, Vegemite Alcoholic beverages: >16 oz beer or >4 oz red wine/day Nonalcoholic beer: >16 oz/day Coffee and other caffeinated beverages: >16 oz/day

All foods should be fresh or properly frozen. Meat products should not be refrigerated more than 3–4 days. Refrigerated cheeses should be eaten within 2–3 weeks. Combination foods like cheese crackers, submarine sandwiches, and ­stir-fried dishes containing soy sauce should be avoided. Pizza, lasagna, and other cheese-containing dishes, including desserts, may be eaten only if made with “allowed” cheeses and toppings. Source: FDA. Avoid food drug interactions. https://www.fda.gov​ /downloads/Drugs/.../GeneralUseofMedicine/UCM229033.pdf. Accessed August 21, 2018.

Chapter 11 Pharmacology  243

Table 11.2 Selected Grapefruit–Drug Interactions: Avoid or Consume Grapefruit with Caution with These Medications Drug Class

Generic

Trade Name

Antiarrhythmic

amiodarone ranolazine

Cordarone® Ranexa®

Antihistamines

fexofenadine

Allegra®

terfenadine

Seldane®

astemizole

Hismanal®

halofantrine (antimalarial)

Halfan®

primaquine (antimalarial)

No trade name

quinidine

No trade name

felodipine

Plendil®

nimodipine nisoldipine nitrendipine

Nimotop® Sular® Bayotensin

Cholesterol–lowering (HMG–CoA reductase inhibitors) (“–statins”)

lovastatin simvastatin cerivastatin

Mevacor® Zocor® Baycol®

Immunosuppressants

everolimus sirolimus cyclosporine tacrolimus

Afinitor®, Zortress® Rapamune® Neoral® Prograf®

CNS

buspirone

BuSpar®

pimozide

Orap®

ziprasidone

Geodon®

sertraline

Zoloft®

triazolam

Halcion®

quetiapine cisapride

Seroquel® Prefulside®, Propulsid® Viagra® Pletal® Entocort® None Relpax® Vepesid® Mifeprex® Ixempra® Tasigna® Procardia® Sutent® Torisel® Geodon® Vesicare® Flomax®

Anti-infective agents

Calcium channel blockers

Miscellaneous

sildenafil cilostazol budesonide colchicine eletriptan etoposide mifepristone ixabepilone nilotinib nifedipine sunitinib temsirolimus ziprasidone solifenacin tamsulosin

Sources: Elbe D. Grapefruit–drug interactions. In: Pronsky ZM, ed. Food– Medications Interactions. 17th ed. Birchrunville, PA: Food–Medication Interactions; 2015: 410–2. Bailey BG, Dresser G, Arnold JMO. Grapefruit–medication interactions: forbidden fruit or avoidable consequences? CMAJ. 2013; 185(4): 309–16.

Nutritional Complications Secondary to Pharmacotherapy The previous sections of this chapter have focused on the effect of diet and nutritional status on drug ­pharmacokinetics. The other side of nutrient–medication interactions is the effect of drug action on nutritional status. Drugs may affect 244  Part 3  Introduction to Pathophysiology

nutrient ingestion, digestion, absorption, and metabolism. The clinical expertise of the RDN is a critical component in the identification, prevention, and correction of these interactions. Team communication, once again, is crucial to optimize patient care.

Drug Consequence: Effect on Nutrient Ingestion  One only has to evaluate the possible side effects of any medication to understand their potential effect on nutrient ingestion. Nausea, vomiting, diarrhea, constipation, increased appetite, and decreased appetite are all common side effects that dramatically affect dietary intake. Further complicating this situation is the fact that many individuals are prescribed numerous medications and that most older adults take multiple medications each day.31,32 Next, consider the additive effect of OTC medications as well as herbal supplements.32 The literature tells us that the higher use of medications are related to an increase in both morbidity and mortality.32 An evaluation of 100 patients with renal disease indicated an average of one to five dietary supplements were used daily.30 Appetite and subsequent food ingestion can be affected by taste, smell, and saliva production. Many medications either increase or decrease saliva production, or even alter its consistency. For example, amitriptyline, a common antidepressant, may cause a decrease in saliva production. Since substances must be dissolved in fluid to be tasted, many clients on these medications will report difficulty eating, decreased appetite, or anorexia, ultimately due to dry mouth. Other medications may actually cause abnormal taste perception. Patients have reported experiencing metallic, salty, sweet, and simply foul tastes after taking some medications. Chemotherapy agents, analgesics (pain relievers), cardiac drugs, antibiotics, central nervous system drugs, and antifungal agents are common groups of medications that result in these patient complaints. For example, Captopril and cisplatin ingestion may result in a metallic or altered sense of taste.33 Increased appetite secondary to medications can result in unplanned weight gain. A common example is treatment with prednisone or other corticosteroids, antiseizure medications, or antidepressants. Zyprexa (olanzapine) and Clozaril (clozapine), used to treat schizophrenia, almost always result in weight gain. These medications appear to block the serotonin receptor associated with satiety, inhibit histamine and dopamine, and increase the hormone prolactin.34–36 Other antidepressant medications, such as Prozac, can result in the opposite effect: decreased appetite and weight loss. See Table 11.3 for common medications that can result in weight gain and Table 11.4 for those that can result in weight loss.

Drug Consequence: Effect on Nutrient Absorption Any drug that affects GI function has the potential to interrupt nutrient absorption. This includes medications that cause side effects such as nausea, vomiting, diarrhea, and constipation. Adequate and efficient nutrient absorption requires exposure to enzymes in the appropriate metabolic environment, adequate transit time, sufficient GI tract surface area, and any transporters necessary for absorption. Any medication that speeds gastric emptying or affects the pH of

Table 11.3 Selected Medications That May Cause Weight Gain Drug Class Antipsychotic

Generic Name clozapine olanzapine phenothiazines quetiapine risperidone paliperidone aripiprazole asenapine haloperidol ziprasidone

Trade Name Clozaril®, Fazaclo® Zyprexa® Thorazine®, Prolixin®, Trilafon® Seroquel® Risperdal® Kepivance® Abilify® Saphris® Haldol® Geodon®

Drug Class

Generic Name

Anti-hypertensive

captopril Indapamide hydralazine

Capoten® Lozol® Apresoline®

Anti-hyperlipidemia

cholestyramine

Questran®

Anti-inflammatory

mesalamine

Asacol®, Entasa®, Canasa®, Rowasa®

Anti-neoplastic

cytarabine

Cytosar–U®

aldesleukin/interleukin–2

Proleukin®

capecitabine carboplatin fluorouracil (5–FU) tamoxifen citrate

Xeloda® Paraplatin® Adrucil,® Nolvadex®, Nolvadex–D® Arimidex® Platinol–AQ® Cytoxan®, Cytoxan lyophilized® Casodex® Blenoxane® DTIC-Dome® Mutamycin® Roferon-A® Intron-A® Hydrea® Gleevec® Camptosar® Methotrexate®, Rheumatrex® Velban,® Oncovin® Navelbine®

Sources: Leslie WS, Hankey CR, Lean MEJ. Weight gain as an adverse effect of some commonly prescribed drugs: a systematic review. QJM. 2007; 100(7): 395–404. Dent R, Blackmore A, Peterson J, Habib R, Kay GP. Changes in body weight and psychotropic drugs: a systematic synthesis of the literature. PloS One. 2012; 7(6): E36889.

anastrozole cisplatin cyclophosphamide

Table 11.4 Medications That May Cause Weight Loss

bicalutamide bleomycin sulfate dacarbazine mitomycin alpha 2a alpha 2b hydroxyurea imatinib mesylate irinotecan HCL methotrexate

Drug Class

Generic Name

Trade Name

Alzheimer’s

donepezil rivastigmine galantamine

Aricept® Exelon® Reminyl®

Antiarrhythmic

digitalis digoxin hydroxychloroquine sulfate flecainide amiodarone

Digitoxin® Lanoxin® Plaquenil® Tambocor® Cordarone®, Pacerone®

venlafaxine

Effexor®, Effexor XR® Xanax® BuSpar®

Antianxiety

alprazolam buspirone Antibiotic

®

Trade Name

vinblastine sulfate vinorelbine tartrate

pramipexole

Dopar®, Larodopa® Mirapex®

Antipsychotic

loxapine

Loxitane®

Anti–Parkinson’s

levodopa

clindamycin gentamicin sulfate ethosuximide

Cleocin Garamycin® Zarontin®

Antiviral

ganciclovir sodium

Cytovene®

Calcium regulator

calcitriol

Rocaltrol®, Calcijex®

Anticonvulsant/ antiglaucoma

acetazolamide

Diamox®

Laxative

bisacodyl mineral oil

Dulcolax® Agoral plain®

Anticonvulsant/ antipanic

clonazepam

Klonopin®

Oral hypoglycemic

metformin

Glucophage®

DPP-4 inhibitors

Januvia®, ­Onglyza®, Linagliptin®

Thyroid preparations

levothyroxine sodium

Synthroid®, Levoxyl®, Unithroid®

Weight-control agent

orlistat

Xenical®, Alli® (OTC) Adipex-P®, Fastin® Ionamin® Qsymia® Meridian® Belviq® Sold under many names Sold under many names Sold under many names

Anticonvulsant

Antidepressant

bupropion fluoxetine

fluvoxamine maleate sertraline Anti-ADHD

amphetamines methylphenidate

Gout Antifungal

colchicines amphotericin B

terbinafine

®

Wellbutrin , Wellbutrin SR® Prozac®, Prozac Weekly®, Sarafem® Luvox® Zoloft® Adderall®, Dexedrine® Ritalin®, Concerta®, Metadate®, Methylin®, Vyvanse®, Quillivant®

phentermine phentermine resin phentermine–topiramate sibutramine lorcaserin benzphetamine diethylpropion phendimetrazine

None ®

Abelcet , ­AmBisome®, Amphotec®, Fungizone® Lamisil®

Sources: Pronsky ZM, Elbe D, Ayoob K. Food–Medication Interactions. 18th ed. Birchrunville, PA: Food–Medication Interactions; 2015. Weight-control Information Network (WIN), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health. Prescription Medications for the Treatment of Obesity. NIH Publication No. 07–4191. http://win.niddk.nih.gov/publications/prescription.htm.

Chapter 11 Pharmacology  245

gastric juices could therefore interfere with nutrient absorption. Multiple health complications have been identified with the chronic use of PPIs.37 For example, since calcium supplements are absorbed best in an acidic environment, the chronic use of PPIs may affect calcium absorption by decreasing stomach acidity leading to increased risk of fracture and osteporosis.38,39 Additional concerns have been raised as to the effect of chronic PPI use as to its potential effect on the gut microbiome.40 Similarly, both omeprazole and H2 blockers can impair the absorption of vitamin B12.37,41 Medications that interfere with lipid metabolism or absorption can interfere with fat-soluble vitamin absorption. Chronic use of corticosteroids, which are anti-­inflammatory and immune-suppressing medications, is a mainstay of treatment for several medical conditions, including rheumatoid arthritis, Chronic Obstructive Pulmonary Disease (COPD), and others. This class of medications results in decreased absorption of calcium from the GI tract as well as increased urinary loss of calcium. This significant drug consequence places the patient at high risk for bone fracture and osteoporosis.42

Drug Consequence: Effect on Nutrient Metabolism Drugs can interfere with macronutrient, vitamin, and mineral metabolism. For example, corticosteroids increase the rate of gluconeogenesis, resulting in hyperglycemia and increased nitrogen loss. Numerous medications interfere with vitamin and mineral metabolism. Phenytoin (Dilantin), used for treatment of seizures, inhibits both vitamin D and folate metabolism. Long-term use may result in megaloblastic anemia secondary to folate deficiency. See Table 11.5 for examples of common interactions for nutrient metabolism.

Drug Consequence: Effect on Nutrient Excretion Since most drug metabolites are excreted in urine, any drug that increases urinary output places the patient at risk for accelerated nutrient excretion as well. A classic example is potassium-wasting diuretics: use of the diuretic furosemide (Lasix) or any other medications in this class can result in hypokalemia (low serum potassium). Any medication that affects renal function in a significant way—reducing reabsorption of nutrients, for instance—can also cause excessive loss of a nutrient in the urine. An example of a tubular reabsorption deficit involves the use of immunosuppressant medications called cyclosporine (e.g., Neoral, Sandimmune, and SangCya). These medications have been associated with large amounts of magnesium loss in the urine. See Table 11.6 for examples of common medications affecting nutrient excretion.

At-Risk Populations As stated previously, it would be a daunting task to acquire a working knowledge of all potential drug–nutrient interactions. However, a study of the basic principles of pharmacology and categories of interactions reveals that certain situations—notably certain disease states, organ function changes, or treatment modalities—place individuals at risk. Furthermore, certain groups of individuals are more likely than others not only to take more medications but also to have an increased risk of improper or inadequate pharmacokinetics. Knowing these populations are at risk allows the practitioner to target them for monitoring and education.

Drug–Nutrient Interactions in the Older Adult  The older adult population represents one group with an exceptionally high risk for food–medication interactions.31,32,43,44

Table 11.5 Medications That Interfere with Nutrient Metabolism Nutrient Minerals

Drug(s)

Effect on Nutrient(s)

Diuretics (thiazides), corticosteroids, purgatives, amphotericin B (antifungal), digoxin

Potassium depletion

Cortisol, desoxycorticosterone, aldosterone, estrogen–progestogen oral ­contraceptives, phenylbutazone

Sodium and water retention

Sulfonylureas, phenylbutazone, cobalt, lithium

Impair uptake or release of iodine

Oral contraceptives, ethambutol (antitubular agent), amphotericin B (antifungal)

Lower plasma zinc, elevate copper

Corticosteroids, bisphosphonates

Calcium depletion

H2 receptor antagonists, proton pump inhibitors

Decreased absorption of iron

Laxatives

Malabsorption of electrolytes and calcium

Phenobarbital and phenytoin (Dilantin), carbamazepine

Increase metabolism of folic acid, vitamins D and K

Isoniazid (INH), hydralazine

Pyridoxine and niacin antagonists

Laxatives

General malabsorption of fat-soluble vitamins

Pyrimethamine, sulfadoxine, methotrexate, metformin, oral contraceptives, H2 receptor antagonists, proton pump inhibitors

Vitamin B12 and/or folate antagonists

Amino acids

Oral contraceptives, selective serotonin reuptake inhibitors, trazodone

Altered tryptophan metabolism

Blood glucose

Metoprolol, chlorpromazine

Increases blood glucose

Niacin

Decreases blood glucose

Vitamins

Source: Pronsky ZM, Elbe D, Ayoob K. Food–Medication Interactions. 18th ed. Birchrunville, PA: Food–Medication Interactions; 2015.

246  Part 3  Introduction to Pathophysiology

Table 11.6 Medications That Affect Nutrient Excretion Nutrient Minerals

Vitamins

Macronutrients

Drug(s)

Effect on Nutrient

Loop diuretics

Increase excretion of sodium, potassium, chloride, magnesium, calcium

Thiazide diuretics

Increase excretion of most electrolytes

Antifungals

Increase excretion of potassium

NSAIDs

Increase excretion of potassium

Caffeine

Increases sodium excretion

Calcitonin

Increases excretion of phosphorus, magnesium, potassium, chloride, and sodium; may increase or decrease excretion of calcium

Antihyperlipidemics

Increase excretion of calcium and magnesium

Antineoplastics

Increase excretion of magnesium, calcium, potassium, zinc, copper

Clonidine

Decreases excretion of sodium and chloride

Corticosteroids

Decrease excretion of sodium; increase excretion of potassium, calcium, nitrogen, zinc

Cyclosporine

Increases excretion of magnesium; decreases excretion of potassium

Digitalis

Increases urinary excretion of magnesium

NSAIDs

Increase excretion of vitamin C

Corticosteroids

Increase excretion of vitamin C

Tetracycline

Increases urinary excretion of riboflavin, folacin

NSAIDs

Increase excretion of protein

Calcitriol

Increases excretion of albumin

Antineoplastics

Increase excretion of amino acids

Note: NSAID, non–steroidal anti–inflammatory drug. Source: Pronsky ZM, Elbe D, Ayoob K. Food–Medication Interactions. 18th ed. Birchrunville, PA: Food–Medication Interactions; 2015.

There are several reasons. First, older individuals generally have the highest rate of chronic disease and are therefore prescribed the largest number of medications; this sheer volume increases risk. Furthermore, the use of OTC and complementary medications compounds the incidence of interactions. In addition, drug pharmacokinetics is affected by physiological changes that occur with aging. Decreased muscle mass and impaired cardiac, liver, and renal function all are common in older adults and can change how a drug is absorbed, metabolized, and excreted. For example, older adults may experience an exacerbation of drug-related confusion if other neurological diseases are present. Finally, compliance with drug regimens can be an important issue for this population. Financial burdens, complex regimens, or lack of proper drug education can lead to inappropriate drug dosing. Polypharmacy, a term that is often associated with the older adult population, is defined as administration of excessive drugs at one time or concurrent use of a large number of drugs, which increases the risk of interactions. Other features of polypharmacy may include the use of medications without a reason, the use of multiple medications for the same condition, the use of medications that interact with one another, the use of inappropriate dosages, the use of additional drugs to treat side effects of medications, and overall improvement when medications are discontinued.31,32,43,45,46 Protocols and clinical guidelines have been developed to prevent adverse drug effects in this population.46,47 The Beers criteria identify the medications most likely to result in adverse effects. General components of these criteria state that if a patient uses more than five drugs, is noncompliant

with medication regimens, and has a history of adverse effects, the risk of continued interactions is high.48 Box 11.3 provides guidance for prevention of adverse drug reactions in older adults.

Drug–Nutrient Interactions in Nutrition Support  The use of specialized nutrition support (SNS) is another clinical measure that poses a high risk for drug–nutrient interactions (see Chapter 7). Tube feedings have been documented to decrease absorption of some medications (e.g., warfarin, phenytoin, and tetracycline).49,50 Macronutrients present in the tube feeding may cause chelation of some medications. This is an excellent opportunity for the RDN and pharmacist to discuss interprofessional care. The following are the 2016 safe practice recommendations from the American Society for Enteral and Parenteral Nutrition regarding medication and enteral feedings:51 • Develop policies and procedures to ensure safe practices by staff across all departments involved in enteral medication preparation and administration. • Identify drug, dose, dosage form, route, and access device in the prescriber’s order. • Review by pharmacist of each medication order to determine whether the enterally administered medication will be safe, stable, and compatible as ordered. • Institute and follow nursing policies and procedures to prepare and administer each medication safely. • Provide nonsterile compounding pharmacy services to support medication preparation. Chapter 11 Pharmacology  247

BOX 11.3

LIFE CYCLE PERSPECTIVES

Prevention of Adverse Drug Reactions in Older Adults Colette LaSalle, PhD, RD  San Jose State University Adverse drug events (ADEs) are negative reactions that occur in response to administration or discontinuation of pharmacological therapy. Adverse drug reactions (ADRs), which are types of ADEs, include any harmful, unintentional drug reactions that take place at customarily prescribed doses. These reactions contribute to hospitalizations, disability, morbidity, and mortality, consequently adding billions of dollars to health care expenditures. Older patients are considered vulnerable to ADRs as a consequence of physiologic changes that accompany the aging process, a high frequency of comorbid conditions, and the large numbers of medications prescribed to them. Many ADRs result from inescapable patient eccentricities, but many others are believed to be preventable. One way to prevent ADRs is to avoid prescribing potentially inappropriate medications (PIMs), but older individuals are particularly vulnerable to ADRs due to age-related physiological changes. The Beers criteria, which are evidence-based recommendations, are some of the most commonly used methods for assessing appropriateness of prescribing medications for older patients. The most common causes of ADRs are as follows: • Decline in physiological functions that naturally occur with aging (may influence disposition of drugs) • Impaired organ function from prior disease or aging (alters drug kinetics, organ responses, and homeostatic counterregulatory drug effects) • Number of medications prescribed (probability of toxicity increases with number of medications prescribed) Noncompliance with medication regimens is another cause of ADRs in older patients. Noncompliance may be a ­result of the following: • Inadequate instructions for taking medications • Switching to alternative medical practices • Illiteracy

• Use best practices as per USP for any enteral drug preparations compounded in advance. • Do not add medication directly to an enteral feeding formula. • Administer each medication separately through an appropriate access. • Avoid mixing together different medications intended for administration through the feeding tube. • Use available liquid dosage forms only if appropriate for enteral administration. • Prepare approved immediate-release solid dosage forms of medication for enteral administration. • Use only appropriate instruments to measure and prepare enteral medication. • Use only clean enteral syringes to administer medications through enteral device. 248  Part 3  Introduction to Pathophysiology

• Poverty • Misconceptions • Inability to recall complicated medical regimens Common drug interactions identified by pharmacoepidemiological studies and summarized by Safe Medication ­Practices Canada include the following: • • • • • • • • • • • • • • •

Warfarin and NSAIDs1 Warfarin and trimethoprim–sulfamethoxazole (TMP–SMX) Warfarin and ciprofloxacin Glyburide and trimethoprim–sulfamethoxazole (TMP–SMX) Digoxin and clarithromycin Digoxin and macrolide antibiotics such as erythromycin Lithium and ACE inhibitors or loop diuretics Clopidogrel and proton pump inhibitors (PPIs) ACE inhibitors and potassium-sparing diuretics ACE inhibitors/angiotensin receptor blockers and TMP–SMX Tamoxifen and paroxetine Calcium channel blockers and macrolide antibiotics Theophylline and ciprofloxacin Phenytoin and TMP–SMX Spironolactone and TMP–SMX and nitrofurantoin

1

NSAID class does not include COX-2 inhibitors.

References 1. American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2015; 63: 2227–46. 2. Nothelle SK, Sharma R, Oakes AH, et al. Determinants of potentially inappropriate medication use in long-term and acute care settings: a systematic review. J Am Med Dir Assoc. 2017; 18: 806.e1–806.e17. 3. Leya M, Stone NJ. Statin prescribing in the elderly: special considerations. Curr Atheroscler Rep. 2017; 19: 47. 4. Welker KL, Mycyk MB. Pharmacology in the geriatric patient. Emerg Med Clin North Am. 2016; 34: 468–81. 5. Institute for Safe Medication Practices Canada. https://www.ismp -­canada.org/index.htm. Accessed August 22, 2018.

• Provide appropriate tube irrigation around timing of drug administration: • Prior to administering medication, stop the feeding and flush the tube with at least 15 mL water; administer the medication using a clean enteral syringe; flush the tube again with at least 15 mL water, taking into account the patient’s volume status; repeat with next medication; and flush the tube one final time with at least 15 mL. • Restart the feeding in a timely manner to avoid compromising nutrition status. Hold the feeding by 30 minutes or more only if separation is indicated to avoid altered drug bioavailability. • Consult with an adult or pediatric pharmacist for patients who receive medications coadministered with EN.51

11.6  NUTRITION THERAPY Nutritional Implications Any use of prescribed drugs, OTC medications, or complementary treatments has the potential to affect nutritional status, interfere with drug pharmacokinetics, and/or alter nutrient metabolism. Additionally, regulatory agencies for health care, including The Joint Commission and Centers for Medicare and Medicaid Services, require an established protocol for identification of, intervention for, and patient education for drug–nutrient interactions.

Nutrition Assessment Nutrition assessment will focus on factors that could affect absorption, distribution, metabolism, or excretion of drugs (see Chapter 3). First, the clinician should evaluate past and current medical history for any diagnosis affecting kidney, liver, or cardiac function. Baseline laboratory measurements for kidney function (blood urea nitrogen, creatinine), liver function (ALT, AST, bilirubin, alkaline phosphatase, prothrombin time), and hemoglobin A1C should then be evaluated. The medical history should identify any treatment regimens (e.g., enteral nutrition or dialysis) that may potentiate drug–nutrient interactions or adverse effects. Overall, nutritional status will need to be quantified to ensure that consistent physiological response to medications is possible. If the patient is malnourished, for example, the amount of protein-bound drug can be reduced due to hypoalbuminemia, increasing the effect of the medication. Next, all drugs, OTC medications, dietary supplements, and other complementary medical regimens should be reviewed. Patient interviews and social history should

identify any potential barriers to compliance with, understanding of, or access to medical or nutrition therapies. For each prescription drug, OTC medication, and dietary supplement, drug–drug interactions should be identified, along with any nutrition implications.6,52,53 Figure 11.4 provides an overview of the assessment process. Consider the nutrition assessment data presented in Box 11.4. Figure 11.5 outlines the factors considered during assessment of this patient’s risk for drug–­nutrient interactions. Based on this assessment, the nutrition diagnosis will be food–medication interaction 5 and the nutrition interventions will focus on modification of diet and/ or medication to reduce the risk of compromising the patient’s nutritional or health status. Interventions to optimize both drug efficacy and nutritional status include recommending appropriate timing of medication (Toprol should be taken with meals), avoiding alcohol, and avoiding foods high in potassium. The patient should be educated on specific foods high in potassium that are likely to be consumed. The last step in the nutrition care process will be to determine when and what to monitor and evaluate based on the nutrition diagnosis and intervention. If the patient in Box 11.4 is hospitalized, this evaluation might be obtained within 48 hours of his admission: 1. Diet history to evaluate consumption of potassium and alcohol and determine whether a meal was consumed when the Toprol was administered. 2. Discuss with health-care team members. 3. Review of laboratory values for serum potassium. At discharge, the patient’s knowledge of foods high in potassium may also be assessed.

Figure 11.4 Nutrient Assessment of Food–Medication Interactions Past and current medical history

Treatment regimens that may potentiate drug–nutrient interactions

Diagnoses affecting:

Kidney function Nutritional implications of medications used

Drug–drug interactions

Drug–nutrient interactions

Liver function

Biomedical assessment

Cardiac function

Kidney function

BUN Creatinine

Liver function

Glucose

ALT AST Bilirubin

Chapter 11 Pharmacology  249

BOX 11.4

CLINICAL APPLICATIONS

Assessment of a Patient at Risk for Drug–Nutrient Interactions Client History

Food-/Nutrition-Related History

AGE AND MEDICAL HISTORY 65-year-old adult male; PMH: hypertension; myocardial infarction; 4-vessel coronary artery bypass graft; type 2 diabetes mellitus; prostate cancer status post TURP; long-term use of alcohol MEDICAL DIAGNOSES Cardiac function: hypertension, previous Ml, and cardiac surgery Liver function: probable alcohol abuse Renal function: related to type 2 diabetes mellitus; hypertension

Biochemical Data, Medical Tests, and Procedures Treatment regimens that may potentiate drug–nutrient interactions: none at this time Glucose 180 mg/dL; BUN 21 mg/dL, Cr 1.2mg/dL Interpretation of data: Poor glycemic control; possible renal insufficiency

Review medication and herbal supplement use to determine the nutrition implications of the current or ordered medications. This includes determining the dosage and timing of the medications, the medical effect of the medication(s), and possible drug– drug interactions and drug–nutrient interactions.

Medication Regimen Once daily: Toprol 50 mg; Plavix 5 mg; Aspirin 325 mg; Altace 5 mg Twice daily: Metformin 1000 mg

DEFINE CURRENT DRUGS • Toprol (metoprolol)—beta-blocker used to reduce the overall workload of the heart • Plavix (Clopidogrel)—inhibits platelet aggregation; used to prevent stroke and myocardial infarction in patients with cardiac history or history of previous stroke • Aspirin—inhibits platelet aggregation; used to prevent stroke and

myocardial infarction in patients with cardiac history or history of previous stroke • Altace (ramipril)—ACE inhibitor used to treat hypertension • Metformin—oral medication prescribed for type 2 diabetes mellitus

DRUG–DRUG INTERACTIONS • Plavix and aspirin—These drugs together may increase chance of bleeding. Patients should avoid other over-the-counter medications that contain aspirin. FOOD–MEDICATION INTERACTIONS • Altace may cause hyperkalemia (high serum potassium). Patients should be instructed to avoid foods high in potassium, especially salt substitutes. • Toprol absorption increases with food intake. Daily dosages should be consistently taken with meals so that therapeutic levels can be reached. • The patient should avoid all alcohol because interactions between alcohol and both Altace and Metformin can occur.

Figure 11.5 Nutrition Assessment of Food–Medication Interactions: A Clinical Example Past and current medical history: 65 YOM

Treatment regimens that may potentiate drug–nutrient interactions: none

Diagnoses affecting:

Kidney function: type 2 DM hypertension

Nutritional implications of medications used

Drug–drug int: Toprol–Amaryl Altace–Amaryl Plavix–Aspirin

Drug–nutrient int: Altace–serum K Toprol–food Altace/Amaryl– alcohol

250  Part 3  Introduction to Pathophysiology

Liver function: probable alcohol abuse

Biomedical assessment

Cardiac function: hypertension previous MI cardiac surgery

Kidney function

Liver function

BUN: 21 mg/dL Creatinine: 1.2 mg/dL

No lab values available at this time

Glucose: 180 mg/dL

11.7 CONCLUSION The AND’s position regarding the integration of nutrition therapy and pharmacotherapy “promotes a team approach and encourages active collaboration among registered dietitians and other health care team members.” 6 This chapter has provided a foundation in the principles of pharmacology for future dietitians, which is the first step in ensuring this collaboration. If practitioners use their understanding

of the common categories for food–medication interactions to guide assessment and intervention during the nutrition care process, adverse drug, herbal/botanical, and nutritional effects can be prevented. This level of aggressive monitoring will decrease overall morbidity and mortality, maintain optimal nutritional status, prevent polypharmacy, and maximize the effect of prescribed medical and nutrition therapies.

CHAPTER REVIEW QUESTIONS 1. Match the following examples to these routes of administration. (Choose from: oral, sublingual, ­buccal, rectal, intramuscular, ­intravenous, and inhalation.)

3. Define drug distribution. Which major physiological factors can affect distribution? 4. Metabolism of drugs primarily occurs in which body organ?



a. Tablet dissolved under the tongue



b. Insulin given into the muscle



c. Dextrose given into a peripheral vein

6. How are drugs excreted? Name a disease that affects drug excretion by altering an organ’s function.



d. Asthma medication that is delivered by puffs through a breathing device

7. Define polypharmacy. Which age group is most likely to be at risk for this condition?

5. What are factors that can affect metabolism of a drug?

8. Explain the following drug–­ nutrient interactions.

a. Methotrexate causes a change in taste



b. Antacids bind phosphorus



c. Lasix increases the renal excretion of potassium



d. Phenobarbital decreases folate metabolism

2. What factors could affect the dissolution of a medicine?

REFERENCES 1. History of the FDA. FDA History Office. https://www.fda.gov/AboutFDA/History/default​ .htm. Accessed August 22, 2018. 2. Therapeutic Drug Use. National Ambulatory Medical Care Survey 2014. National Center for Health Statistics. Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/fastats​ /drug-use-therapeutic.htm. Accessed August 22, 2018. 3. Health Expenditures. National Center for Health Statistics. Centers for Disease Control and Prevention. https://www.cdc.gov/nchs/fastats​ /health-expenditures.htm. Accessed October 27, 2017. 4. Clarke TC, Black LI, Stussman BJ, et al. Trends in the use of complementary health approaches among adults: United States, 2002– 2012. National Health Statistics Reports No. 79. Hyattsville, MD: National Center for Health ­Statistics; 2015. https://www.cdc.gov/nchs/data​ /nhsr/nhsr079.pdf. 5. Academy of Nutrition and Dietetics. ­Nutrition Terminology Reference Manual (eNCPT): Dietetics Language for Nutrition Care. http://www.ncpro.org. Accessed July 31, 2018. 6. Position of the American Dietetic ­Association: Integration of medical nutrition

therapy and pharmacotherapy. J Am Diet Assoc. 2010; 110: 950–56.

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7. Backman JT, Filppula AM, Niemi M, ­Neuvonen P. Role of cytochrome P450 2C8 in drug metabolism and interactions. Pharmacol Rev. 2016; 68: 168–241.

13. Sun D, Hu M, Browing M, et al. Dissolution failure of solid oral drug products in field alert reports. J Pharm Sci. 2017; 106: 1302–09.

8. Chen M, et al. Food–drug interactions precipitated by fruit juices other than grapefruit juice: An update review. J Food and Drug Anal. 2018; https://doi.org/10.1016/j.jfda.2018.01.009. 9. Jacobson TA, Maki KC, Orringer CE, et al. National lipid association recommendations for patient-centered management of dyslipidemia: part 2. J Clin Lipid. 2015; 9S: S1–S22. 10. Sarasua SM. Opportunities for improving cardiovascular health outcomes in adults younger than 65 years with guideline-recommended statin therapy. J Clin Hypertension. 2017; 19: 850.

14. Gonzalez FJ, Coughtrie M, Tukey RH. Drug metabolism. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s: The Pharmacological Basis of Therapeutics. 12th ed. New York, NY: McGraw-Hill. http://accesspharmacy​ .mhmedical.com/content.aspx?bookid=1613&​ sectionid=102124003. Accessed August 22, 2018. 15. Chan LN. Drug-nutrient interaction in clinical nutrition. Curr Opin Clin Nutr Metab Care. 2002; 5: 327–32. 16. Herbs and Supplements. Medline Plus. http://www.nlm.nih.gov/medlineplus/druginfo​ /herb_All.html. Accessed August 22, 2018.

11. Epstein S, Cryer B, Ragi S, et al. Disintegration/dissolution profiles of copies of Fosamax (alendronate). Curr Med Res Opin. 2003; 19: 78–89.

17. Pronsky ZM, Elbe D, Ayoob K, Crowe JP, Epstein S, Roberts WH. Food ­Medication ­Interactions. 18th ed. Birchrunville, PA: Food Medication ­Interactions. 2015.

12. Perkins AC, Blackshaw ΡΕ, Hay PD, et al. Esophageal transit and in vivo disintegration of branded risedronate sodium tablets and two generic formulations of alendronic acid tablets: a single-center, single-blind, six-period crossover

18. Milton JC, Hill-Smith I, Jackson SHD. Prescribing for older people. BMJ. 2008; 336: 606–09. 19. Gonzalez FJ, Coughtrie M, Tukey RH. Pharmacogenetics. In: Brunton LL, Chabner BA,

Chapter 11 Pharmacology  251

Knollmann BC, eds. Goodman & Gilman’s: The Pharmacological Basis of Therapeutics. 12th ed. New York, NY: McGraw-Hill. http://accesspharmacy​ .mhmedical.com/content.aspx?bookid=1613&​ sectionid=102124003. Accessed August 22, 2018. 20. Padol S, Yuan Y, Thabane M, Padol IT, Hunt RH. Clinical impact of CYP2C19 polymorphism on the action of proton pump inhibitors: a review of a special problem. Int J Clin Pharmacol Ther. 2007; 45: 188; author reply 189–90. 21. Riley, KM (2007, August 16). Transcript of FDA press conference on warfarin. www.fda.gov​ /bbs/transcripts/transcript081607.pdf. 22. Wadelius M, Chen LY, Downes K, et al. Common VKORC1 and GGCX polymorphisms associated with warfarin dose. Pharmacogenomics J. 2005; 5: 262–70. 23. Cotreau MM, von Moltke LL, Greenblatt DJ. The influence of age and sex on the clearance of cytochrome P450 3A substrates. Clin Pharmacokinet. 2005; 44: 33–60. 24. Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. J Am Diet Assoc. 1995; 95: 791–97. 25. Loboz KK, Shenfield GM. Drug combinations and impaired renal function—the “triple whammy.” Br J Clin Pharmacol. 2005; 59: 239–43. 26. Tsai HH, Lin HW, Simon Pickard A, et al. Evaluation of documented drug interactions and contraindications associated with herbs and dietary supplements: a systematic literature review. Int J Clin Pract. 2012; 66: 1056–78.

31. Kim J, Parish AL. Polypharmacy and medication management in older adults. Nurs Clin N Am. 2017; 52: 457–68.

http://summaries.cochrane.org/CD000952/calcium​ -and-vitamin-d-for-treating-osteoporosis-caused​ -by-the-use-of-steroids. Accessed July 7, 2010.

32. Little MO. Updates in nutrition and polypharmacy. Curr Opin Clin Nutr Metab Care. 2017; doi: 10.1097/MCO.0000000000000425.

43. Hajjar ER, Cafiero AC, Hanlon JT. Polypharmacy in elderly patients. Am J Geriatr Pharmacother. 2007; 5(4):345–51.

33. Naik BS, Shetty, N, Maben EVS. Drug-­ induced taste disorders. Eur J Intern Med. 2010; 21(3): 240–43.

44. deSouza Silba JE, Suoza S, da Silva TB, et al. Use of herbal medicines by elderly patients: a ­systematic review. Arch Gerontol Geriatr. 2014; 59: 227–33.

34. Dayabandara M, Hanwella R, Ratnatunga S, et al. Antipsychotic-associated weight gain: management strategies and impact on treatment adherence. Neuropsychiatr Dis Treat. 2017; 13: 2231–41. 35. Verhaegen AA, Van Gaal LF. Drug-­induced obesity and its metabolic consequences: a review with a focus on mechanisms and possible ­therapeutic options. J Endocrin Invest. 2017; 40: 1165–74. 36. American Diabetes Association; American Psychiatric Association; American Association of Clinical Endocrinologists; North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004; 27: 596–601. 37. Vaezi M, Yang Y, Howden CW. Complications of proton pump inhibitor therapy. Gastroenterology. 2017; 153: 35–48. 38. Vries F, Staa T-P, Leufkens HGM. Proton pump inhibitors, fracture risk and selection bias: three studies, same database, two answers. Osteoporos Int. 2010; 22: 1641–42.

27. Fasinu PS, Bouic PJ, Rosenkranz Β. An overview of the evidence and mechanisms of herb– drug interactions. Front Pharmacol. 2012; 3: 69.

39. Yang YX, Lewis JD, Epstein S, et al. Longterm proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006; 296: 2947–53

28. Marsh J, Hager C, Havey T, Sprague S, ­Bhandari M, Bryant D. Use of alternative ­medicines by patients with OA that adversely interact with commonly prescribed medications. Clin Orthop Relut Res. 2009; 467: 2705–22.

40. Minalyan A, Gabrielyan L, Scott D, et al. The gastric and intestinal microbiome: role of proton pump inhibitors. Curr Gastroenterol Rep. 2017; 19: 42–52.

45. Rochon PA, Schmader KE, Sullivan DJ. Drug prescribing for older adults. UpToDate; 2017. https:// www.uptodate.com/contents/drug-­prescribing-for​ -older-adults. Accessed August 22, 2018. 46. Nothelle SK, Sharma R, Oakes AH, et al. Determinants of potentially inappropriate medication use in long-term and acute care settings: a systematic review. J Am Med Direct Assoc. 2017; 18: 806.e1–806.e17. 47. Levy HB. Polypharmacy reduction strategies: tips on incorporating American Geriatrics Society Beers and screening tool of older people’s prescriptions criteria. Clin Geriatr Med. 2017; 33: 177–87. 48. American Geriatrics Society 2015 Updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2015; 63: 2227–46. 49. Jory C, Shankar R, Oak K, et al. Going down the tubes! Impact on seizure control of antiepileptic medication given via percutaneous feeding tubes. Epilepsy Behav. 2017; 64: 114–18. 50. AuYeung SC, Ensom, MH. Phenytoin and enteral feedings: does evidence support an interaction? Ann Pharmacother. 2000; 34: 896–905. 51. Boullata J, Carrera A, Harvey L, et al. ASPEN safe practices for enteral nutrition therapy. J Parenter Enteral Nutr. 2017; 41: 15–103.

29. Grünfeld JP, Rossier BC. Lithium nephrotoxicity revisited. Nat Rev Nephrol. 2009; 5: 270–76.

41. Howden C. Vitamin B12 levels during ­prolonged treatment with proton pump inhibitors. J Clin Gastroenterol. 2000; 30: 29–33.

52. Sanford MG, Ryan C, Cummings AD, et al. Protocols for identifying drug-nutrient ­interactions in patients: the role of the dietitian. J Am Diet Assoc. 2002; 102: 729–30; discussion 730–31.

30. Spanner ED, Duncan AM. Prevalence of dietary supplement use in adults with chronic renal insufficiency. J Ren Nutr. 2005; 15: 204–10.

42. Homik J, Suarez-Almazor ME, Shea B, et al. Calcium and vitamin D for treating osteoporosis caused by the use of steroids. Cochrane Reviews.

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252  Part 3  Introduction to Pathophysiology

Part 4 Nutrition Therapy IN THIS PART Chapter 12 DISEASES AND DISORDERS OF ENERGY IMBALANCE

Chapter 13 DISEASES OF THE CARDIOVASCULAR SYSTEM

Chapter 14 DISEASES OF THE UPPER GASTROINTESTINAL TRACT

Chapter 15 DISEASES OF THE LOWER GASTROINTESTINAL TRACT

Chapter 16 DISEASE OF THE LIVER, GALLBLADDER, AND EXOCRINE PANCREAS

Chapter 17 DISEASES OF THE ENDOCRINE SYSTEM

Chapter 18 DISEASES OF THE RENAL SYSTEM Chapter 19 DISEASES OF THE HEMATOLOGICAL SYSTEM

Chapter 20 DISEASES AND DISORDERS OF THE NEUROLOGICAL SYSTEM

Chapter 21 DISEASES OF THE RESPIRATORY

Courtesy of Peter Madril, MS, RDN, LD

Source: Courtesy of Marcia Nelms.

SYSTEM

Chapter 22 METABOLIC STRESS AND THE CRITICALLY ILL

Chapter 23 NEOPLASTIC DISEASE Chapter 24 DISEASES OF THE MUSCULOSKELETAL SYSTEM

Chapter 25 METABOLIC DISORDERS

253

CHAPTER 12

Courtesy of Peter Madril, MS, RDN, LD

Diseases and Disorders of Energy Imbalance Marcia Nahikian-Nelms, PhD, RDN, LD, FAND The Ohio State University

LEA RNING O B JECTIV ES LO 12.1  Identify the components of energy expenditure. LO 12.2  Explain how to estimate energy requirements. LO 12.3  Discuss the pancreatic and gastrointestinal hormones that impact appetite. LO 12.4  Understand the role adipose tissue hormones have in energy balance and fat storage. LO 12.5  Explain how obesity can be assessed and identified.

254

LO 12.6  Identify how socioeconomic status can impact the likelihood of becoming overweight or obese. LO 12.7  Understand the etiology of obesity. LO 12.8  Know the adverse health effects associated with obesity and their appropriate treatments. LO 12.9  Discuss how information gathered during the nutrition assessment can be used to develop a nutrition diagnosis. LO 12.10  Identify appropriate interventions for treating obesity.

LO 12.11  Understand the importance of behavioral change therapy for weight loss. LO 12.12  Identify risk factors that can contribute to weight loss and malnutrition in older adults, infants, and children. LO 12.13  Describe the different types of eating disorders and their etiology. LO 12.14  Understand the diagnostic criteria for eating disorders. LO 12.15  Know the health risks and complications associated with eating disorders. LO 12.16  Identify treatment possibilities for eating disorders.

G LOSSARY 24-hour energy expenditure—the total amount of energy expended by a human in a 24-hour period, made up of three main components: resting energy expenditure, thermic effect of food, and physical activity–related energy expenditure adaptive thermogenesis—energy expenditure above and beyond the thermic effect of food and resting energy expenditure that is seen in response to overfeeding, traumatic injury, changes in hormonal status, and exposure to a cold environment algorithm—a finite set of well-defined instructions for accomplishing a task; given an initial state, an algorithm will terminate in a corresponding recognizable end-point anorexigenic—appetite inhibiting basal energy expenditure (BEE)—the minimum level of energy expended by the body to sustain life; it is measured in the morning when a subject is in a postabsorptive state, comfortably lying motionless in a supine position, and in a thermally neutral environment body mass index (BMI)—weight in kilograms divided by height in meters squared (BMI 5 kg ÷ m2); although technically not a body composition assessment technique, it correlates well with estimates of body composition derived from skinfold measurements and underwater weighing (hydrodensitometry) and can easily be calculated from weight and height; it is also known as Quetelet’s index, named after its developer, Adolphe Quetelet (1796–1874), a Belgian statistician, astronomer, mathematician, and sociologist; the formula for calculating BMI is: body mass index 5

weight (kg) height (m)2

developed nation—a nation that is generally regarded as one with a high standard of living, a high per capita income, a well-developed infrastructure (e.g., public utilities and systems for transport, public health, and public education), high literacy, long life expectancy, and so on, when compared with the global average developing nation—a nation that is generally regarded as one with a low standard of living, a low per capita income, a relatively

poorly developed infrastructure (e.g., public utilities and systems for transport, public health, and public education), low literacy rates, low life expectancy, and so on, when compared with the global norm direct calorimetry—a technique to determine energy expenditure using a highly sophisticated chamber capable of measuring the amount of heat released by a subject’s body through evaporation, convection, and radiation doubly labeled water—a technique to determine energy expenditure in which subjects drink a known amount of water containing two different stable isotopic forms of water: H218O and 2H2O; the rate that this water disappears from the subject’s body is used to calculate the subject’s energy expenditure estimated energy requirement (EER)—the average dietary energy intake that is predicted to maintain energy balance in a healthy adult of a defined age, gender, weight, height, and level of physical activity, consistent with good health; in children and pregnant and lactating women, the EER includes the needs associated with the deposition of tissues or the secretion of milk at rates consistent with good health iatrogenic—resulting from treatment, usually by a health care provider (in reference to an adverse condition); iatrogenic literally means “brought forth by a physician” indirect calorimetry—an approach to determine energy expenditure by measuring a subject’s oxygen consumption, carbon ­dioxide production, and minute ventilation (the amount of air a subject breathes in 1 minute) kilocalorie (kcalorie or kcal)—the amount of heat required to raise 1000 mL (1 liter) of water 1°C (1.8° F) kilojoule (kjoule or kJ)—the SI (Système International d’Unités or International System of Units) unit of measurement for energy; the amount of work required to move 1 kilogram for 1 meter with the force of 1 newton; 1 kcal = 4.2 kJ (to convert kcal to kJ, multiply kcal by 4.2) lipogenesis—the synthesis of triglyceride from carbohydrates and proteins

12.1  INTRODUCTION The purpose of this chapter is to discuss the spectrum of ­conditions and diseases associated with energy imbalance and altered weight status: overweight and obesity, ­underweight, malnutrition, and eating disorders. All these conditions ­represent significant problems that are associated with health risks. Overweight and obesity are the most common, as their incidence has increased over the past decades. Registered dietitian nutritionists (RDNs) have the potential to mitigate the negative effects of these diseases and conditions by accurately assessing them and implementing evidence-based

obesity—an excess of body fat or adipose tissue; obesity can be defined as a proportion of body weight composed of adipose tissue (percent body fat) that is greater than some standard; because it is often impractical in the clinical setting to measure the percent of body fat using body composition analysis, obesity is generally defined as a BMI ≥ 30.0 kg/m2 for adults; for children and adolescents, obesity is defined as a BMI-for-age at or above the 95th percentile using the Centers for Disease Control and Prevention (CDC) growth charts; the term obesity comes from the Latin ­obesus, meaning “one who has become plump through eating” obesogenic—promoting or encouraging the development of obesity; an obesogenic environment is one that promotes weight gain and the development of obesity by encouraging consumption of energy and discouraging physical activity orexigenic—appetite stimulating overweight—an excess of body weight in relationship to height; for adults, overweight is generally defined as a BMI of 25.0–29.9 kg/m2; for children and adolescents, overweight can be defined as a BMI-for-age-and-sex at or above the 85th percentile but less than the 95th percentile using the CDC growth charts physical activity–related energy ­expenditure—energy expended in voluntary body movement resulting from the daily activities of life, physical exercise, sports, and play, and nonvoluntary behaviors such as spontaneous muscle contractions, maintenance of posture, and fidgeting; it is the most variable component of 24-hour energy expenditure, depending on how physically active a person is resting energy expenditure (REE)—energy expended by the body at rest to keep vital organ systems including the heart, kidneys, brain, liver, and lungs functioning; it accounts for approximately 60%–75% of 24-hour energy expenditure and is roughly 1 kcal/kg body weight/hour thermic effect of food (TEF)—energy expended by the body to digest, absorb, and metabolize food; it accounts for about 10% of 24-hour energy expenditure

practices and nutrition interventions that assist individuals to obtain and maintain a healthy weight. Balancing energy intake with energy expenditure is ­e ssential to maintaining a person’s body weight within a ­desirable range. Also important are the accurate determination of a person’s energy requirements and evaluation of possible causes of an energy imbalance. Therefore, the first sections of this chapter discuss energy balance, energy requirements, and mechanisms that help regulate appetite and intake. (See Chapter 3 for more on nutrition assessment of dietary intake and comparative standards.) Chapter 12  Diseases and Disorders of Energy Imbalance   255

12.2  ENERGY BALANCE Energy Intake Humans obtain the energy and nutrients that their bodies need from the foods and beverages they consume. The human body derives energy from the oxidation of the macronutrients carbohydrate, protein, and fat and the drug alcohol. Internationally, the most commonly used unit of measurement of food energy is the kilojoule (kJ), whereas the kilocalorie (kcal) is the unit of measurement of food energy most familiar to those living in the United States. The amounts of energy released by the oxidation of carbohydrate, protein, fat, and alcohol are shown in Box 12.1. These values, rounded for the sake of convenience, initially were derived from experiments in which a small amount of each macronutrient was incinerated in a device known as a bomb calorimeter, which allowed scientists to accurately measure the amount of heat released from the macronutrient when it was burned. Today, the energy content of a food or beverage is generally determined by first measuring the amount of carbohydrate, protein, fat, and alcohol it contains using relatively simple laboratory techniques and then multiplying the number of grams of carbohydrate, protein, fat, and alcohol in the food or beverage by the energy values for each of the macronutrients shown in Box 12.1. Information on the energy and nutrient content of foods is widely available to consumers and health professionals from a variety of sources, including the Nutrition Facts labels on commercial food containers, brochures provided by fast-food restaurants, online applications, food composition tables and databases, and dietary analysis software. The USDA Food Composition Database provides extensive information on nutrient composition on all foods in the United States. See the website: https:// ndb.nal.usda.gov/ndb/.

Energy Expenditure The total amount of energy expended in one day is referred to as 24-hour energy expenditure or total energy ­expenditure, and can be divided into three major components: r­ esting energy expenditure (REE), the thermic effect of food (TEF), and physical activity–related energy expenditure. Figure 12.1 illustrates the relative proportions of each of these three ­components for the majority of people living in developed countries, where much of the work is done by labor-saving devices.

R e s t i n g E n e r g y E x p e n d i t u r e   Re sting energ y e­ xpenditure is the energy necessary to sustain life and to keep such vital organs as the heart, lungs, brain, liver, and kidneys functioning. For the average North American, REE accounts for approximately 60%–75% of 24-hour energy expenditure and is roughly 1 kcal/kg body weight/hour. Factors affecting REE are shown in Box 12.2. Of these factors, the most important determinant is lean body (or fat-free) mass, with REE being greater in persons having a higher lean body mass. Basal energy expenditure (BEE) is defined as the lowest rate of energy expenditure of an individual. It is measured in the morning when a subject is in a postabsorptive state (no food consumed during the previous 12–24 hours) and is comfortably lying motionless in a supine position (lying on one’s back) in a thermally neutral environment (a room temperature that is perceived as neither hot 256  Part 4  Nutrition Therapy

BOX 12.1

CLINICAL APPLICATIONS

Energy Content of Food Components The energy contents in kilocalories (kcal) and kilojoules (kJ) per gram for each of the macronutrients and alcohol are listed below (1 kilocalorie = 4.2 kilojoules). kcal/g

kJ/g

Carbohydrate

Food Component

4

17

Protein

4

17

Fat

9

38

Alcohol

7

29

Figure 12.1 Components of Energy Expenditure For most North Americans who are sedentary and rely on labor-saving devices to accomplish most of their work, energy expended in physical activity accounts for less than one quarter of the energy expended in a typical 24-hour period. Surprisingly, resting energy expenditure accounts for about 67% of 24-hour energy expenditure and the thermic effect of food accounts for the remaining 10%. Thermic Effect of Food 10%

Physical Activity Energy Expenditure 23% Resting Energy Expenditure 67%

nor cold). These strict conditions often make obtaining a true BEE impractical in the clinical setting. REE, on the other hand, can be measured at any time of day after a subject has quietly rested for the previous 30 minutes. BEE is generally 10%–20% less than REE.1

Thermic Effect of Food  The TEF is a measurable

increase in energy expenditure over and above REE that can be measured for several hours following a meal. The TEF is the energy required to digest, absorb, metabolize, and store the nutrients contained in foods that are consumed and to ­eliminate the resulting by-products and wastes. Originally referred to as the specific dynamic action of food, it accounts for about 10% of the 24-hour energy expenditure for a person consuming a typical mixed meal.1 The TEF of a meal is influenced primarily by the amount and macronutrient composition of the food consumed. Large meals have a greater TEF than small meals. Fat has the lowest TEF, while protein has the highest TEF due to the relatively high energy cost of processing the amino acids released from the proteins in food, including the synthesis of urea. TEF peaks at about 60–120 minutes following a meal and can last up to 4–6 hours,

BOX 12.2

CLINICAL APPLICATIONS

Factors Affecting Resting Energy Expenditure (REE) Lean Body Mass

Age

Because muscle and other lean tissues are generally more metabolically active than adipose tissue, the greater the lean body mass (also known as the fat-free mass), the greater the REE. This is the primary determinant of REE.

REE decreases about 2% for every decade after 30 years of age, even after adjusting for changes in lean body mass.

Energy Restriction

Because males tend to have a greater ­percentage of lean body mass than females, males tend to have a greater REE.

After several weeks of energy restriction, for example to lose weight, REE declines. This is at least part of the reason that, after several weeks of dieting, some people experience a decline in the rate of weight loss, a phenomenon some refer to as a “plateau.”

Body Temperature

Genetics and the Endocrine System

REE increases in persons who have a fever or an elevated body temperature.

Depending on genetic influences, some people inherit a predisposition to a

Male Sex

depending on the size and composition of the meal. TEF is generally not factored into calculations of BEE due to the high variability of its contribution to energy requirements.

PA Energy Expenditure  The most highly variable

c­ omponent of 24-hour energy expenditure is that expended in physical activity (PA). For most people in developed nations, it accounts for about 20%–25% of 24-hour energy expenditure. However, in very active individuals, such as heavy laborers and some athletes, the amount of energy expended in PA can exceed REE by twofold or more.1 PA energy expenditure is influenced by the person’s body weight, the number of muscle groups used in the activity, and the intensity, duration, and frequency of the activity. For any given activity, heavy people expend more energy than lighter weight people because heavier people have a greater body mass to move. Activities requiring multiple groups of large muscles (e.g., cross-country skiing or handball) expend more energy than those requiring fewer groups of muscles (e.g., walking or golfing). The following are PA coefficients used in the determination of energy requirements for the DRI.1 The PA represents one of four different categories of PA level: sedentary, low active, active, and very active. Energy expenditure descriptions and factors for each of these levels are as follows.1 • Sedentary: Includes BEE, the TEF, and PAs required for independent living (adult female and male PA = 1.00). • Low active: Roughly equivalent to the energy expended by a 70-kg (154-lb) adult walking 2.2 miles per day at a rate of 3–4 miles per hour (or an equivalent amount of energy expended in other activities) in addition to the activities necessary for independent living (adult female PA = 1.12; adult male PA = 1.11). • Active: Roughly equivalent to the energy expended by a 70-kg (154-lb) adult walking 7 miles per day at a rate of 3–4 miles per hour in addition to the activities related to independent living (adult female PA = 1.27; adult male PA = 1.25).

higher REE, while others are predisposed to a lower REE. Hypothyroidism and ­hyperthyroidism can dramatically decrease or increase REE, respectively. Injury and Metabolic Stress The metabolic response to illness and injury increases overall energy ­expenditure. Hormones, acute-phase ­proteins, the immune system, and altered cellular metabolism direct the ­physiological changes that c­ haracterize metabolic stress and impact energy requirements.

• Very active: Equivalent to walking 17 miles per day in addition to the activities a normal person would ordinarily engage in (adult female PA = 1.45; adult male PA = 1.48).

Estimating and Measuring Energy Requirements For a detailed discussion of estimating and measuring energy requirements in clinical practice, refer to Chapter 3 (for healthy persons) and Chapters 5 and 22 (for acute care and the critically ill). An individual’s energy requirements can either be estimated using a predictive equation or, if a more accurate determination is necessary, measured using such methods as indirect calorimetry, doubly labeled water, or direct calorimetry. For most patients in the clinical s­ etting, it is usually adequate to estimate energy requirements by means of a predictive equation that uses variables such as sex, age, weight, stature (height), and PA level or by a s­ imple ­normogram. However, in critically ill patients, it may be necessary to more accurately d ­ etermine energy requirements using indirect calorimetry. Doubly labeled water is commonly used in human m ­ etabolic research, while use of direct calorimetry is limited by the small number of research facilities having the necessary technology.

Equations  In most instances, an individual’s energy requirements are estimated using one of several empirically derived equations. Three examples are the Harris–Benedict equations developed in the early 1900s by researchers J. A. Harris and F. G. Benedict, those developed in the 1980s by the World Health Organization (WHO), and the Mifflin–St. Jeor ­equation, which was first published in 1990, all of which are shown in Table 12.1. Harris and Benedict measured the REE of 239 healthy young adult males and females using indirect calorimetry (discussed later in this chapter) and then developed a set of regression equations that best predicted REE using the variables sex, weight, stature (height), and age.2 The WHO equations were developed by a group of experts using an approach similar to Chapter 12  Diseases and Disorders of Energy Imbalance   257

Table 12.1 Examples of Equations for Estimating Resting Energy Expenditure in Healthy Persons Mifflin–St. Jeor Females Males

REE 5 10 W 1 6.25 H 2 5 A 2 161 REE 5 10 W 1 6.25 H 2 5 A 1 5

Harris-Benedict Females Males

REE 5 655.1 1 9.6 W 1 1.9 H 2 4.7 A REE 5 66.5 1 13.8 W 1 5.0 H 2 6.8 A

Schofield (Pediatrics) Females A 0–3 Females A 3–10 Females A 10–18 Males A 0–3 Males A 3–10 Males A 10–18

16.252 W 1 1023.2 H 2 413.5 16.969 W 1 161.8 H 1 371.2 8.365 W 1 465 H 1 200 0.167 W 1 1517.4 H 2 617.6 19.59 W 1 130.3 H 1 414.9 16.25 W 1 137.2 H 2 515.5

Institute of Medicine: EER equation for overweight males aged 3–18 years: EER = 114 – (50.9 × age in years) + (physical activity × [19.5 × weight in kilograms + 1161.4 × height in meters]) Male physical activity factors: • Sedentary: 1 • Low active: 1.12 • Active: 1.24 • Very active: 1.45 Estimated EER equation for overweight females aged 3–18 years: EER = 389 – (41.2 × age in years) + (physical activity × [15 × weight in kilograms + 701.6 × height in meters]) Female physical activity factors: • Sedentary: 1 • Low active: 1.18 • Active: 1.35 • Very active: 1.60

World Health Organization (WHO) Females

Males

0–3 years old 3–10 years old 10–18 years old 18–30 years old 30–60 years old .60 years old 0–3 years old 3–10 years old 10–18 years old 18–30 years old 30–60 years old .60 years old

61.0 W 2 51 22.5 W 1 499 12.2 W 1 746 14.7 W 1 496   8.7 W 1 829   9.2 W 1 637 H 2 302 60.9 W 2 54 22.7 W 1 495 17.5 W 1 651 15.3 W 1 679 11.6 W 1 879   8.8 W 1 1128 H 2 1071

W = weight in kg; H = height in cm; A = age in years. Sources: Harris JA, Benedict FG. A biometric study of basal metabolism in man. Publication No. 279. Washington, DC: Carnegie Institution of ­Washington; 1919. World Health Organization. Energy and protein requirements. Report of a joint FAO/WHO/UNU expert consultation. Technical Report Series 724. Geneva: World Health Organization; 1985. Mifflin MD, St Jeor ST, Hill LA, Scott BJ, Daugherty SA, Koh YO. A new predictive equation for resting energy expenditure in healthy individuals. Am J Clin Nutr. 1990; 51: 241–47. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: The National Academies Press; 2005. https://doi.org/10.17226/10490.

258  Part 4  Nutrition Therapy

that used by Harris and Benedict. A key difference between the two sets of equations is that the WHO equations do not include stature as a variable because it was not found to improve their predictive ability.3 The Mifflin–St. Jeor formula was derived from data from 498 healthy subjects. Both normal-weight and obese subjects were studied and REE was measured by indirect calorimetry.4 When these equations were compared using a systematic review of the literature to evaluate their accuracy in predicting resting metabolic rate (RMR) for nonobese and obese people, the Mifflin–St. Jeor equation was determined to be the most r­ eliable, predicting REE within 10% of that measured when compared to indirect calorimetry.5 An additional set of prediction equations are those ­e stablished by the Institute of Medicine (as part of its ­development of the Dietary Reference Intakes or DRIs) to calculate the estimated energy requirement (EER). See the DRI table in the back of this textbook for EER values. The EER is defined as the average dietary energy intake that is predicted to maintain energy balance in a healthy person of a defined age, gender, weight, height, and level of PA consistent with good health.1 For infants, children, and adolescents, the EER includes the energy needed for a desirable level of PA, as well as the energy needed for optimal growth and development at an ageand gender-appropriate rate that is consistent with good health, including maintenance of a healthy body weight and appropriate body composition. For females who are pregnant or lactating, the EER includes the energy needed for PA, for maternal and fetal development, and for secretion of milk at a rate consistent with good health. The EER for adults used the PA level of active as defined before. The publication Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients) includes a complete set of equations for each of the age and gender groups.1 It is important to note that the EER values apply only to persons having a healthy weight and that EER values have not been established for persons who are overweight or obese.1 Instead, the DRI Committee has developed a separate set of equations for calculating TEE for the maintenance of weight for adults aged 19 years and older who are overweight (i.e., have a body mass index (BMI) between 25.0 kg/m2 and 29.9 kg/m2) and/or obese (BMI ≥30.0 kg/m2), and an additional set was developed for children and adolescents aged 3–18 years who are obese (a BMI-for-age-and-sex ≥95th percentile).1 These equations are included in the same publication as the EERs.

Indirect Calorimetry  The gold standard approach for

measuring energy requirements in critically ill patients and in human metabolic research is indirect calorimetry.6 It is based on the fact that energy expenditure is proportional to the body’s oxygen consumption and carbon dioxide production. Expired air contains less oxygen and more carbon dioxide than inspired air. When the differences in oxygen and carbon dioxide in inspired and expired air are known and the volume of air moving through a subject’s lungs is measured, the body’s energy expenditure can be calculated. Chapter 3 provides additional detail about indirect calorimetry.

Regulation of Energy Balance and Body Weight In the simplest of terms, energy balance is defined as the condition in which calories consumed equal those expended

on a regular basis. However, the regulation of energy balance and body weight is much more complex than that basic equation alone. Research has identified multiple factors that ­influence appetite and body weight, including interactions of the n ­ ervous system and various hormones, produced by the gut, pancreas, and fat cells.7–10 Genetics also influences energy balance and body weight but is discussed later in this chapter under etiology of obesity. A decrease in energy intake and loss of body fat mass typically result in orexigenic neural and h ­ ormonal stimuli that lead to increased appetite and decreased REE. Modest increases in energy intake and increased body fat mass typically result in anorexigenic ­stimuli that lead to decreased appetite and an increase in energy expenditure known as adaptive thermogenesis.

Figure 12.2 An Adipocyte or Fat Cell Newly imported triglycerides first form small droplets at the periphery of the cell, then merge with the large, central globule. Large central globule of (pure) fat Cell nucleus

Neurochemicals That Regulate Appetite and Food Intake Appetite is influenced by a number of signals to the brain that are primarily orchestrated by the hypothalamus region, including neural signals from mouth, stomach, and small intestine during and following eating and the secretion of pancreatic and gastrointestinal hormones such as insulin, glucagon, amylin, cholecystokinin, glucagon-like peptide-1, peptide YY, and ghrelin.7–10 Pleasurable taste sensations within the mouth stimulate appetite and encourage eating. As the stomach fills, it becomes distended, stimulating stretch receptors in the stomach wall that provide neural signals to the hypothalamus that inhibit appetite. Proteins, monosaccharides, and fatty acids in the chyme (semiliquid mass of partially digested food) leaving the stomach stimulate neural and endocrine receptors in the mucosa of the small intestine, resulting in neural signals to the brain that decrease appetite and food intake, and the release of the hormones cholecystokinin, glucagon-like peptide-1, and peptide YY, which also decrease appetite and food intake.7–10 As plasma glucose level rises following a meal, the beta cells of the pancreas release insulin and amylin, which decrease appetite and food intake. During fasting, these beta cells release glucagon, which also decreases appetite and food intake.7–10 Ghrelin is a peptide hormone that is mainly produced by the stomach and stimulates appetite. Ghrelin levels are normally elevated during fasting but immediately decline following food intake. This drop in ghrelin appears to decrease appetite and food intake.7,8 However, in patients with Prader–Willi syndrome, a genetic disorder characterized by voracious appetite and massive obesity, ghrelin levels are increased by as much as threefold or fourfold compared to individuals of similar age, sex, and BMI.11 These numerous and diverse neural and hormonal signals influence the release of various peptides from the hypothalamus, resulting in the final expression of appetite and eating behavior.7

Metabolic Activity of the Adipocyte and ­Adipose Tissue The adipocyte (fat cell) is a large, rounded cell primarily filled with a droplet of triglyceride. The cytoplasm containing the nucleus, mitochondria, and other cell organelles is forced to occupy a thin layer immediately beneath the plasma membrane (see Figure 12.2).12 Throughout the body, adipocytes occur individually or in small groups joined by connective tissue.13

Cytoplasm As the central globule enlarges, the fat cell membrane expands to accommodate its swollen contents. Source: S. Rolfes, K. Pinna, and E. Whitney, Understanding Normal and Clinical Nutrition. 7th ed., copyright © 2006, p. 157.

When found in large aggregations in conjunction with fibrous connective tissue, they form adipose tissue, which serves as the storage site for more than 90% of the body’s energy reserves.7 In addition, adipose tissue fills body crevices, provides thermal insulation to the body, surrounds and shields internal organs, gives shape and form to the body, and cushions such body areas as the feet, hands, shoulders, and buttocks.13 There are two types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). The predominant type is WAT, which in reality is light yellow in color due to the presence of carotenoids. The cells of WAT store triglycerides derived from dietary fats or those synthesized from carbohydrates and proteins through the process of lipogenesis. BAT derives its color from the large number of mitochondria in the adipocytes and from its abundance of blood vessels. BAT is primarily found in fetuses, infants, and young children and accounts for up to 6% of an infant’s body weight. As humans age, the amount of BAT diminishes. In WAT, triglyceride is stored within a single large droplet, whereas in BAT, there are multiple smaller droplets. It appears that the primary function of BAT is maintaining body temperature in human neonates and in hibernating animals by generating heat through a process known as diet-induced thermogenesis or nonshivering thermogenesis. However, because of the small amount of BAT in adult humans, it has a minimal effect on energy expenditure.9,11,12 Although once thought to be a relatively inert storage site for energy consumed in excess of the body’s needs, the adipocyte is metabolically active in the uptake, synthesis, storage, and mobilization of triglycerides. There is a constant turnover of triglycerides in the adipocyte as new triglycerides are synthesized and stored and older triglycerides are hydrolyzed and released from the adipocyte into the circulation.11 Chapter 12  Diseases and Disorders of Energy Imbalance   259

Recent research has shown the adipocyte to be a metabolically active endocrine cell releasing numerous hormones involved in regulating appetite, energy balance, body fat content, and reproduction. In addition, adipocytes release numerous molecules that influence blood pressure, blood coagulation, insulin sensitivity, lipid oxidation, and serum lipid levels. In obesity, the increased release by adipocytes of several potent pro-­ inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and C-reactive protein results in a state of low-grade chronic inflammation, which appears to be linked to many of the adverse health risks discussed later in this chapter.14,15 Two hormones produced by adipose tissue that are involved in energy balance and fat storage are adiponectin and leptin. Research suggests that adiponectin signals that the body has the capacity to store fat, while leptin appears to signal that ample fat has been stored.7 Adiponectin levels increase as the body fat content decreases and decrease as the body fat mass increases.7 Increased levels of adiponectin improve the body’s sensitivity to insulin, which, in turn, enhances the body’s capacity to store fat. Higher levels of adiponectin are associated with decreased risk of coronary artery disease, whereas low levels accompany obesity and its associated health complications such as type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD). In contrast, leptin levels increase as body fat mass increases. Although understanding of this hormone is limited, it is known that leptin regulates body mass by inhibiting food intake through its action on the hypothalamus. In addition, leptin appears to regulate reproduction by promoting fertility and initiating puberty when the body’s energy stores are adequate for the demands of reproduction, and inhibiting reproduction when energy stores are inadequate.7 Adipose tissue mass increases in two ways. First, fully mature adipocytes can increase in size (undergo hypertrophy) as they accumulate more triglyceride during periods when energy intake exceeds energy expenditure. Second, adipocytes can increase in number (undergo hyperplasia) as immature adipocytes divide to produce more cells.7,9 Overweight (BMI 25.0–29.9 kg/m2) and moderate obesity (BMI 30.0– 34.9 kg/m2) are characterized by hypertrophy (enlargement) of adipocytes, and with weight loss, these enlarged adipocytes become smaller. However, as BMI approaches extreme obesity (BMI ≥ 40.0 kg/m2), adipocytes reach their maximum size and then experience hyperplasia (an increase in number). As persons with extreme obesity lose weight, the adipocytes become smaller in size, but the number of adipocytes does not decrease. The clinical implication of this fact is that overweight and moderately obese people who have experienced only fat cell hypertrophy are more successful at maintaining their weight loss than are extremely obese people who have undergone fat cell hypertrophy and hyperplasia. Achieving and maintaining a healthy body weight is more likely if an increase in fat cell number can be avoided.

12.3  OVERWEIGHT AND OBESITY Assessment and Identification of Overweight and Obesity Body Composition  Technically, obesity is an excess of adipose tissue or body fat. It can be defined as a proportion of 260  Part 4  Nutrition Therapy

body weight composed of adipose tissue (percent body fat) that exceeds a range that is considered healthy. Adult males are generally considered obese when their percent body fat is ≥25%, and adult females are considered obese when their percent body fat is ≥32%.The problem with this definition is that it requires that the body’s composition be assessed in order to determine the relative proportions of fat and lean tissue.16–22 The human body is composed of different types of ­tissues—adipose tissue or body fat, muscle, bone, blood, cartilage, ligaments, tendons, the brain and nervous tissue, and the viscera located within the thoracic and abdominal cavities. The most common approach to body composition analysis views the body as consisting of two different compartments: fat and fat free. This is referred to as the “two-compartment model.” Using this model, body composition is expressed as a ratio of fat to fat-free mass, or as a percentage of the body composed of adipose tissue or lean tissue. As discussed in Chapter 3, a variety of methods are available to clinicians for assessing body composition, and the most common of these body composition assessment methods are based on the two-compartment model. They include the following: • Skinfold measurements • Underwater weighing (hydrodensitometry) • Bioelectrical impedance analysis • Air-displacement plethysmography • Dual-energy X-ray absorptiometry (DEXA) Most clinicians do not have the time, expertise, or equipment to accurately assess body composition using the techniques just mentioned. In contrast, accurately measuring weight and height is relatively easy and quick, and the necessary equipment is inexpensive and readily available. Consequently, weight and height measurements are often used in place of body composition analysis to determine whether a person is obese. The problem with this approach is that body composition cannot be determined by merely evaluating body weight and height because these measurements cannot differentiate between the weight of the body’s lean tissue and the weight of the body’s adipose tissue.

Body Mass Index  Because it is often impractical to ­ etermine body composition in the clinical setting, and d because accurate measurements of height and weight are routine measures, obesity in adults has been historically defined as a BMI ≥30.0 kg/m2. Though not a direct measure of body fatness, BMI (also known as Quetelet’s index) can be considered a proxy for measures of body fatness and is regarded as a convenient and reliable indicator of obesity. It is reasonable to assume that for most people a high BMI (i.e., ≥30 kg/m2) represents an increased amount of adipose tissue in the body rather than unusually well-developed musculature or a large, dense skeleton. Because changes in BMI parallel changes in body composition obtained by direct measures of body fat such as underwater weighing and DEXA, it is a convenient and useful approach for tracking improvements in body composition. Therefore, BMI is used as a routine clinical approach to use in evaluating the body weights of patients.16–22 Despite this, it is imperative to also recognize

that obesity should be defined as a situation when weight can impair health.20 Overweight is a body weight in excess of some reference standard weight, usually in relation to height. In adults, overweight is generally defined as a BMI of 25.0–29.9 kg/m2, “healthy weight” is defined as a BMI of 18.5–24.9 kg/m2, and underweight is defined as a BMI < 18.5 kg/m2.16–22 For example, for an adult whose height is 5'4", a weight of 174 pounds or more would fall within the obesity weight range; for a 5'9" adult, a weight of 203 pounds or more would be considered obese. Box 12.3 discusses the calculation of BMI and shows these BMI classifications for adults. For children and adolescents, overweight is defined using the US CDC growth charts that provide the BMI-for-age percentiles for males and females 2–20 years of age (see ­Chapter 3). Using these charts, children and adolescents having a BMI-for-age ≥85th percentile but 102 cm) Women >35 in (>88 cm)

Underweight

Age 2 Overweight

BMI ≥ 85th Percentile but < 95th percentile

Obese

BMI ≥ 95th percentile

Extreme obesity

≥120% 95th percentile or ≥35 kg/m2

1

Disease risk for type 2 diabetes, hypertension, and cardiovascular disease.

2

Increased waist circumference can also be a marker for increased risk even in persons of healthy weight.

Sources: National Heart, Lung, and Blood Institute. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 2000. Styne DM, Arslanian SA, Connor EL, et al. Pediatric obesity—assessment, treatment and prevention: an Endocrine Society clinical practice guideline. J Clinc Endocrinol Metab. 2017; 102: 709–57.

BOX 12.4

LIFE CYCLE PERSPECTIVES

Interpretation of BMI in Older Adults Colette LaSalle PhD, RD  San Jose State University While body mass index (BMI) correlates with health risks in the general population, it is not without limitations. The BMI equation is potentially problematic due to its lack of sensitivity and inability to differentiate body composition. One of the main criticisms of BMI as an assessment tool is that the numerator (weight) does not distinguish among lean mass, adipose tissue, or water content. This is an important consideration when using BMI to assess older individuals because these components can change in response to the physiologic effects of aging.1,2 Older adults typically have less muscle and bone mass due to decreased hormone levels, inadequate intakes of protein and other nutrients, decreased cellular turnover, side effects of certain medications such as glucocorticoids, and/or physical inactivity. This leads to a higher proportion of adipose mass, so BMI calculations in this population will overestimate the contribution of lean mass and underestimate the proportion of adipose tissue, thus failing to capture the true risk. Older people are also more susceptible to alterations in hydration status such as edema or dehydration, which can also impact BMI results. Additionally, the denominator (height) may be decreased because of bone loss, osteoporosis, vertebral compression, or spinal curvatures (kyphosis), further compromising the validity of the BMI.3,4 A greater amount of lean mass is associated with better health status. Because a smaller proportion of body weight is composed of lean mass in older adults as compared to younger people, a higher weight (and thus BMI) corresponds to a

262  Part 4  Nutrition Therapy

healthful amount of lean tissue in this population. It is important to note that while BMIs of 18.5–24.9 are usually classified as “normal,” in people over age 65 this does not correlate with reduced risk. One meta-analysis found that those individuals over age 65 had a lower mortality risk when BMI fell between 27 and 27.9. In fact, in this population a BMI of 40 in (>102 cm)

Females

>35 in (>88 cm)

Asian Males

≥35.4 in (≥90 cm)

Females

≥31.5 in (≥80 cm)

Source: Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the obesity society. J Am Coll Cardiol. 2014; 63: 2985–3023.

that adipose tissue located within the lower body is inversely related to (i.e., lowers) risk of cardiovascular disease (CVD) and diabetes mellitus. The use of magnetic resonance imaging (MRI) or computed tomography (CT) allows for a more accurate quantification of adipose tissue within the regions of the abdomen, hips, and thighs using.24–27 .

Waist Circumference  Waist circumference of ≥40 inches

(102 cm) for men or ≥35 inches (88 cm) for women is considered predictive of obesity and chronic disease risk in Caucasian, African-American, Hispanic, and Native American populations. Within Asian populations, risk is defined at ≥90 cm in men and ≥80 cm in women. As stated previously, fat accumulation, primarily in the abdominal region (or android obesity), is linked to an increased risk of T2DM, metabolic syndrome, and other obesity-related diseases. The current recommendations from the 2013 AHA/ACC/TOS and the AACE guideline are that waist circumference should be used as a part of routine physical examination.21,22,28 See Table 12.3.

Waist-to-Hip Ratio and Waist-to-Height Ratio Alternative approaches to evaluating the impact of body fat distribution on disease risk include the waist-to-hip ratio (WHR) and the waist-to-height ratio (WHtR). The WHR is calculated by dividing the WC measurement by the hip circumference measurement. A WHR >1.0 results when WC is greater than hip circumference. The WHtR is calculated by dividing a person’s WC by his or her height. Both have been shown to better identify health risks than BMI alone.29

Epidemiology In the early 1960s, the National Center for Health Statistics launched a series of surveys examining the health and nutritional status of the U.S. population, in which participants completed questionnaires evaluating diet and lifestyle habits and underwent diagnostic and laboratory testing as well as extensive anthropometric assessment. In these surveys (initially called the National Health Examination Survey and then renamed the National Health and Nutrition Examination Survey [NHANES]), all anthropometric measurements, including height and weight, were taken by trained health technicians using standardized measuring procedures and equipment yielding highly accurate data for calculating BML.

A key finding from these surveys is that the percentage of people in the United States who are overweight or obese has increased since the early 1960s. Data from 2015 to 2016 indicate the rate of obesity was approximately 39.8% affecting more than 93 million adults.30 In children and adolescents, the rate was approximately 18.5% affecting approximately 13 million individuals aged 2–19 years.31

Socioeconomic Status: Race, Gender, and Education  There are associations between obesity and socio-

economic status measured in terms of educational level or income. Data were stratified by income (reported as a ­p overty–income ratio: 130%, between 130% and 350%, and over 350%), sex, and ethnicity. NHANES data from 2011 to 2014 indicated that obesity rates were lower in the higher income groups (31.2%) and for those with college degrees (27.8%).32 The prevalence of obesity was higher in women (38.3%) than men (34.3%). Prevalence of obesity was higher in non-Hispanic black adults (48.1%) and Hispanic adults (42.5%) and lowest in non-Hispanic Asian adults (11.7%).32

Adverse Health Consequences of Overweight and Obesity The health effects of being overweight and obese are significant. Long-term research demonstrates that the risk of developing T2DM, hypertension, stroke, CHD, sleep apnea, liver and gallbladder disease, osteoarthritis, and cancers of the endometrium, breast, prostate, and colon are all increased as people become overweight and obese.20–22,33 It is estimated that the annual medical cost of obesity in the United States is $147–$210 billion and that the lost wages associated with work-related absenteeism was an additional $4.3 billion each year.34,35

Psychosocial and Emotional Consequences  In North

America, the combination of a thin standard of beauty with fat ways of living has resulted in the current era being referred to by some as “the age of caloric anxiety.” The media are relentless in promoting the consumption of foods and beverages having a high caloric density while simultaneously advancing an “ideal” body shape that is impossible to attain for practically all females and males. Because of the strong pressures from society to be thin, overweight and obese people often suffer feelings of guilt, depression, anxiety, and low self-worth. 36,37 Furthermore, the presence of weight bias throughout our society contributes to the psychological impact for those individuals living with obesity. This includes bias amongst health professionals, which poses an important concern for RDNs to consider as a leading member of weight loss interventions.37,38

Physiological Consequences Type 2 Diabetes  T2DM is three times as prevalent among

the obese as compared with normal-weight persons. Excess body fat, especially if located within the abdominal region, elevates fasting and postprandial levels of plasma free fatty acids and is a major risk factor for metabolic syndrome. Elevated plasma free fatty acids can stimulate secretion of insulin from the beta cells of the pancreas, cause insulin resistance in Chapter 12  Diseases and Disorders of Energy Imbalance   263

peripheral tissues, inhibit cellular uptake of glucose from the blood, reduce glycogen storage, and increase hepatic glucose production, all of which lead to hyperglycemia, hyperinsulinemia, impaired glucose tolerance, and eventual development of T2DM.7,20,22 Even modest weight loss in persons with T2DM can result in dramatic improvements in blood glucose control and a reduced need for medications to control blood glucose levels (see Chapter 17).39

Hypertension  There is a strong linear relationship between BMI and blood pressure.40 Important longitudinal studies such as the Framingham Heart Study and the Nurses’ Health Study have supported this evidence. 41,42 Furthermore, there is an even higher correlation between increasing waist circumference and abdominal adiposity to high blood pressure.40 Obesity may contribute to hypertension through the release of adipocyte-related factors containing angiotensinogen and metabolites of fatty acids, both of which stimulate aldosterone secretion. D y s l i p i d e m i a   Obese adults are more likely than

­ ormal-weight adults to have elevated serum levels of total n and low-density lipoprotein (LDL) cholesterol and triglycerides, as well as lower serum levels of high-density lipoprotein (HDL) cholesterol. 22,25 The Nurses’ Health Study reported that among women, the relative risk for CHD was twice as high at BMIs of 25–28.9, and more than three times as high at BMIs of 29 or greater, compared with BMIs of less than 21.16 Elevated serum LDL-cholesterol and low serum HDL-cholesterol are major risk factors for CHD. Consequently, obesity places individuals at greater risk of CHD. Obesity results in the overproduction of very-low-density lipoprotein (VLDL) by the liver. Because the body eventually converts VLDL to LDL, increased serum levels of VLDL result in elevations of serum LDL. The prevention of the onset of obesity in early life is important for reducing the risk of CHD in later life (see Chapter 13).42,43

Hepatobiliary Disorders  The risk of gallstones

(cholelithiasis) increases with adult weight. According to the NHANES III data, the prevalence of gallstones increased more than threefold from normal BMI to the obese category.16 Central or abdominal obesity is a major risk factor for nonalcoholic fatty liver disease (NAFLD), considered the most common chronic liver condition in the Western world.44,45 Although the histological damage to the liver is similar to that seen in alcoholic liver disease, NAFLD arises from causes other than the consumption of alcoholic beverages. Although generally asymptomatic, NAFLD can range from simple steatosis (increased accumulation of fat in the hepatocytes) to nonalcoholic steatohepatitis (steatosis with inflammation and necrosis of the hepatocytes), and eventual liver failure. NAFLD is a fairly recent health concern, being first described in the 1950s. Risk factors associated with NAFLD include central obesity, T2DM, dyslipidemia, and metabolic syndrome.44,45

Cancers  The American Institute for Cancer Research states that aside from smoking cessation, maintaining a healthy weight is the most important factor to prevent cancer. 46 Research consistently supports our understanding that obesity is a significant risk factor for death from cancer generally 264  Part 4  Nutrition Therapy

and from cancer in several specific sites. Obesity in males is associated with increased death from cancer of the esophagus, rectum, pancreas, liver, and prostate. In females, obesity increases risk of death from cancer of the gallbladder, bile duct, breast, endometrium, cervix, and ovaries.46

Reproductive Disorders  Obesity is associated with reproductive disorders in both sexes. In males, obesity is associated with gynecomastia (enlarged mammary glands in the male), hypogonadism, reduced testosterone levels, and elevated estrogen levels. In females, obesity is associated with menstrual abnormalities (particularly in those with abdominal or central body fat distribution) and polycystic ovarian syndrome (PCOS), a common endocrine disorder affecting 5%–10% of females of reproductive age. Approximately 50% of women diagnosed with PCOS are obese. The disorder is characterized by menstrual irregularities, acne, excess body hair, male-pattern hair loss, and a chronic failure to ovulate leading to infertility.47 Box 12.5 provides additional information on the health consequences of overweight and obesity.

Etiology of Obesity Obesity develops when the body’s chronic energy intake exceeds its energy expenditure. At first glance, this may seem simple and straightforward. However, because of the multiple and complex neuroendocrine and metabolic systems influencing energy intake and energy expenditure, obesity is actually a heterogeneous group of disorders. Its etiology remains elusive, and its successful, long-term treatment is difficult.7,20 Among the key factors contributing to obesity are specific medical and psychiatric disorders or their treatment, genetics, and an obesogenic environment that promotes a high energy intake and discourages PA.48,49

Additional Etiology  Obesity can result from a specific

medical disorder such as Cushing’s syndrome, hypothyroidism, or Prader–Willi syndrome, but these are relatively rare. Certain pharmacologic agents (see Table 12.4) are also associated with weight gain (which is then categorized as i­ atrogenic, or “brought forth by a physician”).7,20 Because nicotine in tobacco smoke increases 24-hour energy expenditure by about 10%, smoking cessation results in a normalization of energy expenditure and a tendency for people to gain weight. In addition, some people tend to snack more and drink more alcoholic beverages after they quit smoking. Compared to the males and females who continue to smoke, males who quit smoking gain an additional 9.7 lb (4.4 kg) over 10 years and females who quit smoking gain 11 lb (5.0 kg) over a 10-year period.50

Genetic Effects on Body Weight Obesity has a clear link to genetics, demonstrated by numerous studies showing that obesity persists in families even where food intake and PA patterns differ. However, the escalating obesity epidemic in recent decades supports the idea that, while susceptibility to obesity is genetically and epigenetically determined, the development of obesity itself is the result of a susceptible genome in the presence of a conducive environment. In other words, placing susceptible individuals in an obesogenic environment—one characterized by plentiful energy-dense, high-fat foods and technological advances requiring little in the way of PA—results in obesity.

BOX 12.5

CLINICAL APPLICATIONS

Health Consequences of Overweight and Obesity Premature Death

Arthritis

• An estimated 300,000 deaths per year in the United States may be attributable to obesity. • The risk of death rises with increasing weight. • Even moderate weight excess (10–20 pounds for a person of average height) increases the risk of death, particularly among adults aged 30–64 years. • Individuals who are obese (BMI >30 kg/m2) have a 50%–100% increased risk of premature death from all causes, compared to individuals in the healthy weight range (BMI 18.5–24.9 kg/m2).

• For every 2-pound increase in weight, the risk of developing arthritis is increased by 9%–13%. • Symptoms of arthritis can improve with weight loss.

Heart Disease • The incidence of heart disease (myocardial infarction, congestive heart failure, sudden cardiac death, angina, and abnormal heart rhythm) is increased in persons who are overweight or obese (BMI >25 kg/m2). • High blood pressure is twice as common in adults who are obese as in those who are at a healthy weight. • Obesity is associated with elevated serum triglycerides and decreased serum HDL-cholesterol.

Diabetes • A weight gain of 11–18 pounds increases a person’s risk of developing type 2 diabetes to twice that of individuals who have not gained weight. • Over 80% of people with type 2 diabetes are overweight or obese.

Cancer • Overweight and obesity are associated with an increased risk of some types of cancer including endometrial, colon, gallbladder, prostate, kidney, and postmenopausal breast cancer. • Women gaining more than 20 pounds from age 18 to midlife double their risk of postmenopausal breast cancer, compared to women whose weight remains stable.

Breathing Problems • Sleep apnea is more common in obese persons. • Obesity is associated with a higher prevalence of asthma.

Reproductive Complications • Obesity is associated with increased risk of menstrual abnormalities and polycystic ovarian syndrome (PCOS) in females and reduced levels of testosterone, increased levels of estrogen, and gynecomastia (enlarged mammary glands) in males. • Obesity during pregnancy is associated with an increased risk of fetal and maternal death and increases the risk of maternal high blood pressure tenfold. • In addition to many other complications, women who are obese during pregnancy are more likely to have gestational diabetes and problems with labor and delivery. • Infants born to women who are obese during pregnancy are more likely to have high birth weights and, therefore, are more likely to be delivered by Cesarean section and experience hypoglycemia, which can be associated with brain damage and seizures. • Obesity during pregnancy is associated with an increased risk of birth defects, particularly neural tube defects such as spina bifida. • Obesity in premenopausal women is associated with irregular menstrual cycles and infertility.

Additional Health Consequences • Overweight and obesity are associated with increased surgical risk as well as increased risks of gallbladder disease, nonalcoholic fatty liver disease, incontinence, and depression. • Obesity can affect the quality of life through limited mobility and decreased physical endurance as well as through social, academic, and job discrimination.

Children and Adolescents • The most immediate consequence of overweight, as perceived by children themselves, is social discrimination.

• Risk factors for heart disease, such as hyperlipidemia and hypertension, occur more frequently in overweight and obese individuals than those in the healthy weight range. • The prevalence of type 2 diabetes, often considered a disease primarily affecting adults, has increased dramatically in children and adolescents. Overweight and obesity increase the risk of type 2 diabetes. • Overweight adolescents have a 70% chance of becoming overweight or obese as adults. This increases to 80% if one or more parent is overweight or obese.

Benefits of Weight Loss • Weight loss as modest as 5%–15% of total body weight in a person who is overweight or obese reduces the risk of certain diseases, particularly heart disease. • Weight loss can result in lower blood pressure, lower blood glucose, and improved serum lipid and lipoprotein levels. • A person with a BMI >25.0 kg/m2 may benefit from weight loss, especially if he or she has other health risk factors such as high blood pressure or elevated lipid and lipoprotein levels, is a cigarette smoker, has diabetes, has a sedentary lifestyle, or has a personal and/or family history of heart disease. Sources: U.S. Department of Health and Human Services. The Surgeon General’s Call to Action to Prevent and Decrease Overweight and Obesity. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, Office of the Surgeon General; 2001. Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the obesity society. J Am Coll Cardiol. 2014; 63: 2985–3023. Garvey WT, Mechanick JL, Brett EM, et al. American Association of Clinical Endocrinologists and American College of Endocrinology comprehensive clinical practice guidelines for medical care of patients with obesity. Endocr Pract. 2016; 22: 843–84. Styne DM, Arslanian SA, Connor EL, et al. Pediatric obesity—assessment, treatment and prevention: An Endocrine Society clinical practice guideline. J Clinc Endocrinol Metab. 2017; 102: 709–57.

Chapter 12  Diseases and Disorders of Energy Imbalance   265

Table 12.4 Medical Conditions and Pharmacologic Agents Known to Cause Obesity Congenital Causes • Prader–Willi syndrome

• Alstrom syndrome

• Down syndrome

• Cohen syndrome

• Bardet–Biedel syndrome

• Carpenter syndrome

Neuroendocrine Disorders • Cushing’s syndrome

• Polycystic ovary syndrome

• Hypothalamic disorders

• Growth hormone deficiency

• Hypothyroidism Pharmacologic Agents (Examples) Indication or class

Weight gain associated with use

Weight loss or weight neutrality associated with use

Antidepressants, mood ­stabilizers, MAO inhibitors

Amitriptyline, doxepin, imipramine, nortriptyline, trimipramine, mirtazapine, fluoxetine

Bupropion, nefazodone, fluoxetine (short term), sertraline (2 years of age, the AAP suggests to limit media to less than 1 hour per day. It is recommended to have no screen time during meals or up to 1 hour prior to bedtime.59 The majority of scientific evidence suggests that the high prevalence of overweight in developed countries is more a function of excessive energy intake than of low activity level. However, increased PA is important for the long-term prevention of weight gain and management of healthy body weight and should be included as a component of every nutrition intervention for treatment of overweight and obesity. The choices an individual makes about energy expenditure have an important impact on his or her body weight. However, an individual’s environment is an important factor influencing that person’s behavior, either by facilitating or impeding regular PA. In addition to encouraging energy consumption, the current obesogenic environment in North America and throughout the developed world discourages expenditure of energy, and is widely regarded as a causal factor in the increased prevalence of obesity in North America in the past several decades. For example, most areas in the United States and Canada have been designed to be accessed by motor vehicles with little thought, if any, given to the needs of pedestrians or bicyclists. For many people, PA is impeded by an environment lacking convenient, pleasant, and safe areas for walking, bicycling, or other forms of recreation. Urban sprawl and lack of public transportation force most to resort to the automobile for commuting to work and school, and for shopping for food and other items. There is a growing awareness among researchers and public health experts that successfully addressing the problem of overweight and obesity will require identifying feasible ways to cope with and to change the current environment. A first step in this process would be to give people strategies to better manage within the current environment and to better resist the many factors promoting weight gain. A second, long-term approach would be to build an environment that is more conducive to the adoption and maintenance of healthy dietary and exercise habits.60–63 The Academy of Nutrition and Dietetics position paper states: “For weight maintenance the RDN should encourage physical activity as part of a comprehensive weight-­ management program, individualized to gradually accumulate 200 to 300 minutes or more of physical activity per week, depending on intensity, unless medically contra- indicated.”60 The Physical Activity Guidelines for Americans recommend a minimum of 150 minutes of moderate-­intensity PA combined with muscle strengthening exercises on at least 2 days per week.61 Table 12.5 outlines the specific recommendations from these guidelines. The RDN should provide PA guidance when counseling for weight loss. The scope of practice for dietitians prevents the provision of an exercise prescription unless additional education and training is pursued (fitness certification or educational training in exercise science).64 This is an excellent example of how essential team based care

is for obesity treatment where success is supported by a full team of professionals including medicine, exercise science, dietetics and psychology. PA guidance is provided for healthy or medically cleared individuals by the RDN within the context of nutrition assessment. Questions are asked to understand the patient’s current PA level, goals for PA, and readiness to change. The PA readiness questionnaire can be used to determine patient readiness for activity and the types of question to be used in assessment are included to assess current exercise habits. Comparing the individual to the current PA national guidelines will provide an important starting step to provide guidance.62,63 See Table 12.5.

Table 12.5 Physical Activity Guidelines for Americans Age

Recommendations

3-5 years

Encourage active play (light, moderate, or vigorous intensity) and aim for at least 3 hours per day.

6–17 years

Children and adolescents should do 60 minutes (1 hour) or more of physical activity daily. • Aerobic: Most of the 60 or more minutes a day should be either moderate-[a] or vigorous-intensity[b] aerobic physical activity, and should include vigorous-­ intensity physical activity at least 3 days a week. • Muscle-strengthening:[c] As part of their 60 or more minutes of daily physical activity, children and adolescents should include muscle-strengthening physical activity on at least 3 days of the week. • Bone-strengthening:[d] As part of their 60 or more minutes of daily physical activity, children and adolescents should include bone-strengthening physical activity on at least 3 days of the week. • It is important to encourage young people to participate in physical activities that are appropriate for their age, that are enjoyable, and that offer variety.

18–64 years

• All adults should avoid inactivity. Some physical activity is better than none, and adults who participate in any amount of physical activity gain some health benefits. • For substantial health benefits, adults should do at least 150 minutes (2 hours and 30 minutes) a week of moderate-­intensity, or 75 minutes (1 hour and 15 minutes) a week of vigorous-intensity aerobic physical activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity. Any length of activity period appears to contribute to health benefits. • For additional and more extensive health benefits, adults should increase their aerobic physical activity to 300 minutes (5 hours) a week of moderate-­ intensity, or 150 minutes a week of vigorous-­ intensity aerobic physical activity, or an equivalent combination of moderate- and vigorous-intensity activity. Additional health benefits are gained by engaging in physical activity beyond this amount. Adults should also include muscle-strengthening activities that involve all major muscle groups on 2 or more days a week. (continued)

Chapter 12  Diseases and Disorders of Energy Imbalance   269

Table 12.5 Physical Activity Guidelines for Americans (continued) Age 65 years and older

Recommendations *Older adults should follow the adult guidelines. When older adults cannot meet the adult guidelines, they should be as physically active as their abilities and conditions will allow. *Older adults should do exercises that maintain or improve balance if they are at risk of falling. Older adults should determine their level of effort for physical activity relative to their level of fitness *Older adults with chronic conditions should understand whether and how their conditions affect their ability to do regular physical activity safely.

a) Moderate-intensity exercise: aerobic activity that increases heart rate and breathing to some extent. b) Vigorous-intensity physical activity: aerobic activity that greatly increases a person’s heart rate and breathing c) Muscle-strengthening activity: physical activity, including exercise that increases skeletal muscle strength, power, endurance, and mass. d) Bone-strengthening activity: physical activity that produces an impact or tension force on bones, which promotes bone growth and strength. Sources: Physical Activity Guidelines Advisory Committee. 2018 Physical Activity Guidelines Advisory Committee Scientific Report. Washington, DC: U.S. Department of Health and Human Services, 2018. U.S. Department of Health and Human Services. 2008 Physical Activity Guidelines for Americans. Washington, DC: U.S. Department of Health and Human Services; 2008. ODPHP Publication No. U0036. http://www. health.gov/paguidelines. Accessed July 24, 2018. U.S. Department of Health and Human Services. Office of Disease Prevention and Health Promotion. Dietary Guidelines for Americans 2015–20. http://www.health.gov/dietaryguidelines/. Accessed July 27, 2018.

When an individual presents with a BMI that places them as overweight or obese, an initial medical evaluation for comorbidities should occur The degree of obesity and the presence of complications will then guide the decision making for medical and nutritional interventions. These can include lifestyle modifications (diet, PA, and behavioral therapies), the use of pharmacological agents, and the consideration of bariatric surgery. Table 12.6 and Figure 12.4 demonstrate the algorithm of care supported by these evidence-based guidelines.21,22

Pharmacologic Treatment  Drug therapy can be an

adjunct to diet, PA, and behavior therapy in patients whose BMI is ≥30 kg/m2 or in patients whose BMI is ≥27 kg/m2 and who have obesity-related risk factors or diseases.20,21,22 Prescription drugs, approved for obesity treatment act by different mechanisms, are recommended for different use durations and can produce a wide variety of side effects.

Table 12.6 A Guide to Selecting Treatment of Overweight and Obesity Combined therapy with a low-calorie diet (LCD), increased physical activity, and behavior therapy provides the most successful intervention for weight loss and weight maintenance. Consider adjunctive therapies (pharmacotherapy and/or bariatric surgery) if weight loss is 27 and patient is unable to lose weight or sustain weight loss

Comprehensive lifestyle treatment: energy deficit with diet and physical activity and behavioral therapy

Monitor BMI

With comorbidities

With comorbidities Consider pharmacotherapy BMI 35.0

Comprehensive lifestyle treatment: energy deficit with diet and physical activity and behavioral therapy

Consider bariatric surgery if not responsive to behavioral treatment (with or without pharmacotherapy)

With comorbidities Consider pharmacotherapy Sources: Jensen MD, Ryan DH, Apovian CM, et.al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Obesity Society. J Am Coll Cardiol. 2014; 63: 2985–3023. http://circ.ahajournals.org/content/suppl/2013/11/07/01 .cir.0000437739.71477.ee.DC1.html. Accessed August 28, 2018

Figure 12.4 An Algorithm for the Treatment of Overweight and Obesity The American Association of Clinical Endocrinologists and American College of Endocrinology provide an example of evidence-based guideline for obesity evaluation and treatment.

AACE/ACE Algorithm for the Medical Care of Patients with Obesity Patient Presentation

Screen positive for overweight or obesity BMI ≥ 25 kg/m2 (≥23 kg/m2 in some ethnicities)

Medical history Physical examination Clinical laboratory Review of systems, emphasizing weight related complications Obesity history: graph weight vs age, lifestyle patterns/preferences, previous interventions

Diagnosis

Evaluation

Confirm that elevated BMI represents excess adiposity Measure waist circumference to evaluate cardiometabolic disease risk

Anthropometric Diagnosis

BMI kg/m2 25–29.9 OVERWEIGHT

< 25

NORMAL WEIGHT

Clinical Diagnosis

Diagnostic Categories

Presence of weight-related disease or complication that could be improved by weight- loss therapy

< 23 in certain ethnicities

Checklist of Obesity-Related Complications

None

Mild to Moderate

Severe

STAGE 0

STAGE 1

STAGE 2

No complications

OVERWEIGHT BMI 25–29.9 OBESITY BMI ≥ 30

Phases of Chronic Disease Prevention and Treatment Goals

PRIMARY Prevent overweight/obesity

Healthy meal plan

Treatment Based on Clinical Judgment

Follow-Up

Physical activity Health education Built environment

≥ 30 OBESITY

(staging and risk stratication based on complication-specic criteria)

Waist circumference below regional/ethnic cutoffs

NORMAL WEIGHT (no obesity)

|

SECONDARY Prevent progressive weight gain or achieve weight loss to prevent complications

One or more mild-tomoderate complications or may be treated effectively with moderate weight loss

At least one severe complication or requires more aggressive weight loss for effective treatment

BMI ≥ 25

BMI≥25

TERTIARY Achieve weight loss sufficient to ameliorate the complications and prevent further deterioration

Lifestyle/behavioral therapy

Lifestyle/behavioral therapy

Lifestyle/behavioral therapy

Consider pharmacotherapy if lifestyle alone not effective

Consider pharmacotherapy (BMI ≥27)

Add pharmacotherapy (BMI ≥27) Consider bariatric surgery (BMI ≥35)

Once the plateau for weight loss has been achieved, re-evaluate the weight-related complications. If the complications have not been treated to target, then weight loss therapy should be intensified or complication-specific interventions need to be employed. Obesity is a chronic disease and the diagnostic categories for obesity may not be static. Therefore, patients require ongoing follow-up, re-evaluation, and long-term treatment.

Abbreviation: BMI = body mass index

There are currently nine FDA-approved medications for use in obesity treatment. These currently include benzphetamine, phentermine, diethylpropion, orlistat, lorcaserin, phendimetrazine, phentermine/topiramate, naltrexone/ bupropion, and liraglutide.21,22 Table 12.7 reviews each of

these for mechanism and potential side effects. In addition to these FDA-approved obesity drugs, other prescription drugs including bupropion (an antidepressant) and metformin (a biguanide used to treat T2DM) have also been used to promote weight loss. Chapter 12  Diseases and Disorders of Energy Imbalance   271

Table 12.7 Medications Approved for Use in Obesity Treatment Drug

Mechanism of action

Common Side Effects

Orlistat

Pancreatic lipase inhibitor

Steatorrhea, oily spotting, fecal urgency, fecal incontinence

Lorcaserin

5-HT2 serotonin agonist: reduces food intake

Headache, dizziness, nausea, dry mouth, fatigue, constipation

Phentermine– topiramate ER

Sympathomimetic anticonvulsant: reduces food intake

Insomnia, dry mouth, constipation, paresthesias, dizziness, dysgeusia

Naltrexone SR– bupropion SR

Opioid receptor antagonist: reduces food intake

Nausea, constipation, headache, vomiting, dizziness

Liraglutide

GLP-1 receptor agonist: reduces food intake

Nausea, vomiting, diarrhea, constipation, headache, dyspepsia, fatigue, dizziness, abdominal pain

Sources: Apovian CM, Aronne LJ, Bessesen DH, et al. Pharmacologic management of obesity: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2015; 100: 342–62. Ryan DH, Kahan S. Guideline recommendations for obesity management. Med Clin North Am. 2018; 102: 49–63. National Institute of Diabetes and Digestive and Kidney Diseases. https:// www.niddk.nih.gov/health-information/weight-management/prescription -medications-treat-overweight-obesity. Accessed July 27, 2018.

Bariatric/Metabolic Surgical Interventions  Bariatric/

metabolic surgical interventions for obesity have not only increased in use but have also led to important changes in comorbidities. There have been demonstrated improvements in sleep apnea, high blood pressure, hepatic steatosis after bariatric surgery, and subsequent weight loss.67–70 For morbidly obese patients with T2DM, bariatric surgery is considered superior to standard medical treatment.70 Bariatric surgical procedures are considered treatment options in both the adult population and for a select group of pediatric/adolescent patients.21,71

Patient Selection For adults, qualifications for bariatric surgery include BMI ≥ 40, or more than 100 pounds overweight; BMI ≥35 and at least one or more obesity-related comorbidities such as T2DM, hypertension, sleep apnea and other respiratory disorders, nonalcoholic fatty liver disease, osteoarthritis, lipid abnormalities, gastrointestinal disorders, or heart disease and inability to achieve a healthy weight loss sustained for a period of time with prior weight loss efforts.21,22 Adolescents who are BMI ≥35 kg/m2 or 120% of the 95th percentile with clinically significant comorbid conditions such as obstructive sleep apnea (AHI >5), T2DM, idiopathic intracranial hypertension, severe nonalcoholic steatohepatitis, Blount’s disease, slipped capital femoral epiphysis, gastroesophageal reflux disease (GERD), or hypertension; or BMI ≥40 kg/m2 or 140% of the 95th percentile (whichever is lower). A multidisciplinary team must also consider whether the patient and family have the ability and motivation to adhere to recommended treatments pre- and postoperatively, including consistent use of micronutrient supplements. Factors that would be a contraindication for surgery in adolescence would be the following: a 272  Part 4  Nutrition Therapy

medically correctable cause of obesity; an ongoing substance abuse problem (within the preceding year); and a medical, psychiatric, psychosocial, or cognitive condition that prevents adherence to postoperative dietary and medication regimens or a current or planned pregnancy within 12–18 months of the procedure.71 For all bariatric and metabolic surgical procedures, a board certified surgeon in bariatric surgery as well as the use of an interdisciplinary team for both pre-/postoperative care is recommended. The primary bariatric surgical procedures used in the United States can be classified as either restrictive (limits the volume of food that ultimately enters the small intestine for digestion and absorption) or malabsorptive (bypasses portions of the small intestine so that less digestion and absorption can occur) or a combination of both. The four most common procedures are the following: • Roux-en-Y gastric bypass (RYGB): restrictive and malabsorptive • Laparoscopic vertical sleeve gastrectomy (LVSG): restrictive • Laparoscopic adjustable gastric banding (LAGB): restrictive • Duodenal switch, biliopancreatic diversion (DS-BPD): malabsorptive (slight level of restriction) (See Figure 12.5.) The RYGB is the most common procedure in the United States accounting for 60%–70% of all bariatric procedures. Weight loss is achieved by decreasing food intake, increasing satiety, and decreasing absorption. There are dramatic improvements in diabetes, sleep apnea, hypertension, cancer, and CVD risk. This procedure creates a small (20–30 mL) pouch at the top of the stomach, restricting food intake and causing easy satiety. The path for ingested food then bypasses remainder of the stomach, the duodenum, and first part of the jejunum. This ultimately reduces food digestion and nutrient absorption. The jejunum is cut and the distal end (roux limb) is surgically connected to the pouch that creates a bypass for a portion of the small intestine; thus, decreasing absorption of nutrients. The proximal end of the jejunum that drains the stomach and duodenum is anastomosed to a lower segment of the jejunum allowing secretions from the stomach, liver, gallbladder, and pancreas to eventually enter the jejunum and mix with the food contents leaving the pouch.21,22,24 The LVSG is considered a restrictive procedure. Up to 85% of the stomach is surgically removed, leaving a narrow, tubular, banana-shaped portion of the stomach between the esophagus and duodenum. The remaining portion of the stomach restricts capacity to 50–150 m. The procedure leaves the pylorus intact, and therefore there is minimal nutrient malabsorption. The detached section of the stomach is the area that is primarily responsible for the release of ghrelin. Earlier in this chapter, ghrelin was discussed as a neuropeptide that stimulates appetite. It appears that weight loss from this procedure is further enhanced by lower serum levels of ghrelin found in these patients.21,22,24 The LAGB procedure is also considered a restrictive procedure in that it also creates a smaller initial pouch for food consumption. A silicone ring or band is laparoscopically introduced into the abdominal cavity and secured around the

Figure 12.5 The Four Most Commonly Used Surgical Procedures for Weight Loss (a) Adjustable gastric banding; (b) vertical sleeve gastrectomy; (c) Roux-en-Y gastric bypass; (d) duodenal switch with biliopancreatic diversion

Gastric pouch (30 mL capacity)

Stomach (50–150 mL capacity) capac city ity))

Adjustable gastric band

Small intestine

Access port (placed under the skin)

Small intestine S

(a)

(b)

Stomach (50–150 150 0 mL capacity) capac pac city ity))

Gastric pouch (20–30 mL capacity)

Biliopancreatic limb

Roux limb

Biliopancreatic limb Alimentary limb Common channel

(c)

upper part of the stomach. This creates a small pouch with a narrow opening at the bottom of the pouch. Food passes through narrow opening into the rest of the stomach. Band is connected by a tube to an access port that is placed under the skin of the abdomen and is inflated when saline is injected into the access port using a syringe. Inflation of the band can be adjusted. As inflation occurs, the opening becomes narrower so that it delays the emptying of the pouch. This gives the patient a sensation of fullness or satiety. This procedure restricts the amount of food that can be consumed at one time. It initially has capacity of 30 mL but can stretch up to 90 mL. This procedure is the simplest from a technical sense and is least invasive. Despite a slower rate of weight loss, outcome data indicate that over time LAGB appears to have comparable weight loss results to the RYGB. 21,22,24 In the DS-BPD procedure, the intestinal pathway is rerouted to separate the flow of food from the flow of bile and pancreatic juices which inhibits the absorption of

Common channel

(d)

energy-yielding nutrients. This procedure is the most technically complicated and is less commonly performed. It yields the greatest rate of weight loss and, therefore, is typically used for those individuals with BMI >50. The procedure is conducted in two stages. The first stage involves using an LVSG to support the initial weight loss. This initial weight loss will reduce potential complications when second stage is performed. In the second stage of the procedure, the distal part of the small intestine is surgically anastomosed to the stomach. Secretions from the liver, gallbladder, and pancreas are rerouted allowing them to enter the small intestine for their subsequent use in digestion and absorption.21,22,24 Long-term outcomes for bariatric surgery in adults indicate that there is a greater overall weight loss for those who are treated with surgery and has a greater impact on the treatment for T2DM, dyslipidemia, and hypertension. 67–70,72,73 Evaluation of outcomes in a cohort of 544 adolescents indicated the largest weight loss occurred with the RYGB and Chapter 12  Diseases and Disorders of Energy Imbalance   273

LVSG with −29% to 25% were estimated three years after surgery. The lowest amount of weight loss occurred with the LAGB with −8% to −10% changes in BMI.74 Newer procedures for treating obesity include the use of intragastric balloons that received FDA approval in 2015. In one study comparing intragastric balloon to diet and exercise, the intragastric balloon resulted in significantly greater weight loss (25% vs. 10% change in weight loss).75

Preoperative care  Since early 2000, the Enhanced Recov-

ery after Surgery (ERAS) society has attempted to build protocols that promote steps for improving surgical outcomes. The rationale for the ERAS protocols include, in part, ­nutrition-related steps to minimize starvation by reducing the time spent nil per os (NPO) both pre- and postoperatively, decrease the metabolic stress induced by surgery with the use of presurgical carbohydrate loading, and optimize gastrointestinal recovery after surgery by introducing oral intake as soon as possible. These protocols have been established for surgeries involving colorectal, pancreatic, gynecological, urological, and liver procedures. One recent review of the literature attempted to evaluate the use of ERAS protocols for bariatric surgery. It was determined that the use of such protocols resulted in reduced operative time, decreased length of stay, and reduced mortality risk.76,77 Prior to surgery, the patient will undergo routine testing assessing laboratory indices such as complete blood cell count, basic metabolic panel, liver function tests, albumin, hemoglobin A1c, international normalized ratio, prothrombin time, partial thromboplastin time, thyroid-stimulating hormone, vitamin B1, vitamin B12, vitamin D, micronutrients, urinalysis, and urine human chorionic gonadotropin for females. Other screenings will include malignancy screening, sleep apnea, electrocardiogram, and other cardiac/pulmonary tests based on comorbidities. Evaluation for substance abuse and overall functional status will be conducted. Both an in-depth nutrition assessment and psychology consult are crucial components of the preoperative care of the bariatric surgical patient.

Postoperative care The diet progression after surgery is staged with the goal of patients to tolerate solid food within one month of surgery. Food choices should maximize weight loss while preserving lean body mass. Table 12.8 outlines the stages of the typical progression of oral intake. Nutritional supplementation is followed closely with a prescribed regimen of micronutrient supplementation to avoid development of deficiencies. Table 12.9 describes these recommendations. Medical complications that may occur include cardiac arrhythmias, hypoglycemia, gallbladder disease, hyperuricemia, and changes in blood pressure. These potential complications can be prevented with adjustments in medication and close monitoring postoperatively.78–81

Nutrition Therapy for Overweight and Obesity Nutritional care for overweight and obesity is guided by the use of multiple sources of evidence-based resources including medical and nutritional guidelines. 21,22,43,60,82 As you have seen throughout this chapter, nutrition therapy for 274  Part 4  Nutrition Therapy

overweight and obesity is a complex health problem, making it a target for quackery and commercialism. The RDN must be diligent in using evidence-based care to support the nutrition care process.

Nutrition Assessment (See Table 12.10 and Chapter 3 for additional information.)

Client History  Prior to meeting with the patient and any

family that may be present, the RDN will assess pertinent medical history including comorbidities such as hypertension, CHD, the presence of other atherosclerotic diseases (peripheral arterial diseases, abdominal aortic aneurysm, and symptomatic carotid artery disease), T2DM, prediabetes, NAFLD, and sleep apnea.21,22 Box 12.8 identifies the cardiovascular risk factors that would increase the need for weight loss interventions. Medications; supplement use; complementary, alternative, or integrative medical use; previous weight loss interventions, any previous interventions from the health care team members; sleep patterns; food security; education level; employment status; socioeconomic data; and family background should be reviewed. If preliminary food diaries or other nutrition questionnaires are requested, it is efficient to review these prior to the personal meeting with the patient.60 In pediatric and adolescent populations, additional information will include family dynamics, rearing patterns, and eating environment that impact diet and exercise habits.60,66

Anthropometric Measurements  Determining the degree of overweight or obesity through accurate anthropometric measurements is an important source of data.21,22,43,60 The weight and height used to calculate BMI in adults should be measured with the patient wearing light clothing or an examination gown and no shoes. (See Chapter 3.) As stated previously in this chapter, clinical judgment must be used in interpreting the BMI of persons who are very muscular, have lost significant amounts of lean body mass, are short, or have edema or ascites. Waist circumference is used as an index of abdominal adiposity and is interpreted using the classifications shown in Table 12.3. In patients with a BMI ≥ 35 kg/m2, measuring waist circumference is not necessary because it does not materially contribute to disease risk classification. Table 12.3 incorporates BMI and waist circumference to arrive at a disease risk relative to normal weight and low-risk waist circumference for patients having a BMI 30 ng/mL At least 45–60 mg/d in F with menses and/ patients with history of anemia

DV: 2 mg WLS = weight loss surgery, UL = upper intake level, DV = daily value, AGB = adjustable gastric band, LSG = laparoscopic sleeve gastrectomy, RYGB = Rouxen-Y gastric bypass, BPD/DS = biliopancreatic diversion/duodenal switch, SL = sublingual, IM = intramuscular, RAE = retinol activity equivalents, SQ = subcutaneous supplementation for non-WLS patients, DR1 = Dietary Reference Intake, DV = daily value , UL = Tolerable upper intake level, supplementation for WLS patients = actual dose for nutrients by type of WLS Source: Parrott J, Frank L, Rabena R, et al. American Society for Metabolic and Bariatric Surgery integrated health nutritional guidelines for the surgical weight loss patient 2016. Surg Obes Relat Dis. 2017; 13: 727–41.

A complete blood count will provide values to assess for anemia. Specific testing for vitamins and minerals should be directed by the patient’s history and the data collected about dietary intake. Blood pressure and respiratory and heart rate are typically noted from the physical examination. Pediatric guidelines recommend that children or adolescents with a BMI ≥85 percentile be evaluated for potential comorbidities.82

Food-/Nutrition-Related History  Assessing not only

food and nutrient intake and behaviors but also PA, knowledge and beliefs about food and nutrition, readiness for change, and factors affecting access to food is necessary in order to best identify nutrition diagnoses and develop an appropriate plan of care.60 The common methods and approaches for evaluating diet outlined in Chapter 3 are

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appropriate, but there are some special considerations to be aware of when obtaining diet intake data from obese patients as misreporting dietary intake is common.83 Assessing energy and nutrient content of the diet and identification of potential nutrient deficits including micronutrients are very important as many obese individuals have inadequate micronutrient intake despite adequate caloric intake.84 A 3-day intake record including a weekend day be obtained and averaged to better assess usual intake.83 Food frequency questionnaires (FFQs) and food diaries also provide valuable intake data. In pediatrics and adolescents, the family is a major source of information and will need specific consideration to obtain accurate data from all sources of meals and snacks such as school and day care. Inter view questions are asked to understand the patient’s current level of PA, goals for PA, and readiness

Table 12.10 Nutrition Assessment for Overweight/Obese Patients Client History

• Previous food restrictions

Education—primary language

• Eating patterns

Ethnic, cultural, and religious influences

Factors affecting access to food and food-/nutrition-related supplies

Patient/client/family medical/health history • Comorbidities that may indicate risk of metabolic syndrome: hypertension, diabetes mellitus/impaired glucose tolerance, dyslipidemia

• Ability to consistently purchase adequate amounts of food on a daily basis—food security • Ability to feed self

Treatments/therapy/alternative medicine • Medications (especially medications that might cause weight gain: antidepressants, lithium, beta-blockers, corticosteroids)

• Ability to cook and prepare meals Anthropometrics

Social history

• Height

• Socioeconomic status/food security

• Current weight

• Support systems

• Weight history: highest adult weight; usual body weight

Food-/Nutrition-Related History

• Reference weight/BMI

Food and nutrient intake

• Waist and hip circumferences

• 24-hour recall, diet history, food frequency; focus on portion sizes, meals eaten away from home, food preparation methods, dense sources of energy (fat, concentrated sugar content)

• Nutrition-focused physical examination: evidence of muscle w ­ asting (temporalis, interosseous, pectoralis major, deltoid, trapezius); ­presence of edema; assessment of micronutrient deficiency (skin, hair, eyes, oral cavity)

• Use of alcohol, vitamin and mineral supplements • Previous methods used for weight loss, if applicable

Biochemical Data, Medical Tests and Procedures

Medication and herbal supplement use

• Laboratory measures for comorbidities/assessment of metabolic syndrome: serum glucose, HgBA1c, total cholesterol, LDL, HDL, triglycerides

• Herbal or other type of supplements

• Blood pressure

• Knowledge/beliefs/attitudes • Previous nutrition education or nutrition therapy

• Visceral protein assessment: standard (interpret with caution ­secondary to inflammation)

• Mealtime behaviors

• Hematological assessment: standard

• Food allergies, preferences, or intolerances

BOX 12.8

CLINICAL APPLICATIONS

Cardiovascular Risk Factors Placing Patients at a High Priority for Treatment of ­Overweight and Obesity* • Cigarette smoking. • Hypertension (systolic blood pressure of ≥140 mm Hg or diastolic blood pressure >90 mm Hg) or current use of antihypertensive agents. • Increased low-density lipoprotein (LDL) cholesterol (serum concentration >160 mg/dL). A borderline high-risk LDL-cholesterol (130–159 mg/dL) plus two or more other risk factors also confers high risk. • Decreased high-density lipoprotein (HDL) cholesterol (serum concentration 30% of a person’s maximum weight has been lost.90 Since more rapid or extreme weight loss initially does not necessarily translate to better long-term weight loss maintenance, the desired rate of loss is 1–2 pounds per week. 121,22,43,60 Lowering energy consumption by 500–1000 kcal/day (3500–7000 kcal/week) and increasing energy expenditure with moderate levels of PA should result in this desired weight loss rate.60 There is strong evidence supporting the benefit of patients participating in a comprehensive weight loss program that includes (1) a moderately reduced calorie diet, (2) increased PA, and (3) behavior therapy to promote adherence to diet and activity recommendations. 21,22 The following sections provide an overview of the current evidence and benefits of this threepronged approach to weight loss. Keep in mind that these comprehensive lifestyle interventions should precede, in most cases, adjunct therapies such as obesity drugs and/or bariatric surgery. In pediatrics, often goals are based on weight maintenance until BMI-for-age is < 85th percentile. Depending on the level of obesity, a slow weight loss of 1–2 lbs. per month may be an appropriate goal.82 Using the Institute of Medicine equations, reducing intake by approximately 108 kcal/day should result in approximately 1 lb. weight loss/ month.1 Table 12.12 outlines the goals of weight loss based on age and level of obesity for pediatrics.

Dietary Interventions  The energy deficit desired can often be attained with intakes of 1200–1500 kcal/day for women or 1500–1800 kcal/day for men. 60 For many individuals, this is best achieved by restricting fat intake (30.0) • Personal history of GDM • Strong family history of diabetes (first-degree relative) • Prior poor obstetrical outcome (stillbirth, birth defects, or baby >9 lbs) • Member of a high-risk ethnic group (Hispanic, African American, Native American, South or East Asian, Pacific Islander)

Etiology  During the second or third trimesters of pregnancy, metabolic alterations occur to meet maternal and fetal demands for energy and nutrients. These alterations include changes in both insulin secretion and glucose, amino acid, and lipid metabolism. Although most women with GDM have normal glucose tolerance after delivery, their likelihood of developing GDM in subsequent pregnancies and T2DM later in life is increased. Increasing physical activity and reducing postpartum weight gain can reduce risk of subsequent diabetes.4,7 Pathophysiology  GDM is pathophysiologically similar to

T2DM. Islet cell function abnormalities or peripheral insulin resistance are thought to decrease insulin secretory response and insulin sensitivity. Inability of the β cells to meet increased Chapter 17  Diseases of the Endocrine System   517

insulin needs during pregnancy results in higher levels of circulating glucose. GDM also affects the fetus. When maternal blood glucose levels are elevated, the fetus is constantly exposed to these levels as well, and fetal insulin production is increased. It appears that maternal hyperglycemia induces fetal hyperglycemia, leading to fetal hyperinsulinemia and macrosomia.

Clinical Manifestations  Maternal complications associated with GDM include hypertension (preeclampsia), ­polyhydramnios, difficult birth, preterm delivery (before 38 weeks’ gestation), and a higher rate of cesarean sections. Fetal and neonatal complications include macrosomia, hypoglycemia, respiratory distress syndrome, hypocalcemia, hyperbilirubinemia, and polycythemia.4

MNT (see Table 17.16) should be individualized and based on maternal weight and height. Energy and nutrients adequate to meet the needs of pregnancy should be incorporated with established maternal blood glucose goals. When nutrition therapy alone fails to maintain blood glucose at the following levels, insulin therapy is preferred to ensure glycemic control. Both glyburide and metformin cross the placenta and longterm safety data are limited.7 Target glucose ranges are the following: Fasting #95 mg/dL (5.3 mmol/L); or 1-hour postprandial plasma glucose #140 mg/dL (7.8 mmol/L);

Diagnosis  The Standards of Medical Care in D ­ iabetes—2018

outlines the following screening guidelines for diagnosis of GDM: For patients who meet high-risk criteria for T2DM, screening should occur on the first prenatal visit. For patients with a known history of GDM, screening should occur at 6–12 weeks. Patients with unknown medical history should be screened at 24–28 weeks’ gestation. Finally, patients with a history of GDM should be screened for T2DM every 3 years.7 The OGTT is the standard method for screening and diagnosis of GDM (see Box 17.2).

Medical Treatment  The ADA recommends that all women with GDM receive nutrition counseling from a RDN.

or 2-hour postprandial plasma glucose #120 mg/dL (6.7 mmol/L)

Monitoring  Maternal hyperglycemia increases medical risks in the fetus. SMBG, not A1C, is considered the best method to detect maternal hyperglycemia. Postprandial monitoring is superior to preprandial monitoring when insulin therapy is used. Postprandial blood glucose levels are directly related to rates of macrosomia, neonatal hypoglycemia, and

Table 17.16 Nutrition Recommendations for Gestational Diabetes Mellitus Nutrient or Food Type

Recommendation

Meal Planning Tips

Energy

Intake should be sufficient to promote adequate, but not excessive, weight gain to support fetal development and to avoid ketonuria. Daily minimum of 1700–1800 kcal is an appropriate starting goal.

Include 3 small- to moderate-sized meals and 2–4 snacks. Space snacks and meals at least 2 hours apart. A bedtime snack (or even a snack in the middle of the night) is recommended to diminish the number of hours fasting.

Carbohydrate

A minimum of 175 g CHO daily, allowing for the approximately 33 g needed for fetal brain development. Recommendations are based on effect of intake on blood glucose levels. Intake should be distributed throughout the day. Frequent feedings, smaller portions, with intake sufficient to avoid ketonuria.

Common carbohydrate guidelines: 2 carbohydrate choices (15–30 g) at breakfast, 3–4 choices (45–60 g) for lunch and evening meal, and 1–2 choices (15 to 30 g) for snacks. Recommendations should be modified based on individual assessment and blood glucose self-monitoring test results.

Protein

1.1 g/kg (minimum 71 g).

Protein foods do not raise post-meal blood glucose levels. Add protein to meals and snacks to help provide enough calories and to satisfy appetite.

Fat

Limit saturated fat.

Fat intake may be increased because of increased protein intake; focus on leaner protein choices.

Sodium

Not routinely restricted.

2300 mg/day is consistent with U.S. Dietary Guidelines.

Fiber

For relief of constipation, gradually increase intake and increase fluids.

Use whole grains and raw fruits and vegetables. Activity and fluids help relieve constipation.

Non-nutritive sweeteners

Use only FDA-approved sweeteners.

Saccharin crosses the placenta but has not been shown to be harmful.

Vitamins and minerals

Preconception folate. Assess for specific individual needs: multivitamin throughout pregnancy, iron at 12 weeks, and calcium, especially in the last trimester and while lactating.

Take prenatal vitamin. If it causes nausea, try taking at bedtime.

Alcohol

Avoid all alcohol even in cooking.

Source: Adapted from American Diabetes Association. Management of Diabetes in Pregnancy: Standards of Medical Care in Diabetes—2018. Diabetes Care. 2018; 37(Suppl 1): S137–143.

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cesarean delivery. Additionally, maternal blood pressure and urine protein should be monitored to detect hypertensive disorders.7

Nutrition Therapy for GDM Nutritional Implications  Nutrition therapy goals for

GDM include a goal shared by all pregnant women: to promote nutrition for maternal and fetal health while providing adequate energy for appropriate gestational weight gain. Furthermore, achievement and maintenance of normoglycemia and absence of ketones are goals specific to treatment of GDM.19,20

Nutrition Diagnosis  Nutrition diagnoses related to GDM include excessive energy intake, excessive fat intake, inappropriate intake of fats, inappropriate intake of types of carbohydrates, inconsistent carbohydrate intake, inadequate fiber intake, altered nutrition-related laboratory values, food–­medication interaction, food- and nutrition-related knowledge deficit, harmful beliefs/attitudes about food or nutrition-related topics, not ready for diet/lifestyle change, self-monitoring deficit, undesirable food choices, physical inactivity, and inability or lack of desire to manage self-care. Nutrition Intervention  Adequate energy is necessary for

desirable weight gain during pregnancy. 7,19,20 The DRI for pregnancy recommends ≥175 g of carbohydrate, ≥71 g protein, and 28 g fiber. Energy needs are evaluated indirectly by monitoring the woman’s physical activity, appetite, food intake, blood glucose levels, ketone records, and weight change. It is not necessary to calculate energy needs unless problems with excessive weight loss or gain are experienced. Formulas useful for estimating energy requirements for women with GDM and recommended levels of weight gain are outlined in Box 17.10. Protein requirements increase during the second and third trimesters of pregnancy to nonpregnant needs plus 25 g per day or 1.1 g protein per kg desirable body weight.7,19,20 Two factors should be considered when making recommendations concerning dietary fat intake: impact on the woman’s body weight and plasma lipoprotein profiles. Reduced fat intake may be necessary if total energy intake should be decreased, and types of fat such as saturated fat, trans fat, may need to be addressed. Consequences of folate deficiency in pregnancy (i.e., neural tube defects) have been well documented. All women of reproductive age capable of becoming pregnant should take 400 mcg additional folate daily from food or supplements. Whereas about 10% of the iron is absorbed from food in the nonpregnant state, iron absorption increases to 25% at the beginning of the second trimester. Supplementation of 30 mg/day ferrous iron in the second and third trimesters is recommended. Nutrition recommendations for GDM are outlined in Table 17.16.4,7

Monitoring and Evaluation  Follow-up appointments are crucial for the well-being of the infant as well as the mother. Reclassification of the mother’s glycemic status should be performed by the physician at least 6 weeks after delivery. If glucose levels are normal, glycemic status should be reassessed at a minimum of 3-year intervals.7

BOX 17.10 CLINICAL APPLICATIONS

Estimating Energy Requirements in GDM To calculate a woman’s (19 years and older) energy needs during pregnancy, Estimated Energy Requirements (EER) must first be calculated: EER = 354 − (6.9 3 A) 1 PA 3 (9.36 3 W 1 726 3 H) Where A = age in years; PA = physical activity coefficient (1.0 [sedentary], 1.12 [low active], 1.27 [active], 1.45 [very active]); W = weight in kg; H = height in meters. To estimate energy requirements for pregnant women who are at a normal weight: • 1st trimester = Adult EER + 0 • 2nd trimester = Adult EER + 160 kcal + 180 kcal • 3rd trimester = Adult EER + 272 kcal Institute of Medicine guidelines for recommended total (cumulative) weight gain during pregnancy are based on prepregnancy BMI. These recommendations are: • • • •

Underweight (3 L/24 hour) and polydipsia, resulting from excessive loss of fluid. Treatment of DI depends on its cause. Treatment of the cause usually resolves DI. Common causes of DI include the following: • Malfunctioning hypothalamus • Malfunctioning pituitary gland • Brain injury • Tumor • Tuberculosis • Blockage of cerebral arteries • Encephalitis • Meningitis • Sarcoidosis

Adrenal Cortex Disorders A number of common deficiencies result from either insufficient or excess secretion of adrenal cortex hormones. And, as with other endocrine disorders, symptoms are the result of either the absence or magnification of effects of the hormones involved.

Excess Secretion of Glucocorticoids  Prolonged exposure to high levels of endogenous or exogenous glucocorticoids results in the condition Cushing’s syndrome. Insufficient Secretion of Adrenal Cortex ­S teroids  Both adrenal glands must be nonfunctional (or

removed) before adrenocortical insufficiency can occur.2 As a result of either occurrence, both glucocorticoid (cortisol) and mineral corticoid (aldosterone) hormone production is lacking. Death may result from untreated adrenocortical insufficiency.2,40 Primary adrenal insufficiency is uncommon, but iatrogenic (caused by medical treatment) adrenal insufficiency is more frequent, although exact incidence is unknown. Autoimmune Addison’s disease is the more common form of adrenal insufficiency. Addison’s afflicts men and women and can occur at any age, but it is most common in people aged 30–50 years.40 Adrenal insufficiency can be classified as either primary or secondary. Primary adrenal insufficiency (Addison’s disease) is caused by a dysfunctional adrenal cortex that impairs both glucocorticoid and mineral corticoid production. Secondary adrenal insufficiency results from inadequate ACTH production by the anterior pituitary, resulting primarily in deficient glucocorticoid secretion. Adrenal insufficiency can further be classified as congenital or acquired.40 Primary adrenal insufficiency results from destruction of the adrenal cortex. Aldosterone is produced by the medulla of the adrenal gland; cortisol is produced in the adrenal cortex. Clinical findings manifest after 90% of the adrenal cortex has been destroyed. Potential causes of this destruction are as follows: • Autoimmune • Infectious (e.g., mycobacterial and fungal) • Neoplastic (e.g., primary and metastatic) • Traumatic • Iatrogenic (e.g., surgery and medication) • Vascular (e.g., hemorrhage, emboli, and thrombosis)

With destruction of the adrenal cortex, feedback inhibition of the hypothalamus and anterior pituitary gland is interrupted. Symptoms associated with aldosterone deficiency in Addison’s disease progress slowly and insidiously. Typical symptoms of Addison’s disease reflect loss of glucocorticoid and mineral corticoid action. Since aldosterone is essential for life, the condition can be fatal. Aldosterone deficiency causes reduced potassium loss in the urine, resulting in hyperkalemia, which in turn results in disturbed cardiac rhythm. Hyponatremia caused by excessive urinary loss of sodium results in hypotension.40 Cortisol deficiency results in poor response to stress, hypoglycemia (resulting from reduced gluconeogenesis), and hyperpigmentation (from excessive secretion of ACTH).2 Addison’s disease may coexist with other autoimmune disorders, especially thyroid disease, premature ovarian failure, and T1DM.40 Treatment of Addison’s disease involves replacing or substituting hormones not being produced by the adrenal gland. Surgery, radiation, chemotherapy, immunotherapy, or a combination may be used to treat ectopic ACTH syndrome. Prognosis is also dependent upon cause of the disease. Most cases can be cured, although recovery may be complicated by various aspects of the causative illnes.41 Patients with Addison’s disease should not restrict salt in their diets. Patients with concurrent primary hypertension may restrict salt intake rather than discontinue mineral corticoid replacement. Patients living in warm climates should increase salt intake due to increased loss of salt through perspiration.

17.7 CONCLUSION This chapter has described the physiology behind endocrine function, endocrine control of metabolism, diabetes, hypoglycemia, and thyroid disorders and their clinical consequences for the patient and practitioner. Nutrition therapy must address not only endocrine disorders but also the effect of the medications used to treat these disorders on nutrition and nutrition status. Therapeutic nutrition interventions have been discussed, with particular emphasis on specific modifications to assist in the treatment of disease. Nutrition therapy for endocrine disorders, especially DM, poses a challenge for the not only the RDN but the entire healthcare team but also offers the opportunity to greatly improve clinical outcomes and quality of life for clients and patients.

• Metabolic (e.g., amyloidosis)

Chapter 17  Diseases of the Endocrine System   525

PRACTITIONER INTERVIEW

Jill Weisenberger, MS, RDN, CDE  Private practice nutritionist, author, consultant to the food and health care industries How did you become a certified diabetes educator? The opportunity to become a CDE fell into my lap and I jumped at the chance. As a consulting dietitian, I felt the CDE would make me more marketable by widening my scope of practice, and it did. I was asked to apply for the part-time position of an outpatient diabetes dietitian. I had just your usual diabetes background, but an interest and a willingness to learn more. I worked in that job long enough to earn the right to take the CDE exam. Now the CDE has helped me get other clinical jobs and even public relations and writing jobs.

How has dietetics changed since you began your ­practice? During my career, I have seen substantial changes in how we treat diabetes. Today the medications are better, the diet is much less restrictive, and we focus on the patients being able to manage themselves. When I started out, I mostly just educated the client on what to eat via the exchange system and to avoid excess added sugars. Now I counsel and coach people. I help them to use information to solve their own problems and to recognize their barriers. This change didn’t happen overnight but rather with experience. I always say I’m not in the business of telling people what to eat and what to do. Rather, let’s figure out together what works for you and what doesn’t. The improvement in and options for diabetes medications has helped tremendously by giving patients more options and freedom in planning meals. Dietetics, in general, has also changed. We make better use of scientific evidence today.

What is your typical patient like? Tell us about how you accomplish nutrition therapy with your clients. Most of my patients are overweight or obese. Some, even patients in their 20s, are as much as 100 or 200 pounds overweight. Many of my patients have multiple diagnoses such as nonalcoholic fatty liver, diabetes, hypertension, gastroesophageal reflux disease (GERD), and more. One of my patients was a gentleman who came in with an HbA1C of 13.7%, overweight, and on oral medications. We worked on (1) monitoring blood sugar, (2) eating three meals a day, 60 g of carbohydrate per meal, (3) eating 0–20 g carbohydrate for a snack if hungry, and (4) identifying foods in the diet high in saturated fat. Over three

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visits (3 months), his HbA1C dropped to 6.5%. He lost only a small amount of weight but his blood glucose normalized. My initial appointments run about 90 minutes. In the first half, I take a very thorough history including weight history, medical history, food preferences, cooking abilities, budget constraints, family dynamics, and more. Most of the time, the patient has no idea how much I learn from our interview. In the second half of the appointment, we come up with a plan together to move the patient from current eating and exercise habits to better ones. Typically, a patient will walk out the door with three to five behavioral goals. For example, the goal may be to spread the consumption of carbohydrates throughout the day as a means to normalize blood glucose. This might involve consuming three meals a day (60 g of carbohydrate per meal) and if hungry a snack of 0–20 g carbohydrates. Or a goal might be as simple as eating at least one serving of vegetables at dinner. At follow-up visits, we talk about what worked and what didn’t and what the patient would like to learn or do differently. Then, I find out if they anticipate any issues coming up (wedding, vacation, work) that might interfere with the plan. I want to look at blood glucose records too, but they don’t always bring them. When they do, I can help them see how medications, food, and physical activity affect the numbers. I suggest only small changes in their diet each time I see them. But first I always ask, “What is the first thing you’d like to change and why? How confident are you that you can do this, and how motivated are you? Why?” Changing the diet is very hard. People are busy, tired, have kids, and often have few cooking skills. But I do strongly encourage them to monitor their blood glucose. They learn so much from knowing their blood sugar levels, and it allows them to manage their own disease by seeing firsthand the impact of food and exercise. Working on preventing heart disease is as important as the rest, but it’s sometimes hard to get patients to focus on this. So often patients want to go low carb, but they don’t consider the quality of their food choices. Working on the big picture is always a challenge. My advice to new dietitians is to have compassion for each patient. You will do a better job and will enjoy what you do. Wherever you work, surround yourself with smart, capable people who work hard because that is how you become successful. Keep up to date on all pertinent aspects of nutrition and diabetes. Know the science, and feel confident to discuss your patients with their physician.

APPLICATION OF THE NUTRITION CARE PROCESS: TYPE 2 DIABETES

INTRODUCTION A 71-year-old female who arrives at the emergency room presents with nonhealing wound on right foot between the second and third digits. Patient has a history of frequent bladder infections, slight tingling and numbness in her feet, and today, serum blood glucose of 325 mg/dL. She is admitted for antibiotics, probable surgical debridement of a wound, and stabilization and treatment for T2DM. Past medical history includes a diagnosis of HTN treated with 50 mg Captopril two times daily.

crackers (12) with peanut butter (about 2 tbsp). Dinner: pork chop, 3 oz; 1 cup of corn; cornbread, 1 slice; and applesauce, 1 cup.

Anthropometrics Ht. 5'0", Wt. 155 lbs, usual adult body weight: 145–165 lbs 3. Evaluate this patient’s weight. Calculate and interpret her BMI.

Biochemical Data

1. What is the difference between type 1 and type 2 DM? Why is it assumed that this patient has type 2?

Labs: BUN 26 mg/dL; Cr 1.2 mg/dL; Chol 300 mg/dL; HDL 35 mg/dL; LDL 140 mg/dL; Glucose 325 mg/dL; HbA1C 8.5%

2. What risk factors does this patient present with? What symptoms may indicate that she has complications of type 2 DM?

4. What admission laboratory values are abnormal? Interpret their significance in relationship to both her diagnosis and nutritional status.

NUTRITION ASSESSMENT

NUTRITION DIAGNOSIS

Food-/Nutrition-Related History

5. Identify at least two nutrition problems suggested by the nutrition assessment and medical history. Determine the diagnostic term for each nutrition problem. Next, identify the etiology of each nutrition diagnosis. Finally, identify the signs and symptoms that support the evidence for the diagnoses.

Lives with sister who has T2DM; prepares own meals—rarely eats at restaurants. Likes all foods but avoids “foods with sugar.” 24-hour recall indicates the following: Breakfast: 2–3 slices of toast with margarine (about 1 tbsp); coffee with milk. Lunch: 1 can tomato soup prepared with water; saltine

CHAPTER REVIEW QUESTIONS 1. List the three chemical classes of endocrine hormones. For each class, pick one hormone, name its production site, and briefly describe its function. 2. Describe the action of insulin on carbohydrate, lipid, and protein metabolism. 3. What is the definition of diabetes mellitus (DM)? List the classifications for DM and briefly explain similarities and differences for their epidemiology, etiology, pathophysiology, and clinical manifestations. Describe three ways diabetes can be diagnosed.

4. What is meant by glycemic control, and why is it important? Describe the physiological consequences of poor glycemic control. Which laboratory measurements are indicators of short- and long-term glycemic control? How often are they checked? 5. List the onset, peak, and duration of the types of insulin that are now available. How is insulin dosage determined, and how can insulin be administered? What are the differences in nutrition therapy recommendations for a person with diabetes who is using insulin on the conventional plan versus a person using intensive insulin therapy?

6. Briefly describe several meal planning approaches for individuals with diabetes mellitus. Select a meal plan you would use for a 70-year-old man (T2DM) with an eighth-grade education, a 13-yearold teenage female athlete (T1DM), and a 32-year-old pregnant woman (GDM), and justify your answers. 7. List the classes of diabetes medications (not including insulin). Briefly describe their effects. 8. For individuals with T2DM, why is weight management often included as a component of nutrition therapy? Why is it important for the treatment of T2DM?

ENDNOTES 1. Only endocrine disorders with nutritional implications are discussed. 2. The abbreviations T1DM and T2DM used in this chapter are not standardized abbreviations supported by the ADA, but are used for the sake of brevity.

3. Spontaneous hypoglycemia, as opposed to hypoglycemia related to diabetes, is the subject of this section.

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REFERENCES 1. Sherwood L. Principles of endocrinology. In: Sherwood L, ed. Human Physiology: From Cells to Systems. 9th ed. Boston, MA: Cengage Learning; 2016: 656–64. 2. Sherwood L. The peripheral endocrine glands. In: Sherwood L, ed. Human Physiology: From Cells to Systems. 9th ed. Boston, MA: Cengage Learning; 2016: 665–714. 3. Gropper SS, Smith JL, Carr TP. Carbohydrates. In: Gropper SS, Smith JL, Carr TP, eds. Advanced Nutrition and Human Metabolism. 7th ed. Boston, MA: Cengage Learning; 2018: 61–106. 4. Powers AC, Niswender KD, Evans-Molina C. Diabetes Mellitus: Diagnosis, Classification, and Pathophysiology. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. ­Harrison's Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine. mhmedical.com/content.aspx?bookid=2129§ionid=192288322. Accessed November 24, 2018. 5. Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2017. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2017. https://www.cdc.gov/diabetes/pdfs/data/ statistics/national-diabetes-statistics-report.pdf. Accessed December 9, 2017. 6. International Diabetes Federation. Diabetes Atlas. 8th ed. https://www.idf.org/e-library/epidemiology-research/diabetes-atlas/134-idf-diabetes-atlas-8th-edition.html. Accessed December 9, 2017. 7. American Diabetes Association. Standards of Medical Care in Diabetes—2018. Diabetes Care. 2018; 41(S1): S1–S156. 8. Lernmark A. Environmental factors in the etiology of type 1 diabetes, celiac disease and narcolepsy. Pediatric Diabetes. 2016; 17(Suppl 22): 65–72. 9. Sterling J, Pociot F. Type 1 diabetes candidate genes linked to pancreatic islet cell inflammation and beta-cell apoptosis. Genes. 2017; 8: doi: 10.3390/genes8020072. 10. Chia JAJ, McRae JL, Kukuljan S, et al. A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes. Nutr Diabetes. 2017; 7: e274. 11. Kobayashi T, Nishida Y, Tanaka S, Aida K. Pathological changes in the pancreas of fulminant type 1 diabetes and slowly progressive insulin-dependent diabetes mellitus (SPIDDM): innate immunity in fulminant type 1 diabetes and SPIDDM. Diabetes Metab Res Rev. 2011; 27: 965–70. 12. Beaumont RN, Horikoshi M, McCarthy MI, Freathy RM. How can genetic studies help us to understand links between birth weight and Type 2 Diabetes? Curr Diab Rep. 2017; 16: 22–29. 13. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009; 120: 1640–5.

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14. Moore JX, Chaudhary N, Akinyemiju T. Metabolic syndrome prevalence by race/ethnicity and sex in the United States, National Health and Nutrition Examination Survey, 1988–2012. Prev Chronic Dis. 2017; 14: 160–287. 15. Raynor HA, Davidson PG, Burns H, et al. Medical nutrition therapy and weight loss questions for the evidence analysis library prevention of Type 2 Diabetes Project: systematic reviews. J Acad Nutr Diet. 2017; 117: 1578–611. 16. American Association for Clinical Chemistry. Diabetes-related autoantibodies. Lab Tests Online Web site. https://labtestsonline.org/conditions/diabetes. Updated April 28, 2016. Accessed August 27, 2018. 17. Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993; 329: 977–86. 18. Gubitosi-Klug R. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: summary and future directions. Diabetes Care. 2014; 37(1): 44–49. 19. Franz MJ, Macleod J, Evert A, et al. Academy of Nutrition and Dietetics nutrition practice guideline for type 1 and type 2 diabetes in adults: systematic review of evidence for medical nutrition therapy effectiveness and recommendations for integration into the nutrition care process. J Acad Nutr Diet. 2017; 117: 1659–79. 20. Beck J, Greenwood DA, Blanton L, et al. 2017 National standards for diabetes self-management education and support. Diabetes Care. 2017; 40: 1409–19. 21. Insulin: consumer guide 2018. Diabetes Forecast. March 2018. http://www.diabetesforecast. org/2018/02-mar-apr/diabetes-medications-and​ .html. Accessed August 27, 2018.

https://health.gov/dietaryguidelines/2015/guidelines/. Accessed December 10, 2017. 29. Kerr D, Hoppe C, Axelrod C. Smartphone apps for diabetes management. Diabetes Forecast. March 2017. http://www.diabetesforecast.org/ landing-pages/lp-consumer-guide.html. Accessed December 10, 2017. 30. Academy of Nutrition and Dietetics/American Diabetes Association. Count Your Carbs: Getting Started. Chicago, IL: Academy of Nutrition and Dietetics; 2014. 31. Academy of Nutrition and Dietetics/American Diabetes Association. Choose Your Foods: Food Lists for Weight Management. Chicago, IL: Academy of Nutrition and Dietetics; 2014. 32. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998; 352: 937–53. 33. Lachin J, Orchard T, Nathan D. Update on cardiovascular outcomes at 30 years of the diabetes control and complications trial/epidemiology of diabetes interventions and complications study. Diabetes Care. 2014; 37: 39–43. 34. de Boer I. Kidney disease and related findings in the diabetes control and complications trial/ epidemiology of diabetes interventions and complications study. Diabetes Care. 2014; 37: 24–30. 35. Cryer PE, Davis SN. Hypoglycemia. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.­asp x?bookid=2129§ionid=192288656. Accessed ­November 24, 2018.

22. Blood Glucose Meters. Diabetes Forecast. March 2018. http://main.diabetes.org/dforg/ pdfs/2018/2018-cg-blood-glucose-meters.pdf. Accessed August 27, 2018.

36. Masharani U, Gitelman SE, Long RK. Hypoglycemic Disorders. In: Gardner DG, Shoback D, eds. Greenspan’s Basic & Clinical Endocrinology. 10th ed. New York, NY: McGraw-Hill; http://accessmedicine.mhmedical.com.proxy.lib​ .ohio-state.edu/content.aspx?bookid=2178§ionid=166252794. Accessed December 13, 2017.

23. Wahowiak L. Insulin pens: consumer guide 2018. Diabetes Forecast. March 2018. http://main​ .diabetes.org/dforg/pdfs/2018/2018-cg-insulinpens.pdf. Accessed August 27, 2018.

37. Fayfman M, Pasquel FJ, Umpierrez GE. Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Med Clin North Am. 2017; 101: 86–606.

24. Insulin pumps; continuous glucose monitors: consumer guide 2018. Diabetes Forecast. March 2018. http://www.diabetesforecast.org/2018/02mar-apr/. Accessed August 27, 2018.

38. Qiu H, Novikov A, Vallon V. Ketosis and diabetic ketoacidosis in response to SGLT2 inhibitors: basic mechanisms and therapeutic perspectives. Diabetes Metab Res Rev. 2017; 33: e2886–95.

25. Petrie JR, Chaturvedi N, Ford I, et al. Cardiovascular and metabolic effects of metformin in patients with type 1 diabetes (REMOVAL): a double-blind, randomised, placebo-controlled trial. Lancet Diabetes Endocrinol. 2017; 5: 597–609.

39. Forbes JM, Cooper ME. Mechanisms of diabetic complications. Phys Rev. 2013; 93: 126–88.

26. Griffin SJ, Leaver JK, Irving GJ. Impact of metformin on cardiovascular disease: a meta-analysis of randomized trials among people with type 2 diabetes. Diabetolpgoa. 2017; 60: 1620–9. 27. American Diabetes Association. Lifestyle Management: Standards of Medical Care in Diabetes—2018. Diabetes Care. 2018; 41(Suppl 1): S38–50. 28. US Department of Health and Human Services. Dietary Guidelines for Americans 2015–2020.

40. Jameson J, Mandel SJ, Weetman AP. Disorders of the thyroid gland. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill; 2014. http://accessmedicine. mhmedical.com/content.aspx?bookid=1130§ionid=79751787. Accessed August 29, 2018. 41. Fitzgerald PA. Endocrine disorders. In: Papadakis MA, McPhee SJ, Rabow MW, eds. Current Medical Diagnosis & Treatment 2018. New York, NY: McGraw-Hill; http://accessmedicine​ .mhmedical.com/content.aspx?bookid=2192§ionid=167996562. Accessed August 29, 2018.

CHAPTER 18

Source: PosiNote/Shutterstock.com

Diseases of the Renal System Marcia Nahikian-Nelms, PhD, RDN, LD, FAND The Ohio State University

LEARNING OB JECTIV ES LO 18.1  Describe normal physiological functioning of the kidneys, pathophysiology with subsequent impact on kidney function. LO 18.2  Discuss the etiologies of and risk factors for CKD and medical treatment of end stage renal disease.

LO 18.3  Explain medical nutrition therapy for CKD and kidney transplant from assessment to interventions and recommendations. LO 18.4  Define acute kidney injury (AKI), etiologies, signs and symptoms and its treatment.

LO 18.5  Compare nutrition therapy for AKI to that of CKD. LO 18.6  Define nephrolithiasis, etiology and medical treatment. LO 18.7  Describe nutrition assessment, diagnosis and interventions for nephrolithiasis.

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G LO S SARY acute kidney injury (AKI)—refers to kidney dysfunction of short duration or any sudden, severe impairment of kidney function afferent—carrying blood to the designated site; for example, the afferent arteriole carries blood to the glomerulus arteriovenous fistula (AVF)—a surgically created connection of an artery and vein to provide circulatory access for hemodialysis arteriovenous graft (AVG)—a surgically implanted artificial vessel connecting an artery and vein to provide circulatory access for hemodialysis; used when a patient’s blood ­vessels are fragile and a fistula is not feasible azotemia—a build-up of nitrogenous waste products such as urea in the blood and body fluids bone resorption—a process whereby osteoclasts destroy an area of bone as the first step in bone remodeling chronic kidney disease (CKD)—kidney damage (i.e., pathologic abnormalities or markers of damages) or GFR 3 months continuous renal replacement therapy (CRRT)—type of renal replacement therapy used to treat patients with acute kidney injury, particularly those with multiple organ ­failure; the types of patients treated tend to be ­hemodynamically unstable, have poor cardiac output, and be unable to tolerate hemodialysis cystine—a sulfur-containing amino acid that is produced by the actions of acids on proteins that contain this compound dialysate—fluid used by the dialysis procedure to assist in removal of metabolic byproducts, wastes, and toxins; composition is determined by individual patient requirements dialysis—renal replacement procedure that removes excessive and toxic by-products of metabolism from the blood, thus replacing the filtering function of healthy kidneys diffusion—passage of particles through a semipermeable membrane efferent—carrying blood away from the designated site; for example, the efferent arteriole carries blood away from the glomerulus end-stage renal disease (ESRD)—kidney disease in which kidney function declines to 10%–15% of normal (the term CKD is now preferred for this condition); ESRD is equivalent to CKD stage 5 or when a patient requires renal replacement therapy extracorporeal shock wave lithotripsy (ESWL)—a common procedure used to treat kidney stones whereby shock waves are used to break down the stones into smaller pieces glomerular filtration rate (GFR)—the filtration ability of the glomerulus; used as an index of kidney function; normal value is approximately 125 mL/min

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glomerulonephritis—nephritis marked by inflammation of the capillaries of the renal glomeruli and membrane tissue that serves as a filter glomerulus—a network of thin-walled capillaries closely surrounded by a pear-shaped epithelial membrane called the Bowman’s capsule (within the kidney) hematuria—the presence of blood in the urine hemodialysis (HD)—a type of renal replacement therapy whereby wastes or uremic toxins are filtered from the blood by a semipermeable membrane and removed by the dialysis fluid hydroxyapatite—the apatite form of calcium phosphate present with calcium carbonate hypercalciuria—an excess of calcium in the urine hyperoxaluria—an excess of oxalate in the urine hyperuricosuria—a disorder of uric acid metabolism intravenous pyelogram (IVP)—radiographic imaging of the kidneys, ureter, and bladder using X-ray and contrast dye that is injected intravenously intrinsic (parenchymal) acute kidney injury/AKI—kidney injury associated with damage to the renal cell microalbuminuria—the leaking of small amounts of albumin into the urine by the kidneys nephrolithiasis—kidney stones, a common disorder in the United States nephron—basic functional unit of the normal kidney; each nephron has two main parts: the glomerulus and the tubule nephrotic syndrome—a clinical condition consisting of losses of protein in the urine exceeding 3.5 g/day, hyperlipidemia, and low albumin levels (95%

Bicarbonate—(HCO3)

24–28 mEq/L

of dissolved oxygen (PaO2). Changes in the PaCO2 measure how well carbon dioxide is able to move out of the blood into the airspaces of the lung, and then out with the exhaled air. Changes in PaO2 measure how well oxygen is able to move from the air into the lungs. Oxygen saturation (SaO2) is the measure of the degree to which hemoglobin is carrying oxygen. A normal SaO2 is 95–100%. In patients with pulmonary disease, due to gas exchange issues, fewer red blood cells carry the usual load of oxygen, and oxygen saturation is decreased.5 In addition to the exchange of oxygen and carbon dioxide, the lungs play a major role in regulating acid–base balance, as discussed in Chapter 8. The pH is a measure of hydrogen ion concentration (H+) in blood, which indicates its acid or base (alkaline) nature; a pH of less than 7.40 is acidotic, and a pH greater than 7.40 is alkalotic. Respiratory acidosis, caused by decreased ventilation, results in carbon dioxide retention, while respiratory alkalosis, caused by increased ventilation, results in loss of carbon dioxide. The respiratory system responds quickly to acid– base disturbances through changes in minute ­ventilation that alter blood pH by regulating the retention or excretion of carbon dioxide. Carbon dioxide dissolves more readily in the blood than oxygen and forms bicarbonate and smaller amounts of carbonic acid. When present in normal amounts, the ratio of carbonic acid to bicarbonate helps to keep the body pH normal (7.40). In situations where acidosis occurs, respiratory activity is increased and the lungs quickly compensate to excrete excess CO2. If alkalosis is present, respiratory activity decreases and CO2 is retained, and the system reacts by producing a compensatory respiratory acidosis (see Chapter 8).2

Nutrition and Pulmonary Health

Source: Lisa Eastman/Shutterstock.com

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One of the difficulties in studying the relationship between nutrition and respiratory diseases is the scarcity of evidenced-based research, particularly with specific respiratory diseases. Many studies looking particularly at food and nutrient intake related to the etiology of respiratory disease are retrospective population studies rather than intervention trials. Unfortunately, population studies are often contradictory due to a variety of factors, including sampling errors, selection bias, and low statistical power. Even intervention studies sometimes show conflicting outcomes resulting from differences in study design. Malnutrition has been shown to have an adverse effect on clinical outcomes. The impact of protein-energy malnutrition on lung function has been examined in both clinical and animal studies, and the effects of weight loss on pulmonary function in individuals without lung disease have been described. Malnutrition associated with poor intake appears to have an impact on the strength and endurance of respiratory muscles, particularly the diaphragm, and may also cause reductions in lung

parenchyma (respiratory bronchioles, alveoli, and capillaries). With continued malnutrition, increased incidence of pulmonary infection may result from depressed immune function.6–10 There has been continued research examining the role of dietary antioxidants such as vitamin C, vitamin E, beta-carotene, and selenium with healthy lung function. A variety of antioxidants appear to play an important role in protecting the lungs from oxidant injury as the result of the inflammatory process caused by the inhalation of cigarette smoke, pollutants, and other respiratory conditions. The strong observed relationship between antioxidants and respiratory health has prompted the use of antioxidants as a novel therapy for a reducing inflammation in a variety of respiratory illnesses.11–14 Cigarette smoking is associated with reduced levels of antioxidants in various body fluids. Smokers have been shown to have depleted levels of serum ascorbate, α-tocopherol, beta-carotene, and selenium.15 A meta-analysis examining the relationship between cigarette smoking and nutrient intake showed that smokers had higher intakes of energy, total fat, saturated fat, cholesterol, and alcohol and lower intakes of antioxidants and fiber compared to nonsmokers.15 The metabolic turnover for vitamin C is about 35 mg/day greater for smokers than nonsmokers. Because of this, it is recommended that people who smoke consume an additional 35 mg/day of vitamin C beyond the DRI.16 Respiratory disease often includes a variety of symptoms that may affect dietary intake, including early satiety, anorexia, weight loss, cough, and dyspnea during eating. As the disease progresses, these symptoms may have a marked impact on nutritional status. For this reason, it is important that a nutritional assessment that includes an evaluation of weight history, nutrient intake, medication use, biochemical markers, and functional status be initiated. BOX 21.1

21.3 ASTHMA Definition Asthma is a chronic inflammatory disorder of the airway involving many cells and cellular elements, such as mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. Inflammation is the primary problem in asthma and is thought to be primarily immunoglobulin E (IgE) mediated (see Chapter 9). In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with airflow obstruction that is often reversible either spontaneously or with treatment.17

Epidemiology The prevalence of asthma across all age, sex, and racial groups is approximately 25 million individuals including approximately six million children.18 Asthma is the third leading cause of hospitalization and chronic illness among children under 15 years of age as well as the leading cause of missed school days.18 See Box 21.1 for further discussion of the pediatric implications of asthma.

Etiology Asthma is usually divided into two types: allergic and nonallergic asthma.17 Of the two, allergic asthma is the most common and is triggered predominantly by inhaled indoor and outdoor allergens such as dust mites, pet dander, pollen, and mold. Other risk factors include genetic predisposition, ethnicity,19 gender, tendency to develop allergies (atopy), and obesity.20

LIFE CYCLE PERSPECTIVES

Asthma in Children Colette LaSalle, PhD, RD  San Jose State University Over the last decade, prevalence of asthma in children has increased, with 2011 estimates indicating that over 7 million children1 in the United States have been diagnosed with this common respiratory disorder. The etiology of this increase is uncertain, although there is some evidence linking weight ­status and asthma. While the frequency of asthma is higher2,3 in obese youth, being overweight itself may not increase risk.4,5 Weight status can impact pulmonary function and obese and overweight children do exhibit a lower ratio of percent forced expiratory volume in the first second over forced vital capacity (FEV1/FVC).6 There are no specific nutritional interventions for children with asthma, but given the relationship between weight and pulmonary function, weight control interventions may improve overall respiratory status. It is unclear whether there is a causal relationship between asthma and food allergies, but children often have both and are at risk of more severe asthma attacks if they do have food allergies.7 Thus, children and caregivers should be educated on allergen avoidance strategies. Asthma is also associated with esophageal reflux, so if the child has GER,8 following GER treatment recommendations can be helpful. While respiratory

health is dependent on nutritional status and children with asthma have lower levels of certain antioxidants, vitamin D, and polyunsaturated fatty acids (PUFAs), there are limited data to support dietary interventions in this population.9,10 Because asthma attacks can be life threatening, children are typically prescribed rescue inhalers (to be used in case of acute asthma attacks) along with long-term inhaled corticosteroid (ICS) therapy to control their asthma.11,12 Children represent a particularly vulnerable group as they rely on their caregivers to follow the drug regimen, yet parents do not ­always follow the recommendations.13 While ICS therapy does have some potential side effects, the risk of a severe asthma attack due to poor control outweighs them. Acutely, use of ICS increases the risk of oral infections, which could impair dietary intake, but rinsing out the mouth after inhaling the medication can minimize this. However, long-term use of corticosteroids can affect growth and metabolism by suppressing adrenal function, impairing bone remodeling, and reducing growth velocity and height.14 A recent study found that children who had used inhaled corticosteroid therapy through puberty exhibited reduced growth and short stature.15 Therefore, the primary

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Asthma in Children (continued) objective for the RDN working with this population is to provide nutrition interventions that promote a healthy weight and support growth and development. References 1. Centers for Disease Control and Prevention: National Center for Health Statistics, National Health Interview Survey Raw Data, 2011. Analysis by the American Lung Association Research and Health Education Division using SPSS and SUDAAN software. 2. Black MH, Smith N, Porter AH, Jacobsen SJ, Koebnick C. Higher prevalence of obesity among children with asthma. Obesity (Silver Spring). 2012 May; 20(5): 1041–47. 3. Ahmad N, Biswas S, Bae S, et al. Association between obesity and asthma in US children and adolescents. J Asthma. 2009; 46: 642–6. 4. Mahut B, Beydon N, Delclaux C. Overweight is not a comorbidity factor during childhood asthma: the GrowthOb study. Eur Resp J. 2012; 39(5): 1120–26. 5. Sidoroff V, Hyvärinen MK, Piippo-Savolainen E, Korppi M. Overweight does not increase asthma risk but may decrease allergy risk at school age after infantile bronchiolitis. Acta Paediatr. 2012; 101(1): 43–17. 6. Vo P Makker K, Matta-Arroyo E, et al. The association of overweight and obesity with Spirometrie values in minority children referred for asthma evaluation. J Asthma. 2013; 50(1): 56–63.

Nonallergic asthma is caused by other factors, such as anxiety, stress, exercise, cold air, dry air, hyperventilation, passive smoke, viruses, or other irritants. Patients with asthma are at greater risk for life-threatening allergic reactions to foods. Persistent asthma has been associated with elevated IgE to egg and wheat, though food allergies are rarely a cause of asthma. Epidemiological studies have demonstrated that there is an association between obesity and asthma. Lung function decline has been correlated with obesity for both adults and children.20–23 Obesity is associated with low levels of inflammation and this may impact the overall inflammatory response and the development of asthma. Furthermore, there have been additional concerns for insulin resistance in these populations and this impact on the ability to treat asthma.23 The literature has indicated that weight loss results in the improvement of asthma symptoms and overall measures of lung function. For example, patients with asthma who undergo bariatric surgery have a significant decrease in their requirement for medications.24

Pathophysiology When asthma occurs, the inflammatory response affects all areas of the respiratory tract and especially the bronchi and bronchioles, which respond to stimuli by contraction of their smooth muscle (bronchoconstriction). Multiple cells of the immune system (e.g. mast cells, eosinophils) and chemical mediators (e.g. histamine, leukotrienes) direct the inflammatory response. The mucosa becomes inflamed and edematous, with an increased production of mucus, resulting in a partially or totally obstructed airway.17

Clinical Manifestations The initial symptoms the patient may experience include cough, dyspnea, and a tight feeling in the chest. Signs may include wheezing, increased respiratory rate, and labored breathing. Increased heart rate (tachycardia) and hypoxia may 648  Part 4  Nutrition Therapy

7. Wang J, Liu AH. Food allergies and asthma. Curr Opin Allergy Clin Immunol. 2011; 11(3): 249. 8. Thakkar K, Boatright RO, Gilger MA, El-Serag HB. Gastroesophageal reflux and asthma in children: a systematic review. Pediatrics. 2010; 125(4): e925–30. 9. Allan K, Devereux G. Diet and asthma: nutrition implications from prevention to treatment. J Am Diet Assoc. 2011; 111(2): 258–68. 10. ESPGHAN Committee on Nutrition; Agostoni C, Braegger C, Decsi T, et al. Supplementation of N-3 LCPUFA to the diet of children older than 2 years: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr. 2011; 53(1): 2–10. 11. Jones BR Paul A. Management of acute asthma in the pediatric patient: an evidence-based review. Pediatr Emerg MedPract. 2013; 10(5): 1–23. 12. Jones CC, Becker EA, Catrambone CD, Martin MA. A g ­ uideline­based approach to asthma management. Nurs Clin North Am. 2013; 48(1): 35–15. 13. Klok T, Lubbers S, Kaptein AA, Brand PL Every parent tells a story: why non-adherence may persist in children receiving guideline-based comprehensive asthma care. J Asthma. 2014; 51(1): 106–12. 14. Kelly HW, Sternberg AL, Lescher R, et al. Effect of inhaled glucocorticoids in childhood on adult height. NEJM. 2012; 367(10): 904–12. 15. Roizen J, Alter C, Bamba V. Recent research on inhaled corticosteroids and growth. Curr Opin Endocrinol Diabetes Obes. 2012; 19(1): 53–56.

also be observed. Prolonged exacerbation of asthma may result in respiratory alkalosis if untreated, which can progress to respiratory acidosis if not recognized and appropriately addressed.

Treatment An acute asthma exacerbation requires immediate attention to dilate airways and improve oxygenation and ventilation. These interventions would include the use of a bronchodilator with a β-2 agonist medication such as albuterol to address airway inflammation (see Table 21.5). Chronic and long-term control of asthma is achieved using a variety of agents, including corticosteroids (systemic and inhaled) and leukotriene receptor antagonists. Other treatments will include the environmental control of potential allergens and the development of controlled breathing techniques.17 Treatment of asthma includes removal of any items that are known to be asthma triggers from the patient’s environment. When these measures do not work, there are a variety of medications used to control symptoms. Generally, medications are divided into those that provide quick relief and those designed to provide long-term control. Quick-relief medicines, usually bronchodilators, are used to ease the wheezing, coughing, and tightness of the chest that occur during asthma episodes. Long-term medications include anti-inflammatory agents, such as inhaled steroids, that are designed to make the control inflammation.17

Nutrition Therapy for Asthma Cytokines and T-helper cells are examples of cells and chemical mediators involved in the inflammatory response. ­L eukotrienes are one class of those chemical mediators that contribute to the development of asthma. Leukotrienes, which are synthesized from arachidonic acid, modulate the inflammatory response resulting in tissue edema, mucus secretion, smooth-muscle proliferation, and powerful bronchoconstriction. Two types of leukotriene-based medications

have been developed to combat asthma: leukotriene inhibitors that interfere with the actual synthesis of leukotrienes (Zyflo®), and leukotriene antagonists that block their action at the receptor level (Accolate® and Singulair®) (see Table 21.5). The relationship between diet and asthma has been explored from a variety of hypotheses. The hypotheses have primarily focused on the role of a pro-inflammatory diet pattern and relationship to etiology or the consumption or supplementation of foods considered to be anti-inflammatory. The underlying premise is that certain diet components reduce the inflammatory immune response.25 As you have seen previously in the discussion of inflammation and diet (see Chapters 9, 12, 13, 15), normally, human inflammatory cells contain high amounts of the omega-6 fatty acid, arachidonic acid, and low amounts of omega-3 fatty acids. Because both omega-6 and omega-3 fatty acids are metabolized by a common pathway, an excess of omega-3 fatty acids interferes with the metabolism of the omega-6 fatty acids and reduces their incorporation into tissue lipids. The Mediterranean dietary pattern has been associated with a reduced asthma prevalence.26 The Mediterranean dietary pattern emphasizes increased fruits, vegetables, and food sources higher in omega-3-fatty acids. This dietary pattern has been recommended for many chronic diseases including cardiovascular, fatty liver disease and chronic pancreatitis and is one of the patterns recommended by the U.S. Dietary Guidelines (see Appendix C). A recent meta-analysis examined the relationship between regular fish intake and found that there appeared to be a benefit from introducing fish into the diet at an early age and regular weekly consumption.27 Even though there is much interest and promise from both observational and epidemiological studies exploring the dietary connections to asthma, there is inadequate evidence to recommend supplementation above and beyond food choices. An earlier Cochrane review of nine randomized-controlled studies of omega-3 fatty acid supplementation in asthmatic patients found no consistent effects on clinical outcome measures of asthma, including pulmonary function tests, asthmatic symptoms, medication use, and bronchial hyperreactivity.28 Currently, there is a component of an ongoing prospective 5-year trial examining the role of omega-3-fatty acid supplementation and vitamin D where lung function and onset of respiratory disease will be examined.29 It is this type of research design that will provide the practitioner adequate evidence to make nutrition therapy recommendations in treatment of asthma. One component of nutrition therapy involves the identification of drug–nutrient interactions and providing interventions to counteract. Medications prescribed for treatment of asthma may have a number of nutritionally relevant side effects, including dry mouth, throat irritation, nausea, vomiting, and diarrhea. Long-term use of corticosteroids has been associated with increased serum glucose levels and sodium retention. The short-term use of inhaled corticosteroids at conventional or usual doses (for 2–3 years) has not been associated with loss of bone mineral density (BMD) or fractures in adult patients with asthma or mild chronic obstructive pulmonary disease and actually may improve BMD by reducing the overall level of chronic inflammation.30,31 Until the relationship between diet and the etiology of asthma is confirmed, it is most important to recommend a nutritionally adequate diet for individuals suffering from asthma that promotes the Mediterranean dietary pattern. Appendix C

provides an outline of the Mediterranean diet. As stated earlier, obesity is related to asthma and weight loss improves symptoms in many. The dietitian can play a significant role in assessing nutrition status and creating a personalized plan that addresses anti-inflammatory diet components within the Mediterranean diet pattern and that will promote a healthful weight.

21.4 BRONCHOPULMONARY DYSPLASIA (CONTRIBUTED BY SAMANTHA BATEMAN, MS, RDN, LD) Definition Bronchopulmonary dysplasia (BPD) is a neonatal chronic lung disease that is characterized by pulmonary inflammation and impaired growth and development of the alveoli. The definition of BPD is based on the severity of the condition. In 2001, the National Institute of Child Health and Development/National Heart Lung and Blood Institute Workshop modified the most 2001 classification of BPD to include gestational age (GA) and disease severity. This definition of BPD is: Mild: the need for supplemental oxygen for greater than or equal to 28 days but not at 36 weeks’ postmenstrual age or discharge; Moderate: oxygen supplementation for greater than or equal to 28 days plus treatment with 20 years of age should maintain a BMI of ≥23 kg/m2 and females >20 years of age should maintain a BMI of ≥23 kg/m2.72,77 Other ­nutrition-related complications of CF include malabsorption of fat-soluble vitamins, hyponatremia, and osteoporosis.72

Nutrition Assessment Anthropometric Measurements  Early detection of poor

growth allows for appropriate intervention and treatment. The type of CFTR mutation can influence height, weight, and transverse chest width in children. There are three periods when special attention needs to be focused on growth and nutritional status: during the first 12 months after diagnosis of CF, from birth until 12 months of age for infants diagnosed at birth, and during the peripubertal growth period (9–16 years for girls and 12–18 years for boys). Infants from birth to 24 months old have their weight, length, and weight-forlength plotted using the World Health Organization’s (WHO) growth standards. The Center for Disease Control and Prevention growth charts are used for patients 2−20 years of age to assess weight, height, and body mass index (available at www.cdc.gov/growthcharts). Expectations for growth are similar to those of children without CF. Children are considered to be at nutritional risk if they are between the 10th and 25th

weight-for-length percentile and are considered to exhibit failure to thrive if they are at less than the 10th weight-for-length percentile. Mid-upper arm circumference (MUAC) should be measured for pediatric nutrition assessments and are compared to WHO standards for children 6–69 months. MUAC appears to have a higher sensitivity for changes in body composition than other anthropometric measures in pediatrics.77

Biochemical Data and Medical Tests  As mentioned

previously, CF guidelines outline recommendations for medical care and monitoring. Stable patients are assessed three to four times per year with more frequent monitoring for those who are ill or who are experiencing complications. Regular biochemical monitoring includes glucose, albumin, electrolytes, hemoglobin, hematocrit, and serum levels of vitamins A, D, and E. Glucose intolerance and cystic fibrosis-related diabetes (CFRD) occur in approximately 10–15% of CF patients over the age of 20. CFRD is rarely found in young children and occurs more frequently between 18 and 21 years. The exact cause of diabetes mellitus in CF is not clearly understood but is thought to be related to inflammation and the accumulation of fibrous tissues in the pancreas, which interferes with normal insulin production. Individuals with CFRD have an increased morbidity and mortality. They are often underweight and have more advanced pulmonary involvement than those without CFRD. Malnutrition and low BMI are warning signs of the development of CFRD.78 Like type 2 diabetes (see Chapter 17), CFRD may be present for years before diagnosis. Symptoms of CFRD include polyuria (excessive urination) and polydipsia (excessive thirst), failure to gain or maintain weight despite aggressive nutrition intervention, poor growth velocity, an unexpected decline in pulmonary function, and a failure to progress normally through puberty.78 Diagnosis of CFRD is made using an oral glucose tolerance test (OGTT), a test of the body’s ability to metabolize carbohydrate (see Chapter 17). Micronutrient status is a crucial component of the nutrition assessment and deficiencies are not uncommon. This is especially common for fat soluble vitamins.79 Vitamin A is important for vision, the integrity and proliferation of epithelial cells, and normal immunity. Studies examining the vitamin status of individuals with CF indicate that deficiency of vitamin A may be common.80 Note that since plasma vitamin A levels can be decreased in infection, levels measured during acute illness can be misleading. The major function of vitamin D is to control calcium absorption. Low vitamin D intake has been reported among CF patients and studies have documented low serum 25-hydroxyvitamin D concentrations despite daily supplementation of vitamin D. This is of particular importance because of the increased prevalence of osteoporosis and bone fractures among patients with CF. Serum vitamin D levels need to be carefully monitored to ensure that the patient is receiving an appropriate dosage of the vitamin.81 Vitamin E is a powerful antioxidant. Deficiencies lead to hemolytic anemia, neuromuscular degeneration, and retinal and cognitive changes. Low vitamin E levels as well as symptomatic deficiency states have been reported in patients with CF, even those taking pancreatic enzymes and multivitamins (see Table 21.9).79 Chapter 21  Diseases of the Respiratory System   661

Table 21.9 Assessment of Nutritional Status for Individuals with Cystic Fibrosis Nutrition Parameter

Frequency of Assessment

Anthropometric Measurements: Weight (to 0.1 kg)

Every 3 months

Height (length age 8 years if risk factors are present—annually or as indicated

Iron

Annually

Zinc

Annually

Sodium

If dehydration is suspected or exposed to heat stress

Albumin

Annually

Source: Adapted from Borowitz D, Baker RD, Stalling V. Consensus report on nutrition for pediatric patients with cystic fibrosis. J Pediatr Gastroenterol. 2002; 35: 246–59.

Children and adolescents with CF have also been shown to have iron and zinc deficiencies. 82 Iron status should be monitored yearly by checking hemoglobin and hematocrit levels. Zinc deficiency may be present even though plasma zinc levels are normal. Individuals with CF have an increased incidence of osteopenia and osteoporosis, and an increased risk of fractures. Contributing factors include deficiencies of vitamin D, vitamin K, and calcium; use of corticosteroids; disease severity; inactivity and low body mass; hypogonadism; and malnutrition. The bone mass of children age 8 and older who have risk factors for bone disease should be evaluated using dual-energy X-ray absorptiometry (DXA). Additionally, in children at risk for poor bone health, serum calcium, phosphorus, parathyroid hormone, and 25-hydroxyvitamin D levels should be measured.79 Table 21.9 outlines the timeline for nutrition assessment, including growth status assessment, for individuals with CF.

662  Part 4  Nutrition Therapy

Nutrition Diagnosis

Nutrition-Related Medication Management: Pancreatic Enzyme Therapy  Because greater than 80% of

individuals with CF have pancreatic insufficiency, malabsorption of dietary fat, protein, fat-soluble vitamins, and other nutrients often occurs.83 Pancreatic insufficiency has a strong influence on nutrition status and is a predictor of long-term outcome. Individuals with CF are prescribed pancreatic enzyme supplements that contain lipase, protease, and amylase. These enzymes are specifically formulated with an enteric coating that allows for better absorption into the duodenum. Dosing for enzymes is based on the individual’s weight, size and macronutrient of each meal, and any physical signs of malabsorption (i.e. steatorrhea, gas, abdominal pain). The typical recommended enzyme dose for an infant age birth to 12 months is 2 000−4 000 units of lipase per 120 mL of breast milk or formula, but can also be dosed based on units of lipase per kilogram per feed. After 12 months of age, the Cystic Fibrosis Foundation recommends an enzyme dose to be less than 2500 units of lipase per kilogram of body weight per meal. It is recommended that patients do not consume more than 10,000 units of lipase per kilogram of body weight per day.84,85 Children and adults take the enzyme replacement with each meal and infants receive their enzymes mixed with applesauce prior to each feeding.

Energy and Macronutrients  Adequate kcalories to support normal growth and development are essential, especially with pancreatic insufficiency. Energy intake in children should be based on their patterns of weight gain and growth. If an individual has significant growth deficits, lung disease, or malabsorption, energy requirements may be significantly increased (110–200% of the RDA for age). The 2002 Nutrition Consensus Report states that there is no perfect method to estimate the kcalorie needs of a person with CF; instead, a steady rate of weight gain in growing children should be the goal. One starting place is to begin with 130–150% of the RDA for age and then adjust as necessary to maintain a goal weight. As stated earlier in this section, the CF foundation recommends that children with CF maintain a BMI at the 50th percentile. Males who are >20 years of age should maintain a BMI of 20 years of age should maintain a BMI of 8 years

10,000

200–400

400–800

0.3–0.5*

Note: *Currently commercially available products do not have ideal doses for supplementation. These fat-soluble vitamins are given in addition to an age-appropriate dose of non-fat-soluble vitamins. Source: Adapted from Borowitz D, Baker RD, Stalling V. Consensus report on nutrition for pediatric patients with cystic fibrosis. J Pediatr Gastroenterol. 2002; 35: 246–59.

Children need to be monitored for appropriate growth. Additional energy in the form of in-between meal snacks and nutrient-dense foods, particularly foods high in fat, should be added to the diet to support growth. Appropriate feeding behaviors should be encouraged at each age. School-age children (5–10 years) are at higher risk for decreased growth rate. Participation in activities increases energy expenditure and may also lead to limited time for consumption of snacks and taking of enzymes. Adolescence (11–18 years) is a time associated with accelerated growth and pubertal development; nutritional counseling directed specifically toward the adolescent may be necessary (see Table 21.12). The use of nutritional supplements may help to add additional energy, protein, and other nutrients to the diet. Homemade foods high in kilocalories and protein, such as fortified beverages or puddings, may be beneficial. Supplemental enteral feedings may need to be added if adequate kilocalorie intake cannot be achieved or growth is compromised. Nocturnal enteral feedings are encouraged to promote normal eating behaviors during the day. Standard formulas (1.5–2.0 kcal/cc) containing complete protein and long-chain fatty acids are usually well tolerated.

21.10 CONCLUSION The lifetime management of this chronic disease includes many challenges for medical, nutritional, and socioeconomic challenges. The interprofessional team care for these patients is the foundational key to assure positive health outcomes. Future scientific efforts will continue to support the positive impact on life expectancy.

21.11 PNEUMONIA Definition Pneumonia is defined as an infection of the lungs, usually caused by bacteria, viruses, or fungi. Once the offending agent enters the lungs, which usually occurs either through inhalation of infectious particles, aspiration of oropharyngeal secretions or spread of infection into the lung through the blood, it usually settles in the alveoli where it can grow rapidly. The infection causes deterioration of lung function, resulting in fluid accumulation affecting gas exchange and breathing difficulty.86 664  Part 4  Nutrition Therapy

Table 21.12 Developmental Approaches to Nutrition Counseling for Individuals with Cystic Fibrosis Infants: • Breastfeeding is recommended for most infants as the primary source of nutrition during the first year of life. Human milk fortifiers may be used to increase the nutrient density of breast milk, if needed. • Iron-fortified infant formula may be used. The caloric density of the standard infant formula (20 kcal/oz) may need to be increased by concentrating the formula or using fat and/or carbohydrate additives, as appropriate. • Solid foods should be added at 4–6 months developmental age, according to recommendations of the American Academy of Pediatrics. • Infant cereal should be prepared with breast milk or infant formula, not water or juice; additional fat or carbohydrate kilocalories may be added to infant cereal, if needed, to achieve expected rate of growth. • Pancreatic enzymes should be given prior to each feeding using small amount of applesauce • Vitamin supplements with additional fluoride and iron should be given. Toddlers or Preschool Age (1–4 Years): • Whole milk should be encouraged for the child with CF. • Adding kilocalories to table food may help with maintenance of growth at this stage; avoid giving low-fat or low-kilocalorie foods. • Regular mealtimes and snack times should be encouraged. • Dietitians should inquire about feeding behaviors to promote positive interactions and prevent negative behaviors; grazing behavior should be discouraged. • Pancreatic enzymes and vitamins are continued. School Age (5–10 Years): • A normal, healthy diet with a variety of food should be the basis of the diet. • This may be a high-risk period for decreased growth rate in children with CF; identify factors that may interfere with meeting nutritional needs, such as activities that may lead to limited time for snacks and enzyme adherence and the progression of the disease. • Pancreatic enzymes and vitamins are continued. Adolescence (11–18 Years): • Associated with high nutrient requirements due to accelerated growth, pubertal development, and high levels of physical activity. • Nutritional counseling will be more effective if directed toward the adolescent, not the parent. • Adolescents may be more receptive to efforts to improve muscular strength and body image rather than stressing weight gain and improved disease status. • Continue pancreatic enzymes and vitamins. Source: Adapted from Borowitz D, Baker RD, Stalling V. Consensus report on nutrition for pediatric patients with cystic fibrosis. J Pediatr Gastroenterol. 2002; 35: 246–59.

Epidemiology Prior to 1936, pneumonia was the leading cause of death in the United States, but with the use of antibiotics, the incidence of pneumonia has been substantially reduced. In 2015, pneumonia caused 16.1 deaths per 1 00,000 individuals in the United States.87

Etiology Although the microorganisms responsible for pneumonia are present in the environment and are inhaled into the lungs all the time, the cilia and macrophages present in the lungs usually prevent them from entering the alveoli. However, the normal defense mechanisms may be compromised in certain populations, including older adults, infants and young children, and individuals with health problems such as COPD, diabetes mellitus, asthma, alcoholism, stroke, congestive heart failure, and sickle cell anemia. Individuals living with HIV/AIDS and those undergoing chemotherapy or organ transplants who are immunocompromised are also at substantial risk for developing pneumonia. There are three major categories of pneumonia based on the cause: community-acquired pneumonia (CAP), ­hospital-acquired pneumonia (HAP), and ventilator-acquired pneumonia (VAP). CAP occurs when infected persons cough or sneeze and spread the bacteria, primarily Streptococcus pneumoniae (which causes pneumococcal pneumonia), to those around them.86,87 HAP, also known as nosocomial pneumonia or health care-associated pneumonia (HCAP), often affects patients who are in the intensive care unit (ICU). Hospital-acquired pneumonia occurs fairly frequently and has a high rate of mortality. The incidence of hospital-acquired pneumonia is highest among individuals over age 70, the very young, and those who are already debilitated by other diseases.86 HCAP is acquired in other health care settings such as nursing homes, rehabilitation centers, and convalescent homes and may be caused by any of the same causative agents as other forms of pneumonia.86 Accurate diagnosis of HCAP, HAP, and VAP is challenging as there is no specific test to delineate, but often involves collection of specimens for culture and careful monitoring. Bronchoalveolar lavage (BAL) or mini BAL (performed by a Respiratory Therapist), when the lung is lavaged with sterile saline and then the saline (and infectious organisms in the lung causing the infection) is immediately recovered, is a technique that is useful for obtaining the lower respiratory tract specimen to assist in appropriate identification of the infectious agent to determine treatment.

Aspiration Pneumonia Another common cause for the development of pneumonia is aspiration of inhaled materials (saliva, nasal secretions, bacteria, liquids, food, or gastric contents) into the airway below the level of the vocal cords. Aspiration can result, for instance, from inhalation of oropharyngeal and gastric fluids. Aspiration pneumonia occurs when the aspirated material causes an inflammatory response in the lung. There are a number of normal defense mechanisms that help to prevent aspiration. During the swallowing process, the epiglottis, a thin cartilage structure located at the base of the tongue, folds over the top of the larynx to prevent food and liquid from entering the trachea (see Chapter 14). The lower esophageal sphincter (LES) also prevents the upward movement of gastric contents into the esophagus. In addition, food particles and fluids that may be aspirated into the lungs are entrapped in the mucus layer of the respiratory epithelium. The mechanical beating of cilia on the respiratory epithelium advances the

mucus and entrapped particles upward so it can be cleared by the cough. Cough is an important mechanism that allows clearance of foreign material and secretions from the airway. A number of risk factors may contribute to aspiration. Patients with head injuries often have delayed gastric emptying and a decreased gag and cough reflex, and thus are at high risk for aspiration. Individuals who have neurological impairments such as stroke and Parkinson’s disease are at high risk for dysphagia (difficulty in swallowing) and subsequent aspiration (see Chapter 14). Other risks are use of paralyzing agents, improper positioning of a feeding tube, and placement of the head of the patient’s bed at a shallow angle (i.e., not a ≥30° angle). Hyperglycemia can result in disordered motility throughout the gastrointestinal tract. Patients with diabetes who have gastroparesis (delayed gastric emptying, vomiting, nausea, or bloating caused by stomach nerve or muscle damage) may aspirate, particularly if they receive gastric tube feedings. In addition, patients with abnormalities of the gastrointestinal tract including esophageal stricture and gastroesophageal reflux disease (GERD) or who require mechanical ventilation are also at high risk for developing aspiration.86 To avoid aspiration, it is important that the patient’s head be elevated higher than his or her stomach, or at an angle of >30 degrees, during feeding. Residual volumes of liquid in the stomach have also been historically used to determine whether a feeding was emptied from the gastrointestinal tract (and thus potentially placing one at risk for aspiration), but guidelines for this practice are not well established.88 In the Consensus Statement presented by the North American Summit on Aspiration in the Critically Ill Patient, it was recommended that enteral feeding be stopped only if there is definite regurgitation or aspiration of gastric contents or if a residual greater than 500 mL is measured.88 A.S.P.E.N 2016 guidelines do not recommend the use of gastric residuals to monitor tolerance of enteral feeding. If there is a concern for decreased gastric emptying, it is recommended to trial either metachlopramide or erythromycin for treatment.89

Patients with Tracheostomies A tracheostomy is a surgical opening made in the trachea to assist breathing. A tracheostomy tube is inserted through the surgical opening (stoma), as shown in Figure 21.7. A tracheostomy is usually performed for one of the following reasons: (1) to bypass an obstruction in the trachea, (2) to clean and remove secretions from the trachea and prevent them from entering the lungs, or (3) to more easily and safely deliver oxygen to the lungs, usually after long-term mechanical ventilation with an endotracheal tube in place, when the patient is not able to breathe without assistance. Sometimes children or adults require permanent tracheostomies to breathe. Patients who are unable to breathe on their own usually also require a mechanical ventilator (see Figures 21.8 and 21.9) in addition to the tracheostomy. Tracheostomy tubes come in many varieties and sizes, including both cuffed and uncuffed tubes. A cuff is a soft balloon around the distal (far) end of the tube that can be inflated to prevent oral secretions from entering the lungs and to seal the airway to deliver breaths via mechanical ventilation. The cuffs are inflated with air, foam, or sterile water. When the cuff is deflated, the tube allows air around it for vocalization. Chapter 21  Diseases of the Respiratory System   665

Figure 21.7 Tracheostomy Tube

Figure 21.9 Example of beside mechanical ventilator

Mouth

Larynx Source: Courtesy of Marcia Nelms.

Trachea Tracheostomy tube is placed in the tracheostomy (hole) Inflatable cuff

Esophagus

(Anatomy is shown in cross-section)

Figure 21.8 Mechanical Ventilation

support. Once they are weaned (removed) from the ventilator, the tracheostomy tube may remain in place to remove secretions from the trachea. When it is safe for these patients to eat orally, the viscosity of the food often makes a difference. The dietitian often works closely with the speech pathologist to determine whether the patient can safely swallow food without aspiration and, if so, the consistency of food that is appropriate. See Chapter 14 for a complete discussion of dysphagia diets.

Respiratory Failure ET tube Vocal cord

Nasal path Vocal cord Endotracheal tube (oral) Epiglottis

Trachea “Cuff” ballon

Lungs

Nutritional Implications There are many potential complications related to the presence of a tracheostomy tube, including the inability to speak or swallow normally. Patients with tracheostomy tubes who are on mechanical ventilation are often at high risk for aspiration. Frequently these patients require enteral nutrition 666  Part 4  Nutrition Therapy

Respiratory failure (RF) occurs when the respiratory system is no longer able to perform its normal functions. RF is caused by either hypoxemia (low oxygen) or hypercarbia (excess CO2) or both and can be quantified by ABG. It can result from a long-standing chronic lung disease such as COPD or cystic fibrosis, as a result of an acute condition such as drug overdose, or from an insult to the lung as seen with acute respiratory distress syndrome (ARDS). Regardless of the cause, intervention often includes strategies to improve or correct the oxygenation or ventilation issue. ARDS encompasses a variety of changes in lung function associated with critical illness. The diagnostic criteria include an acute onset (within a week of insult), bilateral infiltrates in the lungs, exclusion of hydrostatic edema, and pressure of arterial oxygen/fraction of inspired oxygen (PaO2/ FiO2). Further diagnosis uses the severity of oxygenation impairment and includes the following definitions: mild ARDS as >200 mmHg and 100 mmHg (moderate) but ≤200 mmHg on PEEP or CPAP ≥ 5 cm H2O and severe as ≤100 mmHg PEEP or CPAP ≥5 cm H2O.90 Conditions that may lead to ARDS (see Table 21.13) may result from direct damage to lung tissue as is seen with pneumonia, COPD, and aspiration or from the

Table 21.13 Conditions Associated with the Development of Acute Respiratory Distress Syndrome Direct Injury

Inflammatory (Indirect) Injury

Pneumonia

Sepsis

Aspiration of gastric contents

Severe trauma

Inhalation injury

Acute pancreatitis

Near drowning

Cardiopulmonary bypass

Pulmonary contusion

Massive transfusions

Fat embolism

Drug overdose

Pulmonary edema Postlung transplantation Source: Adapted from Mackay A, Al-Hadded M. Acute lung injury and acute respiratory distress syndrome. Cont Edu Anaesth Crit Care & Pain. 2009; 9: 152–56.

systemic inflammatory response seen in sepsis, trauma, or burns (see Chapter 22). Pulmonary edema invades the alveolar and capillary space, leading to impaired gas exchange, hypoxia, and overall increased work of breathing. Oxygen therapy can be provided by nasal cannula, face mask, CPAP, or bilevel positive airway pressure (BiPAP). Mechanical ventilation is also often required, at least in the acute stages of ARDS, and this can lead to prolonged mechanical ventilation. Pharmacological treatment may include respiratory stimulants, bronchodilators, antibiotics, steroids, sedatives, narcotics, and paralytic agents.

21.12  NUTRITION THERAPY FOR MECHANICALLY VENTILATED INDIVIDUALS Nutritional Implications

ventilation, preserve and restore lean body mass, blunt the inflammatory response, and maintain fluid balance.89

Nutrient Requirements  Total caloric requirements can either be estimated using a predictive equation or directly measured using indirect calorimetry. Indirect calorimetry is the gold standard and is especially important in this population due to the risk of under- or overfeeding. Both under- and overfeeding can lead to difficulty weaning from the ventilator, increased length of stay, and increased risk of complications. Many individuals on mechanical ventilation require propofol as a paralytic. It is important to include the energy provided by this medication (1.1 kcal//mL) in planning nutrition support. Table 21.14 outlines the guidelines for nutrition support for individuals that are mechanically ventilated. The 2016 ASPEN critical care guidelines state that either “trophic or full nutrition by EN is appropriate for patients with ARDS and those expected to have a duration of >72 hours.”89 A standard high-calorie, high-protein polymeric formula can be used for most patients with pulmonary failure on mechanical ventilation. Fluid overload poses a particularly high risk for this population and therefore, a formula with higher energy density in reduced fluid volume may assist. Provision of immunonutrition with omega-3 fatty acids, arginine, glutamine, antioxidants, and nucleic acids have been previously recommended Table 21.14 Nutrition Support Guidelines for Mechanically Ventilated Individuals Nutrition Assessment: • Evaluate weight loss, pervious intake, disease severity, comorbidities, and Gl function. Use of a screening tool such as NUTRIC score or NRS 2002 is recommended to identify high risk individuals. • Indirect calorimetry should be used to evaluate energy requirements whenever possible. (See Chapter 3 for indirect calorimetry best practices.)

Patients who require ventilator support are not able to consume foods orally and will require an alternative form of nutrition support. The route of nutrition support is determined by applying the ASPEN critical care guidelines based on the patient’s underlying illness and gastrointestinal function; nonetheless, enteral nutrition is the preferred method of support due to its role in maintaining gastrointestinal function, the reduced risk of sepsis, and its lower cost. In cases where enteral nutrition support is not possible, and nutritional needs warrant, parenteral nutrition is used.89

• Provide protein to achieve 1.2–2.0 g/kg/day

Nutrition Assessment and Intervention

• Parenteral nutrition may be used alongside EN to meet energy requirements if target volume of EN cannot be tolerated. (after 7–10 days of insufficient EN)

Nutritional needs vary widely depending on the age of the patient, the patient’s prior nutritional status, and the underlying disease process, which is often hypermetabolic. Often patients with RF are poorly nourished, particularly if they have a long-standing history of COPD or CF. Calculation of the NUTRIC score is used to determine nutrition risk in the critical care setting and thus, providing the rationale for nutrition support. A complete nutrition assessment to evaluate the patient’s individual nutritional needs, including anthropometric and laboratory measurements, should be completed. The goals of nutrition therapy during respiratory failure are to meet nutritional needs that will support weaning from mechanical

Nutrition Intervention: • Enteral nutrition support (EN) is preferred when the Gl tract is functional. • Early EN is preferred with hemodynamically stable patients and should be initiated within the first 24–48 hours for those individuals who are anticipated to required support >72 hours. • Attempt to reach 60% of goal within first 7–10 days of feeding. • High-protein polymeric formula is preferred if the Gl tract is functional. Fluid restricted high energy dense formulas may assist with patients who are volume overloaded.

• Head of bed should be elevated 30º–45º. Chlorohexidine mouthwash may be recommended to decrease risk of ventilator associated pneumonia. • Monitor serum phosphate and treat accordingly. Sources: Adapted from Allen KS, Hoffman LA, Jones K, et al. Pulmonary disease. In: Mueller CM, ed. The A.S.P.E.N. Adult Nutrition Support Core Curriculum. 3rd ed. Silver Springs, MD: ASPEN; 2017: 489–502. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assesssment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter Enteral Nutr. 2016; 40: 175–211.

Chapter 21  Diseases of the Respiratory System   667

for use in ARDS but the 2016 ASPEN critical care guidelines state that the use of these formulas for patients with ARDS cannot be supported at this time. The current literature has significant contradictions in outcome data and definitive recommendations cannot be made.89 Typical laboratory assessments for nutrition support monitoring should be followed. In particular, serum phosphorus should be assessed early and regularly. It is not uncommon to see a higher frequency of hyphophosphatemia in this population.91

21.13 TRANSPLANTATION Definition and Epidemiology Lung transplantation is a surgical procedure in which one or both lungs are replaced with healthy organs from a human donor. Lung transplantation is an accepted option for patients with end-stage lung disease. In some cases where the heart has also been weakened, both the heart and lungs will be replaced. Until 1989, combined heart–lung transplants were the most common form of lung transplantation, but more recently single and double lung transplants have become more common.92 Data from the most recent statistical reports on solid organ transplantation indicate 2692 candidates were added to the waiting list for lungs in 2016. In 2016, 2345 lung transplants were performed.93

Pathophysiology Transplant recipients are at high risk for rejection of the transplanted lung. The body’s immune system considers the transplanted organ an invader (similar to infection) and may attack it. Because of the rejection risk, patients must take immunosuppressive (antirejection) medications (see “Transplantation Immunology” section in Chapter 9). Rejection occurs most often during the first 3 months after transplantation, but the immunosuppressive medication may need to be taken indefinitely. Common immunosuppressive drugs used are cyclosporine, tacrolimus, mycophenolate mofetil, azathioprine, and prednisone. The nutritional side effects of these medications may include GI distress (nausea, vomiting, diarrhea, and/or constipation), increases in blood pressure, edema, and alterations in blood sugar levels. They also lower the body’s immunity and increase the risk of infection.

21.14  NUTRITION THERAPY FOR TRANSPLANTATION Nutritional Implications Patients with lung disease may be underweight, normal weight, or overweight. Overweight patients with lung disease, however, are often very sedentary and have significant increases in body fat mass rather than lean body mass (LBM). Lean body mass depletion has been associated with a higher rate of mortality in patients awaiting transplantation. Poor nutritional status, low LBM, as well as the presence of obesity can impact postoperative ventilation days, risk of infection, length of hospitalization, and overall transplant outcomes.94,95,96

Nutrition Assessment A comprehensive nutrition assessment of transplant recipients should include a nutrition-focused physical examination, 668  Part 4  Nutrition Therapy

dietary history, anthropometric measures, and laboratory values.95 Specific assessment issues are included in Table 21.7.

Nutrient Requirements  Protein and energy requirements are affected by the stress of surgery, postoperative complications, episodes of rejection, and the use of immunosuppressant drugs (particularly corticosteroids) but in general transplant, patients are not hypermetabolic unless complications arise. The use of indirect calorimetry to assess energy requirements is indicated when the patient’s medical condition is complicated by posttransplant complications. When indirect calorimetry is not available, 130–150% of BEE (or 35 kcal/kg body weight) is usually adequate. Adequate amounts of protein are required for wound healing and to prevent infection. Protein needs may be increased due to surgical stress and the use of corticosteroids. Suggested protein requirements range from 1.5 to 2.0 g/kg per day. These requirements may decrease to 1 g/kg as the dose of corticosteroids is reduced to maintenance levels during the post-transplant phase.95

Nutrition Intervention The physical and nutritional status of patients awaiting transplant may decline. Therefore, nutrition support is very important during the pretransplant period. The goal is to optimize nutritional status as much as possible by increasing kilocalories and protein. Most patients waiting for an organ transplant are able to eat. Small, frequent meals composed of nutrient-dense foods and supplements should be encouraged. Enteral feedings may be indicated if the patient is unable to eat adequate amounts. The acute posttransplant period may be complicated by rejection, infection, and surgical complications. The nutrition goals during this time are to provide adequate nutrients to promote wound healing, treat changes in electrolyte balance, and achieve optimal blood glucose control. Most transplant patients are allowed to eat 3–5 days after transplantation. Nutrition support should be considered when the patient is not able to eat or if oral feeding is delayed. When nutrition support is required, the use of enteral nutrition is preferred. Patients who are malnourished or at risk for extended NPO (nothing by mouth) status may benefit from immediate posttransplant enteral nutrition. When enteral nutrition support is not possible, parenteral nutrition is advocated. Parenteral nutrition should be administered cautiously because of postoperative hyperglycemia due to metabolic stress, infection, and the use of corticosteroids.95

21.15 CONCLUSION This chapter has reviewed the anatomy and physiology of the respiratory tract along with the detailed changes that occur during common disease processes. Many individuals with respiratory disease are at high nutritional risk and will need specialized nutrition support. Adequate and appropriate nutrition therapy functions to support the normal function of the respiratory tract, to prevent disease, and to support important interventions that serve as crucial components of medical care. The RDN, along with the interprofessional health care team, provide optimal care using an interdisciplinary model (see Box 21.4).

PRACTITIONER INTERVIEW

Susan Gemma, MS, RD  Clinical Dietitian at Nationwide Children’s Hospital—Cystic Fibrosis Program [email protected]

Please describe you current position and responsibilities. I currently work at Nationwide Children’s Hospital in Columbus, Ohio as a clinical dietitian with the Cystic Fibrosis (CF) team. The CF center at Nationwide Children’s Hospital follows over 500 patients with cystic fibrosis. One half of our patient population is 18 years and older, so the CF dietitians are involved in the nutrition management of individuals with CF from newborns throughout the life cycle. I provide nutritional care for hospitalized and clinic patients, in addition to patients in pulmonary rehab. I am also involved with pre- and postlung transplant patients. Standards of care and guidelines for nutrition management of patients with CF have been established by the Cystic Fibrosis Foundation (CFF). Accurate measurements of weight and height or length are paramount for patients when seen in clinic or admitted to the hospital. The CF dietitian uses this anthropometric information to assess trends in weight-forlength in children less than 2 years of age and in BMI for those greater than 2 years. Adequate growth for children is based on weight-for-length or BMI above the 50th percentile or Z score above the median. For adults the goal BMI is 22 and 23 kg/m2 for females and males, respectively. It is well documented in the CF literature that failure to achieve target BMI and/or weight can negatively impact lung function. A nutrition assessment is completed annually, which includes a 24-hour dietary recall, review of the patient’s stool pattern, and nutrition-related lab values. Fat-soluble vitamins A, D, and E are checked with annual labs. The CFF recommends an annual oral glucose tolerance test (OGTT) for patients 10 years and older. A baseline bone density scan (DEXA) is recommended for patients over eight years. At each CF clinic visit, the CF dietitian reviews the ­“nutrition-related” medications. Approximately, 85–90% of individuals with CF are pancreatic insufficient (PI) and require pancreatic enzyme replacement therapy (PERT) with meals and snacks. Enzymes are dosed on the patient’s weight, but can also be calculated based on grams of fat in the meal or snack. Since individuals with CF and PI have fat malabsorption, fat-soluble vitamins may also be malabsorbed. There are several brands of CF-specific multivitamins on the market that provide a water-­ miscible form of vitamins A, D, E, and K to facilitate absorption of these vitamins. Serum vitamin D levels are often suboptimal in patients with CF and an additional single vitamin D supplement is recommended. Moreover, if a patient’s diet history reveals inadequate intake of calcium or if the patient is diagnosed with osteopenia or osteoporosis, a calcium supplement is prescribed.

How has the nutritional care for individuals with CF changed during your professional career? When I started working at the CF center in 1988, the gene mutation had not yet been elucidated. One year later the classic gene, delta F 508, was discovered and over the past 29 years more than 2000 gene mutations associated with CF have been

identified. Once the first gene was discovered, researchers have been vigorously working to find a “cure” for CF, and over the past three decades, a myriad of new pulmonary therapies have been developed. The latest research has focused on new medications to “correct” the defective gene, which has given patients and their families hope for a longer and healthier life. The median age of survival for an individual with CF is currently 47 years old, compared to approximately 25 years of age 30 years ago. Another new development (in the state of Ohio) in the past 12 years has been screening for CF on the newborn panel. If an infant has an elevated marker on the newborn blood test, the same blood sample is tested for the 40 most common CF gene mutations. Identification of a newborn with CF enables the medical team to begin preventative care (initiating pancreatic enzymes, CF vitamins, salt supplementation and respiratory therapies) before the child becomes failure-to-thrive or develops a respiratory infection. Nutrition is an essential part in the medical therapy for individuals with CF. In the mid-1990s research studies funded by the CFF revealed a direct correlation between lung function and nutritional status—the better nourished the patient, the healthier the lungs. A high calorie, high protein diet has been the foundation of nutrition therapy for most individuals with CF. However, in recent years dietitians have emphasized the importance of consuming “healthy” fats such as omega-3 fatty acids found in nuts, avocado, coconut oil, and certain fish.

What are the major components of your nutrition assessment for each of your patients? The CFF recommends that patients meet with the CF team on a quarterly basis for close follow-up. This frequency of clinic visits affords the opportunity for the dietitian to meet with patients and their families on a regular basis. At NCH patients are seen for an annual nutrition assessment, then quarterly for an out-patient progress note. Individuals with poor weight gain or weight loss are seen more frequently by the dietitian. On a typical clinic day, there are usually 20–30 pediatric and adult patients scheduled in an afternoon. The CF dietitians review the patient list to determine who needs an annual nutrition assessment or a quarterly progress note. For patients who have been seen recently, a “screen” note is completed which addresses weight trends and any other nutrition-related concerns. Much of the time spent with the patient or caretakers is often devoted to “problem-solving” or monitoring weights. There is a nutrition template in the electronic medical record for each type of nutrition documentation: annual nutrition assessment, out-patient progress note and screen note. For patients admitted to the hospital, the CF dietitian completes an inpatient nutrition assessment. These templates outline the nutrition care process: anthropometric measurements, pertinent labs, nutrition-related medications, diet order, “impression,” PES statement, and recommendations, which include interventions and monitoring. (continued) Chapter 21  Diseases of the Respiratory System   669

What is the role of the RDN on the health care team in CF clinic? The CF team is a multidisciplinary medical team, consist of physicians, nurse practitioners, nurses, dietitians, social workers, and respiratory therapists. Over the past 3 years, the CF team at NCH has added a physical therapist, pharmacist, and child life specialist to CF clinic. During a clinic visit, the patient meets with most of the team members. As a CF dietitian, I often see the patient with the nurse or physician to gather information pertinent to the nutrition assessment. When there are socioeconomic concerns, the dietitian and social worker may meet with the patient and family together.

What are the most rewarding aspects of your career? The highlight of working with patients with CF is the “continuity of care.” Our patients are usually diagnosed in early infancy and followed throughout their life. At our CF center, patients are seen in clinic at every 2–4 weeks or 2–4 months depending on their medical needs. It is rewarding to see infants and children thrive with the recommended therapies and a high-calorie diet. Although it is very difficult for parents to learn that their newborn infant is diagnosed with CF (a life-shortening, chronic disease), there is now great hope for children to lead normal lives. Over the past 30 years, it has been especially rewarding to see children grow up, attend college, be married, and have children of their own. There are also rewards in gaining a patient or family’s trust and to see adherence to nutrition recommendations. Moreover, working with CF as a disease entity affords the opportunity for learning on a daily basis. Since CF affects the respiratory, gastrointestinal, and endocrine systems in the body, there is ongoing medical information to be learned. The CFF hosts the North American Cystic Fibrosis Conference and the Nutrition/Social work Consortium each year. These two

conferences provide educational opportunities for updates on caring for individuals with CF. I have had the privilege of participating as a roundtable moderator for specific nutrition topics. The daily collaboration in both the clinic and inpatient settings is also very rewarding. For example, with the new oral medications to “correct” the defective CF gene, the pharmacist counsels the patient and/or family on the proper administration of the drug. Since these medications are taken twice a day and best absorbed with 18–20 g of fat, the dietitian provides information on ways to consume adequate fat with each dose. The dietitian is an integral part of the CF team and her opinion on pancreatic enzymes, vitamin/mineral supplements and nutritional supplements is highly valued.

What is the greatest challenge caring for patients with CF? The daily routine for most individuals with CF includes a long list of medications and respiratory therapies: pancreatic enzymes with every meal and snack, vitamins, proton pump inhibitor, therapies with aerosolized treatments and vest therapy 20–30 minutes twice a day, not to mention consuming a high-calorie diet every day. For patients with CF-related diabetes, this means additional medications/therapies: glucose monitoring, carbohydrate counting and insulin coverage with meals. These therapies are very time-consuming, expensive (even with insurance), and the “pill burden” is tremendous. It has been said that “we expect extraordinary things from ordinary people.” It is challenging for individuals with CF to find a balance with adherence to all their therapies and living their daily life. Dietitians, in turn, are challenged with establishing rapport with patients and families in an effort to individualize nutrition counseling and provide realistic goals.

APPLICATION OF THE NUTRITION CARE PROCESS: COPD

NUTRITION ASSESSMENT

24-HOUR RECALL:

FOOD-/NUTRITION-RELATED HISTORY

½ cup coffee, few sips of orange juice, ½ cup oatmeal with 1 tsp sugar, and small amount of 1% milk ½ cup chicken noodle soup, 2 saltine crackers, ½ cup coffee Drank Pepsi throughout the day (~32 ounces) Vitamin/mineral supplements: None

When you talk to Stella about her food intake at home, she indicates that her appetite is poor. “Sometimes I feel bloated; I fill up so quickly—after a few bites of food.” “Food doesn’t taste good anymore.” She tells you that her highest adult weight was 145–150 lbs (about 5 years ago). She complains that her dentures are fitting very loosely.

1. What factors can you identify from her nutrition history that probably contribute to her poor food intake?

USUAL DIETARY INTAKE:

ANTHROPOMETRIC MEASUREMENTS

Coffee, juice, and dry cereal with a small amount of milk in the morning and one other larger meal during the day, usually at lunch—which consists of meat, vegetables, rice, potatoes, or pasta. She admits that she eats only small amounts. At night she often has a bowl of soup. She drinks Pepsi throughout the day (usually three 12-oz cans).

Ht.: 5’3”; Wt.: 119 lbs.

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PHYSICAL EXAM Vital signs: Temperature: 98.8°F, blood pressure (BP): 130/88, respiratory rate (RR): 22

Extremities: 1 + bilateral pitting edema Chest/lungs: Decreased breath sounds; prolonged expiration with wheezing; using accessory muscles at rest. 2. Evaluate Stella’s current weight, usual body weight, ideal body weight, and BMI. How does her bilateral pitting edema affect your evaluation of her weight?

BIOCHEMICAL DATA Sodium: 136 mEq/L; Potassium: 3.7 mEq/L; pH: 7.29; PaCO2: 50.9 mmHg; PaO2: 77.7 mmHg; O2Sat: 92%; HCO3: 29.6 mEq/L 3. Evaluate Stella’s biochemical data. What do they tell you about her nutritional status? Define each of the following blood gases and interpret her values: pH, PaCO2, PaO2, O2Sat, HCO3.

diagnostic term for each nutrition problem. Next, identify the etiology of each nutrition problem. Finally, identify the signs and symptoms that support the evidence for these nutrition problems.

NUTRITION INTERVENTION 5. Identify the nutrition prescription for this patient by recommending the appropriate dietary modification for her diagnosis. 6. Calculate energy and protein requirements for Stella.

NUTRITION MONITORING AND EVALUATION 7. Determine nutrition criteria for monitoring and evaluation for each nutrition diagnosis that you identified.

NUTRITION DIAGNOSIS 4. Identify at least two nutrition problems based on the nutrition assessment and medical history. Determine the

CHAPTER REVIEW QUESTIONS 1. Describe the three major functions of the respiratory system in human health. What methods are used to measure pulmonary function? 2. Describe the role of nutrition in pulmonary health. Which nutrients have been associated with normal pulmonary function? How does smoking affect vitamin C requirements? 3. Based on supportive evidence, what are the important nutrition factors to keep in mind when treating

patients of various age groups with asthma? 4. Define bronchopulmonary dysplasia (BPD). Why does it occur? 5. Define cystic fibrosis (CF). What organ systems are involved in the disease? How does this organ involvement affect nutritional status? You receive a nutrition referral from a physician for a 9-year-old male with CF. He is below the 10th percentile weight for height.

Outline an appropriate nutrition protocol for someone of his age. 6. Describe aspiration pneumonia. As a dietitian, what procedures or methods would you recommend to help prevent aspiration pneumonia in a patient receiving enteral feedings? 7. Define respiratory failure (RF). What are the goals of nutrition therapy for RF? Outline a nutrition protocol for a patient with RF?

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CuZn superoxide dismutase. Pediatrics. 2003; 111: 469–76. 45. Uauy R, Poindexter B, Koletzko B. Nutritional Care of Preterm Infants : Scientific Basis and Practical Guidelines. Basel: S. Karger AG; 2014. 46. Wemhöner A, Ortner D, Tschirch E, Strasak A, Rüdiger M. Nutrition of preterm infants in relation to bronchopulmonary dysplasia. BMC PulmMed. 2011; 11: 7. 47. Uberos J, Lardon-Fernandez M, Machado-Casas I, Molina-Oya M, Narbona-Lopez E. Nutrition in very low birth weight infants: impact on bronchopulmonary dysplasia. Minerva Pediatr. 2016; 68: 419–26. 48. Dani C, Poggi C. Nutrition and bronchopulmonary dysplasia. J Matern Fetal Neonatal Med. 2012; 25(Suppl 3): 37–40. 49. Academy of Nutrition and Dietetics. Bronchopulmonary dysplasia. In: Pediatric Nutrition Care Manual. http://www.nutritioncaremanual.org/. Accessed April 8, 2018. 50. Bozzetti V, Tagliabue P. Metabolic bone disease in preterm newborn: an update on nutritional issues. Ital J Pediatr. 2009; 35(1): 20. 51. Demarini S. Calcium and phosphorus nutrition in preterm infants. Acta Paediatr Oslo Nor 1992 Suppl. 2005; 94(449): 87–92. 52. Cacho NT, Parker LA, Neu J. Necrotizing enterocolitis and human milk feeding: a systematic review. Clin Perinatol. 2017; 44: 49–67. 53. Darlow BA, Graham PJ, Rojas-Reyes MX. Vitamin A supplementation to prevent mortality and short- and long-term morbidity in very low birth weight infants. In: Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd; 2016. http://onlinelibrary.wiley.com/ doi/10.1002/14651858.CD000501.pub4/abstract. Accessed September 11, 2018 54. Spears K, Cheney C, Zerzan J. Low plasma retinol concentrations increase risk of developing bronchopulmonary dysplasia and long-term respiratory disability in very-low-birth-weight infants. Am J Clin Nutr. 2004; 80: 1589–94. 55. Shaikhkhalil AK, Curtiss J, Puthoff TD, Valentine CJ. Enteral zinc supplementation and growth in extremely-low-birth-weight infants with chronic lung disease. J Pediatr Gastroenterol Nutr. 2014; 58: 183–7. 56. Silverman EK, Crapo JD, Make BJ. Chronic Obstructive Pulmonary Disease. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content. aspx?bookid=2129§ionid=192031379. Accessed November 24, 2018. 57. Academy of Nutrition and Dietetics. Chronic Obstructive Pulmonary Disease Guideline. ­Evidence Analysis Library Web site, https://www​ .andeal.org/topic.cfm?menu=5301. Accessed April 8, 2018. 58. Hopkinson NS, Tennant RC, Dayer MJ, et al. A prospective study of decline in fat free mass and skeletal muscle strength in chronic obstructive pulmonary disease. Respir Res. 2007; 8: 25–32. 59. Gronberg AM, Slinde F, Engstrom C-P, Hulthen L, Larsson S. Dietary problems in patients with severe chronic obstructive pulmonary disease. J Hum Nutr Dietet. 2005; 18: 445–52.

60. Engelen MP, Schols AM, Lamers RJ, Wouters EF. Different patterns of chronic tissue wasting among patients with chronic pulmonary disease. Clin Nutr. 1999; 18(5): 275–80. 61. Shols AM, Fredric EW, Soeters PB, Westerterp KB, Wouters EF. Resting energy expenditure in patients with chronic obstructive pulmonary disease. Am J Clin Nutr. 1991; 54: 983–87. 62. Lehouck A, Boonen S, Decramer M, Janssens W. COPD, bone metabolism, and osteoporosis. Chest. 2011; 139: 648–57. 63. Romme E, Smeenk F, Rutten E, Wouters E. Osteoporosis in chronic obstructive pulmonary disease. Expert Rev Respir Med. 2013; 7: 397–410. 64. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press; 2010. 65. Thomsen M, Ingebrigtsen T, Marott J, et al. Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease. JAMA. 2013; 309: 2353–61. 66. Weekes CE, Emery PW, Elia M. Dietary counselling and food fortification in stable COPD: a randomised trial. Thorax. 2009; 64: 326–31. 67. Ferreira I, Brooks D, White J, Goldstein R. Nutritional supplementation for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2012; (12): CD000998. 68. Chapman S. Pulmonary rehabilitation for people with chronic obstructive pulmonary disease: an evidence review. Br J Community Nurs. 2017; 22: 608–10. 69. Costi S, Crisafulli E, Antoni FD, Beneventi C, Fabbri LM, Clini EM. Effects of unsupported upper extremity exercise training in patients with COPD: a randomized clinical trial. Chest. 2009; 136: 387–95. 70. Cystic Fibrosis Foundation. About cystic fibrosis. https://www.cff.org/What-is-CF/ About-Cystic-Fibrosis/. Accessed April 8, 2018. 71. Sorscher EJ. Cystic Fibrosis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content. aspx?bookid=2129§ionid=192280672. Accessed November 24, 2018.

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72. Borowitz D, Robinson K, Accurso F, et al. Cystic Fibrosis Foundation evidence–based guidelines for management of infants with cystic fibrosis. J Pediatr. 2009; 155: S73–93.

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73. Farrell PM, Rosenstein BJ, White TB, et al. Guidelines for diagnosis of cystic fibrosis in

84. Berry AJ. Pancreatic enzyme replacement therapy during pancreatic insufficiency. Nutr Clin

Pract Off Publ Am Soc Parenter Enter Nutr. 2014; 29: 312–21. 85. Lusman S, Sullivan J. Nutrition and growth in cystic fibrosis. Pediatr Clin North Am. 2016; 63: 661–78. 86. Mandell LA, Wunderink RG. Pneumonia. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/ content.aspx?bookid=1130§ionid=79733578. Accessed April 8, 2018. 87. Centers for Disease Control. National Center for Health Statistics. Pneumonia. https://www.cdc .gov/nchs/fastats/pneumonia.htm. Accessed May 7, 2018. 88. McClave SA, Demen MT, DeLegge MH, et al. North American summit on aspiration in the critically 111 patient: consensus statement. J Parenter Enteral Nutr. 2002; 26: S80–5. 89. McClave SA,Taylor BE, Martindale RG, et al. Guidelines for the provision and assesssment of nutrition support therapy in the adult critically ill patient : Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter Enteral Nutr. 2016 ; 40 : 159-211. 90. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin definition the ARDS definition task force. JAMA. 2012; 307(23): 2526–33. 91. Suzuki S, Egi M, Schneider AG, Bellomo R, Hart GK, Hegarty C. Hypophosphatemia in critically ill patients. J Crit Care. 2013; 28(4): 536, e9–19. 92. U.S. Library of Medicine. Medline Plus Web site. https://medlineplus.gov/lungtransplantation. html. Updated March 7, 2018. Accessed April 8, 2018. 93. Valapour M, Lehr CJ, Skeans MA, et al. OPTN/SRTR 2016 Annual Data Report. Lung Am J Transplant. 2018; 18: 363–433. 94. Chamogerogakis T, Mason DP, Murthy SC, et al. Impact of nutritional state on lung transplant outcomes. J Heart Lung Transplant. 2013; 32: 693–700. 95. Hasse JM, Matarese LE. Solid organ transplantation. In: Mueller CM, ed. The A.S.P.E.N Adult Nutrition Support Core Curriculum. 3rd ed. Silver Springs, MD: ASPEN; 2017: 603–18. 96. Jomphe V, Mailhot G, Damphousse V, et al. The impact of waiting list BMI changes on the short-term outcomes of lung transplantation. Transplantation. 2018; 102: 318–25.

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CHAPTER 22

Source: Courtesy of Marcia Nelms

Metabolic Stress and the Critically Ill Marcia Nahikian Nelms, PhD, RDN, LD, FAND The Ohio State University

LEA RNING O B JECTIV ES LO 22.1  Describe the difference in energy and fuel substrate between starvation and metabolic stress. LO 22.2  Define metabolic stress and list potential causes and metabolic abnormalities observed in the stress response. LO 22.3  Describe how estimated nutrient requirements are determined during metabolic stress and the nutrients of concern when selecting formulas for enteral or parenteral nutrition support.

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LO 22.4  Identify diagnostic criteria for sepsis and the role of nutrition therapy. LO 22.5  Classify the types of burns. LO 22.6  Describe how the enteral feeding prescription for the burn patient is developed and provide examples of nutrition supplements for burns.

LO 22.7  Identify factors that place a patient at nutritional risk post-operatively. LO 22.8  Discuss energy and protein requirements for post-operative healing using evidence based guidelines.

G LOSSARY C-reactive protein—a protein released as a response to inflammation ceruloplasmin—a protein used in copper transport Curling’s ulcer—ulceration of gastric or duodenal tissue as a result of burn or trauma debridement—the removal of dead or injured tissue epidural anesthesia—an anesthetic drug placed into the epidural space of the lumbar or sacral region of the spine, causing loss of sensation from the abdomen and pelvis to the lower limbs esophagectomy—a surgical procedure resecting or removing the esophagus fibronectin—an acute-phase glycoprotein involved in the regulation of cell growth and differentiation, wound healing, and vascular integrity

general anesthesia—total loss of sensation and consciousness as a result of an anesthetic drug gluconeogenesis—the metabolic pathway through which glucose is formed from non-carbohydrate sources glycogenolysis—the metabolic pathway through which glycogen is converted to glucose hypoperfusion—reduced blood flow hypotension—low blood pressure hypoxic injury—cellular injury as a result of oxygen deprivation local anesthesia—loss of sensation only in the area where an anesthetic drug is placed menhaden—hydrogenated and partially hydrogenated oils from the menhaden fish (a small plankton-feeding fish)

22.1 INTRODUCTION Chapter 9 discussed the body’s response to injury at the cellular level. The type of cellular response depends on the ability of the cell to react, adapt, and repair itself after exposure to injury. This response may be temporary and completely reversible, but in some situations, the cell is permanently damaged and is no longer functional. Cell responses may include inappropriate accumulation of substances within the cell; changes in size, number, or shape; and the inflammatory response. The inflammatory response can be extreme and ongoing, which results in systemic consequences. This is the situation that may occur in critical illness. This chapter explores the body’s unique responses to specific types of stress and injury and the evidence-based recommendations for medical nutrition therapy. As described in the 2016 ASPEN guidelines for nutrition support therapy in the adult critically ill: “Traditionally, nutrition support in the critically ill population was regarded as adjunctive care designed to provide exogenous fuels to preserve lean body mass and support the patient throughout the stress response. Recently, this strategy has evolved to represent nutrition therapy, in which the feeding is thought to help attenuate the metabolic response to stress, prevent oxidative cellular injury, and favorably modulate immune responses. Improvement in the clinical course of critical illness may be achieved by early EN, appropriate macro- and micronutrient delivery, and meticulous glycemic control. Delivering early nutrition support therapy, primarily by the enteral route, is seen as a proactive therapeutic strategy that may reduce disease severity, diminish complications, decrease length of stay in the ICU, and favorably impact patient outcomes” (p. 161).1 With increased research and experience in nutrition support, we understand that nutritional care in the critically ill can accomplish these previous objectives plus additional goals, including reduction of the stress, inflammatory, and immune responses as well as

necrotizing fasciitis—inflammation of the connective tissue leading to necrosis of the tissue; may be caused by infection, injury, or an autoimmune reaction sepsis—a systemic inflammatory response and immunosuppressive process that prevents an adequate response to infection or trauma; may result in organ dysfunction or hypoperfusion abnormalities serum amyloid A—family of apolipoproteins associated with high-density lipoprotein (HDL) in plasma; considered to be an acute-phase protein released in response to inflammation systemic inflammatory response ­syndrome (SIRS)—a classification for life threatening illness that occurs in response trauma, surgery or infection

the reduction of cellular injury. Nutrition support is a crucial component of the medical care for the critically ill.1 With these goals in mind, this chapter first describes the physiological effects of metabolic stress. We know that the stress condition places the patient at the highest level of nutritional risk. In no other situation can nutritional deficits result in such dramatic and often severe consequences for a patient. Research over the previous three decades has led us to a clearer understanding of not only the body’s need for nutrition support during critical illness but also the role of nutrition in mediating the stress response. Planning nutrition care goes beyond the simple decision to feed the patient during critical illness; it is imperative to understand whom to feed, what to feed, when to feed, and how much to feed.

22.2  PHYSIOLOGICAL RESPONSE TO STARVATION Malnutrition develops when the nutrient supply is inadequate—that is, during starvation. But it can also develop when the body is unable to utilize nutrients appropriately or when nutritional needs are so high that a typically adequate intake cannot meet those demands—that is, during metabolic stress. This is the basis of the recently proposed guidelines for diagnostic criteria for malnutrition. Malnutrition in the context of acute illness is the result of both the inflammatory response and metabolic stress.2 The body’s physiological reaction to starvation is quite different from its response to metabolic stress, the key difference being the adaptation that occurs during starvation. It was not until completion of the hallmark studies of Dr. Ancel Keys and his subsequent publication of The Biology of Human Starvation (1950) that the manner in which the body responds to starvation through physiological adaptations was understood (see Box 22.1). Keys and his research team followed the effects of starvation in 36 conscientious objectors during World War II.3 Chapter 22  Metabolic Stress and the Critically Ill   675

BOX 22.1

HISTORICAL PERSPECTIVES

Ancel Keys’s Human Starvation Study In 1939, as the war in Europe intensified and the United States prepared to enter the conflict, Ancel Keys, a new member of the faculty of the University of Minnesota, was asked by the U.S. War Department to develop a food ration for paratroopers. Keys had just founded the Laboratory of Physiological Hygiene beneath the bleachers of Memorial Stadium. The solution Keys and his collaborators concocted in the lab—the infamous K-ration—was so successful that the U.S. military assigned it to all their troops. Partly because of this success, Keys received support from the U.S. government as the war came to a close to conduct a large-scale comprehensive study on the physiological and psychological effects of starvation. Keys put 36 conscientious objectors through a diet and exercise program designed to recreate the living conditions of occupied Europe. His human subjects ate simple, starchy foods and root vegetables, and were required to walk at least 22 miles per week. After 3 months of this semi-starvation, the young men were refed and rehabilitated. The resulting two-volume publication, The Biology of Human Starvation, was an instant classic, not merely for its detailed investigation of the physical consequences of protein-energy malnutrition, but also for its description of the condition’s psychological

One of the most important distinctions between starvation and metabolic stress is the difference in energy and fuel substrate requirements. During starvation, the body responds to a reduction in food intake by reducing its overall energy needs; the basal metabolic rate is reduced so that fewer kcalories are needed. In contrast, energy requirements are increased during metabolic stress and injury. The next major difference between starvation and metabolic stress is the source of fuel that is used to meet energy requirements. Under normal circumstances, the body uses a mixture of fuels (primarily carbohydrate and lipid) for energy. But since humans have a limited ability to store carbohydrate, the primary source of fuel shifts from glucose to lipids during periods of starvation as glucose availability decreases. Lipolysis becomes preferential and the accumulated lipid stores serve as the primary energy source. This adaptation for the use of lipid as the primary fuel and the subsequent metabolism of ketones allow for preservation of muscle mass and prevent the complications of protein deficiency (suppressed immune response, infection, and decreased protein synthesis).4 The adaptation for use of lipid as a primary fuel does not occur in metabolic stress. Instead, the continued requirement for glucose as the primary fuel necessitates continued breakdown of lean body mass to support gluconeogenesis. Table 22.1 outlines both normal nutrient metabolism and the key adaptations that occur during starvation. Figure 22.1 summarizes the changes in metabolism during starvation. Unfortunately, when the body is faced with an injury, infection, or disease-causing metabolic stress, the normal adaptations that protect the body during simple starvation do not occur. 676  Part 4  Nutrition Therapy

effects.1 Deprived of food, the men became depressed and lost their motivation; later, they became obsessed with food, licking their plates, hoarding food, and even cheating.2 Ancel Keys was one of the 20th century’s most important physiologists and nutritionists. Besides inventing the K-ration and studying starvation, he was the first to uncover a relationship between a high intake of saturated fat, the level of cholesterol, and the development of cardiovascular disease. He was one of the first medical scientists to utilize mathematical regression in the study of human health.3 Finally, and perhaps most importantly, Keys demonstrated the importance of cultural and economic factors in the health of human populations. Throughout his career in physiology, nutrition, and public health, Keys emphasized the mutability of the body and our ability to prevent disease through simple modifications in lifestyle. References 1. Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human Starvation. Minneapolis: University of Minnesota Press; 1950. 2. Kalm LM, Semba RD. They starved so that others are better fed: remembering Ancel Keys and the Minnesota experiment. J Nutr. 2005; 135(6): 1347–52. 3. Vanltallie TB. Ancel Keys: a tribute. Nutr Metab. 2005; 2: 4.

Table 22.1 Comparison of Metabolism during Normal Nutritional State versus Starvation Normal Nutritional State

Starvation

Metabolic rate matches current physical activity requirements and body composition.

Decrease in metabolic rate to ensure conservation of energy.

Carbohydrate and lipid are efficiently metabolized sources of energy providing 55%–85% of energy requirements.

Decreased need for glucose utilization.

Protein is used for maintenance of protein structures and to meet ongoing protein synthesis requirements.

Preservation of lean mass, minimizing protein loss.

Utilization of lipid as main source of energy.

22.3  PHYSIOLOGICAL RESPONSE TO STRESS Definition Metabolic stress is the hypermetabolic, catabolic response to acute injury or disease. Diagnoses that may lead to metabolic stress include trauma as seen in a gunshot wound or motor vehicle accident (MVA); closed head injury (see Chapter 20); burns; severe inflammation such as in pancreatitis; cancer; sepsis; and hypoxic injury as seen in acute kidney injury; or it may occur after major surgery. The degree of metabolic stress typically correlates with the seriousness of the injury.5,6 In critical care medicine, the severity of illness is ranked using numerous scoring systems such as the Glasgow Coma Scale

Figure 22.1 Changes in Metabolism during Starvation Metabolism Response to Starvation (Short Term) No Injury or “Stress” (Protective Adaptation Occurs) Overall energy needs decrease Metabolic rate decreases 20−25 kcal/kg/d Energy from fat storage 90% of kcal Energy from protein 10% for gluconeogenesis Protein stores protected

ENERGY DEPOT FAT, FATTY ACID

Lower metabolic rate 20–25 kcal/kg/d

90% kcal

LIVER Glucose Pyruvate

Urea Intact skin

Gluconeogenesis (10% kcal) Glucose

Brain/tissues requiring glucose

Ketones produced

ENERGY PRODUCTION

Energy for protein synthesis Micronutrients needed Amino acids Alanine Hormone adaptation preserves protein

Protein synthesis

To tissues

LEAN MASS Minimal catabolism to meet glucose needs

Heat loss blocked Source: Reprinted with permission from Medscape.com, 2009. Available at: http://cme.medscape.com/viewarticle/432384.

(see Table 20.12), the Acute Physiology and Chronic Health Evaluation (APACHE), the Injury Severity Score (ISS), or the Abdominal Trauma Index (ATI). Current recommendations use the NUTRIC score or NRS 2002, which have combined measures of metabolic stress and injury with nutrition parameters. This allows the practitioner to identify those individuals who are critically ill and at risk for malnutrition.7,8 Table 22.2 displays both the NRS 2002 and NUTRIC score assessment tools.

Epidemiology Injuries caused by physical force (serious falls, gunshot wounds, stabbing, drowning, and other accidents) are classified as trauma. Trauma is the leading cause of death for individuals aged 1–46 years and the third leading cause of death across all age groups. The economic burden is high: an estimated $406 billion per year including the costs of health care and lost productivity.9

Etiology The metabolic consequences of injury and stress result from numerous factors including hormonal release and influence, acute-phase protein synthesis, sustained inflammatory response, hypermetabolism, increased reliance on gluconeogenesis and its subsequent production of glucose, and shifts in fluid balance and decreased urine output.10–15

Clinical Manifestations The stress response has been described as a progression through three phases: the ebb phase, the flow phase, and finally the recovery or resolution phase. 11 The ebb phase encompasses the immediate period after injury (2–48 hours). This period is characterized by shock resulting in hypovolemia and decreased oxygen availability to tissues. The reduction in blood volume results in decreased cardiac and urinary output. The goal of medical care during this acute period is to stop all hemorrhaging, restore blood flow to organs and maintain oxygenation to all tissues. As the patient stabilizes hemodynamically, the flow phase begins. This phase encompasses the classic signs and symptoms of metabolic stress: hypermetabolism, catabolism, and altered immune and hormonal responses. The final adaptation phase or recovery phase indicates a resolution of the stress with a return to anabolism and normal metabolic rate.11,12

Pathophysiology Hormones, acute-phase proteins, the immune system, and altered cellular metabolism direct the physiological changes that characterize metabolic stress. This same scenario is played out in other serious illnesses such as cancer or heart failure and historically has been referred to as cachexia. Stress and injury activate the hormones that direct a “flight-or-fight” response, including glucagon, cortisol, epinephrine, and Chapter 22  Metabolic Stress and the Critically Ill   677

Table 22.2 NUTRIC Score and NRS 2002: Examples of Nutrition Risk Screening Tools for the Critically Ill. NRS-2002: factors used to determine score (30) Impaired nutritional status

Severity of disease

Absent score 0

Normal nutritional status

Absent score 0

Normal nutritional requirements

Mild score 1

Weight loss >5% in 3 months

Mild score 1

Hip fracture

OR

Chronic patients in paticular with acute complications: cirrhosis, COPD

Food intake 5% in 2 months

Chronic hemodialysis, diabetes, oncology Moderate score 2

OR

Major abdominal surgery, stroke Severe pneumonia, hematologic malignancy

BMI 18.5–20.5 + impaired general condition OR Food intake 25%–50% of normal requirement in preceding week Severe score 3

Weight loss >5% in 1 month (15% in 3 months)

Severe score 3

Head injury

OR

Bone marrow transplantation

BMI 10)

OR Food intake 40, protein should be provided at 2.5 g/kg of ideal body weight.1 Factors that affect the accuracy of energy estimations include the presence of obesity, mechanical ventilation, stress, and trauma. It is also imperative to include consideration of any paralytic drugs and mechanical ventilation that are used to treat the critically ill patient, as these interventions affect energy requirements.22 When providing nutrition support to the critically ill, it is crucial to avoid overfeeding and its subsequent metabolic complications, which include increased carbon dioxide production and hyperglycemia. Biochemical indices to assess visceral protein status (transport proteins/albumin) are typically more reflective 682  Part 4  Nutrition Therapy

of the level of metabolic stress than of the patient’s actual protein status and are also affected by fluid balance, wound losses, and the use of blood products needed for stabilization of the patient. Multiple nutrition guidelines caution against using albumin, prealbumin, and others as measures of protein status.1,18,19 The liver prioritizes the synthesis of acute phase proteins during stress and the synthesis rates for other proteins are downgraded.18 Using the AND/ASPEN malnutrition criteria such as recent weight change, evidence of fat and muscle wasting, fluid accumulation, and loss of functional status (e.g., measured by handgrip dynamometry) may provide additional information that is relevant to the assessment of nutritional status in context of acute injury (see Chapter 3, particularly Table 3.14 and Figure 3.24). Still, the very nature of critical illness often prevents the use of nutrition-focused physical exam. As previously discussed, the use of scoring systems such as the NUTRIC score or NRS 2002 has demonstrated reliability in identification of those individuals with the highest nutrition risk. The NUTRIC score and NRS 2002 use not only nutrition assessment parameters but also a measure of disease severity. Refer to Table 22.1 that outlines the components of the NRS 2002 and NUTRIC score.1,7,8

Nutrition Diagnosis Nutrition diagnoses during metabolic stress and critical illness may include increased energy expenditure, increased nutrient needs, inadequate protein-energy intake, altered GI function, and impaired nutrient utilization.

Nutrition Intervention For critically ill individuals, nutritional needs can rarely be met by the oral route, and alternate feeding routes including both enteral nutrition (EN) and parenteral nutrition (PN) are standard components of the medical and nutritional care. Figure 23.4 provides guidance for selecting a feeding route. ASPEN 2016 critical care guidelines recommend that enteral nutrition should be started early within the first 24–48 hours of admission when the patient is hemodynamically stable and is at nutritional risk.1,23 Many critically ill patients require vasopressor agents to stabilize them after surgery, trauma, and/or injury, and the fear of GI complications has supported the recommendation to postpone initiation of EN until hemodynamic stability has been achieved. EN is always preferred when compared to PN as EN is more cost-effective and is associated with reduced infectious complications, fewer surgical interventions, and, in some studies, fewer hospital days. 1,24 Therefore, whenever possible EN should be chosen over the use of PN. Still, there are common barriers for EN within the critical care population. These include high risk of aspiration, delayed GI motility, and frequent inability to reach goal volume, for example. The ASPEN critical care guidelines state that for most patients feeding directly into the stomach is appropriate, but if concern for aspiration exists, then feeding into the small intestine should be used. 1,25,26 The presence of bowel sounds is not always a consistent nor reliable measure of bowel function. Critically ill patients often have

delayed gastric motility and waiting for normalization may un­n ecessarily delay the initiation of EN. Finally, the use of volume-based feedings and established EN protocols provides the flexibility for health care providers to adjust rates so that when feedings are interrupted there are steps to allow for individual adjustment to achieve the 24-hour volume recommendations.1,26 Additional information concerning prevention and treatment of complications is discussed later in this section. The first step in developing the EN prescription, after access to the GI tract has been established, is choosing the appropriate enteral formula. Formula choices will be influenced by the established institutional formulary as well as the ability to meet energy and protein needs within the fluid volume of a specific formula. ASPEN critical care guidelines indicate that for most critically ill patients, a standard polymeric formula can be recommended. The efficacy of formulas that contain immune-modulating nutrients [glutamine, arginine, docosahexanoic acid (DHA), eicosapentaenoic acid (EPA), and nucelotides] has resulted in mixed results within the literature. This is most likely due to differences in research methodologies and small sample sizes. The ASPEN critical care guidelines suggest that these formulas be reserved for specific populations such as surgical ICU patients, perioperative patients, and those with burns or traumatic brain injuries.1,27 The Canadian guidelines additionally do not recommend immune-modulating formulas except in surgical patients.28 See Table 22.8. Glutamine is the preferred fuel for the enterocytes and assists in maintaining intestinal membrane permeability. Additionally, glutamine supports immune cell growth, reduces levels of pro-inflammatory cytokines, and is a precursor to the antioxidant glutathione. Though glutamine is a nonessential amino acid, the body’s synthesis rate cannot meet the increased needs during the stress of critical illness. Glutamine has previously been recommended for burn, trauma, and ICU patients. Most specialized formulas provide 0.3–0.4 g/kg/day of glutamine, and glutamine can be added to an enteral formula that does not already contain it.29–31 But as stated earlier, until more research is conducted, recommendations for its use is limited to specific populations.1 Arginine performs numerous roles within the body including serving as a precursor for nitric oxide and in numerous ways within the immune system. Since arginine synthesis is dependent on citrulline (and thus glutamine), levels may be inadequate during metabolic stress. Clinical studies for supplementation of arginine have produced mixed results. More positive results for supplementation have been observed in trauma and surgical patients who are hemodynamically stable and as more research is conducted, more specific recommendations can be made.1 Other nutrients of interest for critically ill patients include omega-3 fatty acids, vitamin C, vitamin E, selenium, zinc, and probiotics.1,33 The protocol for supplementation proposed by the Inflammation and the Host Response to Injury Collaborative Research Program includes 100 mg IV vitamin C every 8 hours; 400 μg IV selenium daily; and 1500 IU vitamin E every 12 hours for 7 days or until discharged from the ICU. Vitamin C and selenium are given intravenously for the first

2 days and as enteral dosages thereafter.33 The recommendations for selenium supplementation in the critically ill ranges from 500 to 750 μg/day over a period of 1–3 weeks.1,34,35 Table 22.9 provides examples of recommendations for supplementation within an evidenced-based protocol. Omega-3 fatty acids have been proposed as an intervention to reduce the pro-inflammatory cytokines involved in systemic inflammatory conditions and metabolic stress. Demonstrating the benefit of omega-3 fatty acids in specialized nutrition support, like the other immunomodulating nutrients, has had mixed results within the literature. Further research needs to be conducted to establish benefit, specific dosage, and formulation recommendations. Sources of fiber added to enteral feedings provide ­substrates that assist in maintenance of beneficial bacteria in the GI tract (probiotics, prebiotics, and synbiotics). As ­discussed in Chapter 15, substrates such as inulin, guar gum, and other soluble fibers are fermented to short-chain fatty acids and lactate. Most enteral formulas use guar gum and soy fiber as the source of fiber. ASPEN critical care guidelines state that in critically ill patients in the medical intensive care setting who develop diarrhea may be evaluated for a soluble fiber supplement if their current EN does not have fiber added.1,36 PN should be reserved for those cases of prolonged nothing-by-mouth (NPO) status lasting longer than 7 days, when the patient is malnourished and enteral access cannot be obtained, when EN support cannot meet the patient’s needs or is not tolerated, or when a major surgical procedure will prevent the patient from starting enteral nutrition and the patient will enter surgery in a malnourished state.1 Recent literature has demonstrated increased interest in the benefit of supplemental PN for patients who are critically ill. Patients often do not receive their full caloric requirements when critically ill, and this is due to the interruption of feeding for treatments, reduced tolerance to EN in critical illness, and, in large part, to nutrition’s lower priority within the scope of medical care. When PN is used to supplement EN, a more consistent provision of nutrition with improved health outcomes may result.37–39 The ASPEN critical care guidelines suggest that PN should be considered when the patient is unable to meet at least 60% of energy and protein needs for greater than 7–10 days.1 Chapter 5 provides details regarding the design of PN prescriptions. An important concern for PN in metabolic stress may be its contribution to hyperglycemia. Additionally, the use of parenteral lipids may be immunosuppressive. The ASPEN critical care guidelines recommend avoiding use of soy-based parenteral lipids for the first 7 days of admission.1 Newer formulations of parenteral lipids such as SMOF TM may be advantageous, but the research is too limited at this time for specific recommendations to be made. Other complications of PN may include catheter occlusion, catheter-related infection, hypertriglyceridemia, intestinal atrophy, electrolyte disturbances, and refeeding syndrome in previously malnourished individuals. An example of how current nutrition guidelines are incorporated into a standardized protocol is demonstrated in Table 22.9 and Figure 22.4.

Chapter 22  Metabolic Stress and the Critically Ill   683

Table 22.8 Enteral Formulas in Metabolic Stress Formula/ Manufacturer Oxepa® (Abbott)

Caloric Density 1.5 kcal/mL

Perative® (Abbott)

1.3 kcal/mL

Pivot® (Abbott)

1.5 kcal/mL

Impact® (Nestle)

1.0 kcal/mL

Osmolality 535 mOsm/ kg water

460 mOsm/ kg water

595 mOsm/ kg water

375 mOsm/ kg water

Carbohydrate (% of total kcal, source) 28.1%

Protein (% of total kcal, source) 16.9%

Sugar (sucrose), corn maltodextrin

Lipid (% of total kcal, source) 55.2% Canola oil, mediumchain triglycerides, marine oil (may contain one or more of the following: anchovy, menhaden, salmon, sardine, tuna), borage oil

54.5%

20.5%

25%

Corn maltodextrin

Partially hydrolyzed sodium caseinate, whey protein hydrolysate

Canola oil, mediumchain triglycerides

45%

25%

30%

Corn syrup solids

Hydrolyzed sodium caseinate, whey protein hydrolysate

Structured lipid (interesterified sardine oil and medium-chain triglycerides), soy oil, canola oil

Rationale for Metabolic Stress • Concentrated calories for fluidrestricted patients • Unique, patented oil blend— contains 4.6 g/L of EPA* and 4 g/L of GLA† • Elevated levels of antioxidants vitamin C, vitamin E, and beta-carotene • Includes 1.6 g of NutraFlora® scFOS®/8 fl oz (6.5 g/L and 9.8 g/1500 mL) • Contains added arginine (8 g/L total arginine at 2.5% of kcal) • Arginine—13 g/L (3.5% of calories) • Glutamine (inherent)—6.5 g/L • Omega-3 fatty acids (EPA, 2.6 g/L; DHA, 1.3 g/L) • Elevated levels of vitamin C, E and beta-carotene

53%

22%

25%

• EPA/DHA: 1.7 g/L

Maltodextrin

Sodium and calcium caseinates, L-arginine

Palm kernel oil, refined fish oil (anchovy, sardine)

• Supplemental L-arginine: 12.5 g/L • Dietary nucleotides: 1.2 g/L

Impact Peptide 1.5® (Nestle)

1.5 kcal/mL

Impact Advanced Recovery® (Nestle)

1.2 kcal/mL

Microlipid® (Nestle)

4.5 kcal/mL

510 mOsm/ kg water

730 mOsm/ kg water

37% Maltodextrin

25% hydrolyzed casein, L-arginine

38%

• L-arginine: 18.7 g/L

Palm kernel/coconut oil, refined fish oil (anchovy, sardine), soybean oil; MCT:LCT ratio: 50:50; n6:n3 ratio: 1.4:1

• Dietary nucleotides: 1.8 g/L

Blend of arginine, omega-3 fatty acids and nucleotidesrecommended for peri/ postoperative support

31%

35%

34%

Maltodextrin

Sodium and calcium caseinates (milk), L-arginine

Palm kernel oil, refined fish oil (anchovy, sardine), sunflower oil; MCT:LCT ratio: 16:84; n6:n3 ratio: 1.2:1 100% Safflower oil

®

Beneprotein (Nestle)

25 kcal/1.5T

Benecalorie® (Nestle)

7.5 kcal/mL

ProMod® (Abbott)

100 kcal/oz

100%

glycerine

†

GLA, gamma-linolenic acid (from borage oil);

*EPA, eicosapentaenoic acid (from marine oil).

684  Part 4  Nutrition Therapy

9%

91%

Calcium caseinate

Sunflower oil; mono/ diglycerides

10 g/oz Hydrolyzed collagen

Used as modular to increase caloric density Used as modular to increase protein density (6 kcal/1.5T)

Whey protein isolate 0%

• EPA + DHA: 4.9 g/L

Modular used to increase caloric density Modular used to increase energy and protein density

Table 22.9 An Example of a Trauma and Surgical Critical Care Nutrition Protocol Using Evidence-Based Guidelines

Gastric access

• Long-term: PEG (initiate TF at 6:00 a.m. postPEG placement)

Initial Nutrition Evaluation Resuscitation goals met? No

Continue resuscitation. Hold initiation of nutrition support.

Yes

• Consult Nutrition Service and start enteral nutrition (see below, “Enteral Nutrition”)

Post-pyloric access

• Ensure all patients have nutrition regimen by day 2

• Gastroparesis with persistent high (500 mL) gastric residual volume (GRV) despite prokinetic agents or recurrent emesis

• Enteral nutrition (EN) is preferred over parenteral nutrition (PN) (see protocols below)

• Severe active pancreatitis (endoscopic placement for jejunal feeds) • Open abdomen

GI stress ulcer prophylaxis

Refer to unit-specific protocol.

Antioxidant protocol

• Given to all adult trauma ICU patients for 7 days

• Abdominal Trauma Index (ATI) >15 Parenteral Nutrition (PN) Initiation of PN:

• Supplementation • Ascorbic acid: 1000 mg PO/PT/IV q 8 hours • Selenium: 200 mcg PT/IV qd

• Avoid use of lipids during first week of PN.

• Excludes: • Pregnant patients (ascorbic acid and selenium = pregnancy category C)

Weaning TPN when:

• Patients with creatinine >2.5 mg/dL

TFs tolerated at 60% of goal

• Obtain prealbumin and CRP levels at day 2 if anticipated ICU stay is >3 days. Refer to unit-specific protocol.

Wound healing protocol (for open abdomen, burns, large wounds, or fistulas)

• Ascorbic acid (vitamin C): 500 mg BID PO/PT/ IV × 10 days

Severe cachexia/ malnourishment protocol

Consider use of oxandrolone: 10 mg PO/PT twice daily

• Vitamin A: 10,000 IU, PO/PT/IM × 10 days • Zinc: 220 mg PO × 10 days PO or PT 50 mg/10 mL elemental oral solution

POs tolerated at 60% of meals consumed

Dosing weight

• Wean off PN per clinician judgment

• Use IBW for height if actual body weight is >IBW • Hamwi method for calculating IBW: • Men: 106# (48 kg) 1st 5 ft, then add 6# (2.7 kg) per inch >5 ft, +/– 10% • Women: 100# (45 kg) 1st 5 ft, then add 5# (2.3 kg) per inch >5 ft, +/– 10%

• Start Pivot at 50% of goal (~25–30 mL/hr) within 24–48 hours of admission

• Use actual body weight if weight is 50, use 25–30 kcal/kg IBW

EN Access: Placement

• Decrease PN to ~half, d/c lipids and decrease dextrose/AA per PN team order

Nutritional Goals

Enteral Nutrition (EN)

• Advance as tolerated to goal by day 5 with improvement of SIRS or critical illness

• Decrease PN to ~half, d/c lipids and decrease dextrose/AA per PN team order • Wean off PN as TF rate advances to goal or per clinician judgment

• Repeat and reassess every Monday/Thursday. Glucose control

• If previously healthy, initiate PN only after the first 7 days of hospitalization if EN is not feasible. • If protein-calorie malnutrition present and EN not feasible, start PN immediately after resuscitation.

• -tocopherol: 1000 IU PO/PT q 8 hours

Initiation of EN:

• Short-term: If placement unsuccessful after two attempts consider endoscopic placement of PEG/J (long-term) • Indications:

Protocols:

Lab protocol

• Short-term: OGT, NGT, small-bore feeding tube

• Begin with blind bedside nasogastric feeding tube

Protein needs

• If BMI 20–29.9, use 1.2–2.0 g/kg actual body weight

• Consider bedside endoscopic, fluoroscopic, Cortrak, or intraoperative placement

• If BMI 30–50, use 2.0 g/kg IBW

• OGT and NGT placement confirmed by physical exam

• Renal failure (HD/CRRT): 1.2–2.5 g/kg dosing weight

• Small-bore feeding tube placement confirmed by radiology

• Hepatic failure: 1.2–2.0 g/kg dosing weight

• If BMI >50, use 2.5 g/kg IBW

Chapter 22  Metabolic Stress and the Critically Ill   685

Fluid needs

• 1 mL/kcal baseline • Cover additional losses (i.e., fever, diarrhea, GI output, and tachypnea) • Fluid restriction (HF, renal failure, hepatic failure with ascites, CNS injury, and electrolyte abnormality)

If LOS >7 days and patient has not consistently met near 100% needs, consider nutritional provision from a combination of PO/EN/ PN routes. Note: ICU, intensive care unit; CRP, C-reactive protein; OGT, orogastric tube; NGT, nasogastric tube; PEG, percutaneous endoscopic gastrostomy; TF, tube feeding; PEG/J, percutaneous endoscopic gastrostomy/jejunostomy; PN, parenteral nutrition; IBW, ideal body weight; HD, hemodialysis; CRRT, continuous renal replacement therapy; CHF, congestive heart failure; CNS, central nervous system; LOS, length of stay. Sources: 1. Adapted from Mills B, Collier B. Trauma and Surgical Critical Care Nutrition Guideline. Nashville, TN: Vanderbilt University Medical Center Division of Trauma and Surgical Critical Care. http://www.mc.­vanderbilt. edu/surgery/trauma/Protocols/FINAL%20NUTRITION.pdf. Revised May 10, 2011. Accessed April 25, 2018. 2. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter Enteral Nutr. 2016; 40: 159–211.

22.5 SEPSIS Definition Sepsis has historically been defined as an uncontrolled inflammatory response to infection or trauma. It is now understood that sepsis is actually an immunosuppressive process that prevents an adequate response to infection and includes a range of conditions such as systemic inflammatory response syndrome and multiorgan failure.5,40 The Surviving Sepsis Campaign was formed in 2002 and included the Society for Critical Care Medicine, along with 11 other international organizations. This organization publishes the guidelines for treatment of sepsis.40 In 2016, definitions for sepsis were updated: Sepsis is a “life threatening organ dysfunction caused by dysregulated host response to infection.” Septic shock is “a subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality.” 41 Systemic inflammatory response syndrome (SIRS) is an additional classification of this condition not necessarily caused by an infectious process. SIRS may occur after major surgery or trauma, or with other conditions such as myocardial infarction.8

Epidemiology Over 1.5 million individuals in the United States are diagnosed with sepsis. One out of every three individuals who die during hospitalization are diagnosed with sepsis.42 The number of cases of sepsis worldwide has doubled over the past decade and accounts for an estimated 6 million deaths.43

Etiology As stated previously, sepsis was originally thought to be a result of an overwhelming systemic infection. Researchers are now beginning to realize the complexity of the cascade of 686  Part 4  Nutrition Therapy

events associated with sepsis and recognize that the similar progression characteristic of SIRS can occur without infection. A combination of pro-inflammatory cytokine release, imbalance of coagulation factors, altered cellular metabolism, hypoperfusion, and hypotension direct the physiological changes that occur with sepsis.5,40,41

Clinical Manifestations The initial major signs of sepsis include increased white blood cell count (>12,000 mm3), increased heart rate (>90 beats per minute), respirations (>20 breaths/minute), and fever (>100.4°F [38°C]) or hypothermia (15% BSA. 50 Additional vitamins, minerals, and trace elements are often supplemented for wound healing (see Table 9.5). In burn patients, higher amounts of these nutrients are often prescribed to replace the large amounts lost via the wound exudates, but also to ensure adequate support for engraftment and overall wound healing. Supplementation with vitamins A, C and E, copper, selenium, and zinc may be included in nutrition protocols in burn intensive care units (see Table 22.11).50,55 Depending on the route of nutrition support, the supplementation in the formula or PN solution chosen may be adequate to meet the client’s needs. An alternative route for administering micronutrients may be providing supplementation for those nutrients for which deficiencies are identified. As recovery proceeds and the patient is able, oral feedings can be initiated. Weaning from nutrition support is recommended when the patient is able to meet at least 60% of nutritional needs orally (see Figure 22.4). Nutritional requirements will need to be adjusted as the patient heals and the focus of therapy shifts to rehabilitation. 690  Part 4  Nutrition Therapy

Table 22.11 Example of a Nutrient Supplementation Protocol for Burns Micronutrient

Supplementation

Glutamine

0.3–0.5 g/kg/day for 10-g doses via feeding tube 2–4 × daily

Zinc

≥20% TBSA full thickness or ≥30% TBSA: 30 mg elemental/day intravenously × 5 days and then 50 mg elemental zinc daily by mouth or feeding tube

Selenium

≥20% TBSA full thickness and intubated or ≥30% TBSA: 1000 μg/day parenterally × 14 days and then 200 μg twice daily by mouth or feeding tube

Vitamin C

≥20% TBSA full thickness or ≥30% TBSA: 500 mg/day twice daily by mouth or feeding tube

Vitamin E

400 units twice daily by mouth or feeding tube

Source: Hall KL, Shahrokhi S, Jeschke MG. Enteral nutrition support in burn care: a review of current recommendations as instituted in the Ross Tilley Burn Centre. Nutrients. 2012; 4: 1554–65.

22.9 SURGERY Definition Surgery is defined as an operative procedure used to diagnose, repair, or treat an organ or tissue. Surgery can be further classified by the seriousness of the procedure (major or minor), the necessity (elective or emergency), or the specific purpose of the procedure (diagnostic, excision, palliative, reconstructive, or transplant).

Epidemiology In 2014, 17.2 million surgical procedures were performed in the United States.56 These included a wide range of procedures such as cardiac catherizations, reduction of fracture, coronary artery bypass graft, Cesarean section, and hysterectomy.

Etiology Many surgical procedures do not pose nutritional risk. Nonetheless, if the patient enters surgery malnourished or overnourished, or if the surgical procedure will interrupt normal nutrition processes, the individual will be at nutritional risk postoperatively. Age and coexisting diagnoses will have an impact on the outcome and recovery from the surgical procedure. Malnutrition increases the risk of the most common postoperative complications, including wound dehiscence (improper wound opening after suture closure), infection, and increased length of stay, as well as increased morbidity and mortality.6,57–58 Despite the fact that most surgeons agree that nutrition impacts surgical outcomes and that peri-/postoperative nutrition will impact the patient’s hospital course and subsequent health outcomes, the use of evidence-based protocols for nutrition intervention is not consistent in the United States.58 See Figure 22.6. As discussed earlier in this chapter, screening and prognostic tools have been developed to identify those patients most likely to be at nutritional risk (Also see Chapter 3). The NRS 2002 and NUTRIC score will allow for identification of those individuals at malnutrition risk and those who may

Figure 22.6 Status of Nutrition Support in Surgical Outcomes

R.I.P. R.I.P. + HOSPITAL HOSPITAL + + +

66% of of gastrointestinal gastrointestinal 66% surgery surgery patients patients are are malnourished malnourished at at the the time of of surgery. surgery. time

These Patients Patients are are three three These times times more more likely likely to to have have complications complications during during surgery, and and five five times times surgery, more likely likely to to die. die. more

Only 20% 20% of of all all Only hospitals hospitals have have a a formal formal nutrition nutrition screening process process screening in place. place. in

$ 75% of of surgeons surgeons 75% agree that that perioperative perioperative agree nutrition nutrition delivery delivery will will reduce reduce complications. complications.

For every every dollar dollar spent spent For on nutrition nutrition therapy therapy for for on patients, patients, $52 $52 is is saved saved in in hospital hospital costs. costs.

Currently, only only 20% 20% of of Currently, patients receive receive any any patients preoperative preoperative Nutrition Nutrition Intervention. Intervention.

of gas or bowel movement was a sign of resolution of ileus. Because it is difficult to ascertain when GI function has returned, however, the determination of when to actually begin postoperative feeding has been debated. The factors that have traditionally prevented early feeding postoperatively include lack of understanding of the benefits of early feeding, misunderstanding of postoperative ileus, concern for complications, lack of skills for tube placement, perception of an inability to feed when a patient is receiving vasopressor agents, and, finally, lack of communication.60 As more and more literature confirms that these factors can be overcome, an early feeding step may become standard in postoperative protocols. Many patients who have entered surgery with nutritional deficits cannot withstand additional weight loss. Allowing a patient to be fed as soon after surgery as is possible and safe is recommended.61–66

Nutrition Assessment

Energy and protein requirements are established individually and should support postoperative healing. REE is adjusted as appropriate to address postoperative requirements in order to Sources: Leremy/Shutterstock.com; RedKoala/Shutterstock.com; Imagination lol/Shutterstock .com; Leremy/Shutterstock.com; Aha-Soft/Shutterstock.com; grmarc/Shutterstock.com. estimate energy needs. A standard nomogram Source: Wischmeyer PE, Carli F, Evans DC, et al. American Society for Enhanced Recovery of 25–35 kcal/kg per day can be used, but as disand Perioperative Quality Joint Consensus Statement on Nutrition Screening within a cussed throughout this chapter (see also Chapters Surgical Enhanced Recovery Pathway. Anesth Analg. 2018; 126: 1896-1907. 3 and 5), energy needs estimation has its limitations. ASPEN critical care guidelines and the 2018 American benefit from perioperative nutrition support. An additional Society for Enhanced Recovery and Perioperative Quality Joint screening algorithm suggested by the 2018 American SociConsensus Statement state that meeting protein requirements ety for Enhanced Recovery and Perioperative Quality Joint are a priority even if energy needs cannot be achieved. Protein Consensus Statement is the perioperative nutrition screen requirements are elevated and will generally fall between 1.5 (PONS). This screen asks the following: Does the patient have and 2.5 g/kg IBW per day but vary depending on the type of a low BMI 10% in past 6 months? Has the patient had a reduced oral intake by >50% in the past week? 22.10 PERI-/POSTOPERATIVE (and/or) Does the patient have a preoperative serum albumin 50% in the past week? (and/or) – Does the patient have a preoperative serum albumin 1.2 g/kg/d.   6. We recommend that patients who are screened as being at nutritional risk before major surgery receive preoperative ONSs for a period of at least 7 d. This may be achieved with either of the following. – IMN formulas (containing arginine and fish oil) – High-protein ONS (2–3x a day, minimum of 18 g protein/dose)   7. We recommend that for patients who are screened as being at nutritional risk before major surgery, where oral nutrition supplementation via ONS is not possible, that a dietitian be consulted and an enteral feeding tube be placed and home EN initiated for a period of at least 7 d.   8. If neither oral nutrition supplementation via ONS nor EN is possible, or when protein/kcal requirement (>50% of recommended intake) cannot be adequately met by ONS/EN, we recommend preoperative PN to improve outcomes   9. Preoperative IMN should be considered for all patients undergoing elective major abdominal surgery. 10. We recommend preoperative fasting from midnight be abandoned. 11. In patients undergoing surgery who are considered to have minimal specific risk of aspiration, we encourage unrestricted access to solids for up to 8 h before anesthesia and clear fluids for oral intake up to 2 h before the induction of anesthesia. 12. We recommend a preoperative carbohydrate drink containing at least 45 g of carbohydrate to improve insulin sensitivity (except in type I diabetics due to their insulin deficiency state). We suggest that complex carbohydrate (eg, maltodextrin) be used when available. After Surgery   1. We recommend that a high-protein diet (via diet or high-protein ONS) be initiated on the day of surgery in most cases, with exception of patients without bowel in continuity, with bowel ischemia, or persistent bowel obstruction. Traditional “clear liquid” and “full liquid” diets should not be routinely used.   2. We recommend reaching an overall protein intake goal is more important than total calorie intake in the postoperative period.   3. We recommend standardized protocols for postoperative nutrition support be instituted.   4. IMN should be considered in all postoperative major abdominal surgical patients for at least 7 d.   5. In patients who meet criteria for malnutrition, who are not anticipated to meet nutritional goals (>50% of protein/kcal) through oral intake, we recommend early EN or tube feeding within 24 h. Where goals are not met through EN, we recommend early PN, in combination with EN if possible.   6. We recommend when using gastric residual volume’s as a marker of feeding tolerance, a cutoff of >500 mL should be used before tube feeds being suspended or tube feed/EN rate reduced.   7. In patients started on EN and/or PN, we recommend continuation of EN or PN support for patients who are not able to take in at least 60% of their protein/kcal requirements via the oral route.   8. We recommend posthospital high-protein ONS in all patients after major surgery to meet both calorie and protein needs, especially in the previously malnourished, elderly and sarcopenic patient. Abbreviations: BMI, body mass index; CT, computed tomography; EN, enteral nutrition; IMN, immunonutrition, ONS, oral nutritional supplement; PONS, perioperative nutrition screen; PN, parenteral nutrition. Source: Wischmeyer PE, Carli F, Evans DC, et al. American Society for Enhanced Recovery and Perioperative Quality Joint Consensus Statement on Nutrition Screening within a Surgical Enhanced Recovery Pathway. Anesth Analg. 2018; 126: 1896-1907.

692  Part 4  Nutrition Therapy

If patients require EN, it should be started within 24 hours for those patients who are malnourished. Supplemental PN should be used if the patient is not able to meet their needs by EN alone. The ASPEN critical care guidelines state that immune enhancing enteral formulas should be considered. The use of fish oils and arginine appear to have a synergistic effect and have resulted in reduced postoperative complications.1

22.11  HIV AND AIDS The human immunodeficiency virus (HIV) targets host immune cells and turns them into viral factories for HIV reproduction. Progression to the symptomatic condition of acquired immunodeficiency syndrome (AIDS) may make the infected individual vulnerable to opportunistic infections that can cause a range of disabilities or death. However, the progression from HIV infection to AIDS and from AIDS to death is not an inevitable outcome if effective medical and nutritional interventions are initiated. HIV is transmitted from person to person through infected body fluids. HIV is a relatively weak virus, however, and does not survive well outside the body. Thus, transmission through casual contact and the environment has been deemed unlikely. A review of the early history of HIV infection suggests that although HIV is not as easily transmitted as other infectious diseases, it is nonetheless a significant health threat. HIV and AIDS present a wide variety of challenges for maintenance of nutritional status. Changes in nutritional status can result from HIV infection, disease complications and coinfections, and disease treatments. Social, economic, and clinical issues all interact with nutritional status. Populations already at risk for nutritional compromise because of lack of health care access, lifestyle choices (e.g., smoking, alcohol, and drug abuse), food insecurity or nutrition insecurity (the lack of consistent access to an adequate and appropriate food supply), and comorbidities such as hepatitis, diabetes, or other conditions may find their health status compromised with HIV infection and AIDS. Alterations in nutrient intake, absorption, metabolism, and excretion have been documented throughout the disease spectrum. While these interactions are complex and multifactorial in nature, this chapter concentrates on clinical aspects of the disease and potential interventions.

Epidemiology In 2016, there were 36.7 million people with HIV infection in the world; 2.1 million of them were children, and most resided in southern and eastern African countries. An estimated 1.8 million people were newly diagnosed in 2016.67 Despite the fact that the World Health Organization acknowledges that the HIV epidemic has leveled off, globally, AIDS is still considered to be among the leading causes of death, especially in Africa.67 In 2017, an estimated 1.1 million persons in the United States were living with diagnosed or undiagnosed HIV/AIDS and an estimated 40,000 people were diagnosed with HIV/AIDS.68

Pathophysiology HIV is a retrovirus approximately 0.1 microns in diameter, about l/70th of the diameter of the CD4 lymphocyte (T helper

cell) that it particularly targets. It contains nine genes, six of which are essential to penetrate and infect the target cells and produce copies of the virus. The other three genes are used to provide the necessary information to produce new viral particles in the host cell. HIV is most typically transmitted via blood through sexual contact (generally penile anal or penile vaginal intercourse), blood transfusion, intravenous needle sharing, and perinatally (from mother to child) through blood or breast milk. As with other infections, there is both an exposure and dose requirement for the body to become infected, and it is possible to be exposed without seroconversion, such as in the case of accidental needle sticks with very low doses of HIV transferred.3 The resulting immunodeficiency syndrome is most closely related to the infection of activated CD4 cells. The virus identifies the target CD4 cell and fuses to the surface. HIV injects RNA, enzymes, and other substances that assist in viral integration and replication. Using its own kit of injected substances, HIV RNA is transcribed to DNA particles using reverse-transcriptase enzymes. The DNA is carried to the nucleus and integrated into the host DNA using the HIV’s integrase enzymes. At this point, the integrated viral materials can remain dormant until they are activated, at which time they command the cell to become a viral factory that manufactures viral components. Protease enzymes cleave the viral proteins for assembly into viral cores. Once fully assembled, the virus is ready to bud out of the infected host cell. As the host CD4 cell manufactures, assembles, and releases viruses, it is incapacitated and destroyed. In addition, macrophages harboring HIV are rendered dysfunctional. It is through this process that the immune system is compromised and HIV disease progresses.69 (Refer to Chapter 9 to review the types and functions of immune cells in the body.)

Clinical Manifestations Table 22.12 summarizes the clinical manifestations of HIV along with selected nutritional implications. Primary HIV infection is often accompanied by flu-like symptoms and a reduction in CD4 cell counts. As CD4 and other cells are damaged and rendered dysfunctional, the body’s defenses against infection and malignancy may decline. There is a strong relationship among CD4 cell counts, HIV viral load (in copies per milliliter), and progression to a diagnosis of AIDS.69 The higher the viral burden of HIV, the more CD4 cells are infected, rendered dysfunctional, and destroyed, leaving the body open to opportunistic infections and cancers. Lower viral load set points are associated with prolonged survival and reduced numbers of AIDS-defining diagnoses. However, the level of destruction of CD4 cells appears to be more precisely predictive of survival than viral load. The reduction in numbers and function of CD4 cells is associated with an increase in incidence of opportunistic disease. These opportunistic infections and malignancies further assault the body’s normal functions and are associated with nutritional decline and mortality. The response of the intestinal tract includes the rapid turnover of gut tissue and activation of immune cells on the intestinal surface.68,69 HIV infection is associated with depletion of CD4 cells in the GI tract, where more than 60% of the body’s T lymphocytes reside. This provides a large reservoir of HIV-infected cells in the gut and increases risk for the Chapter 22  Metabolic Stress and the Critically Ill   693

Table 22.12 Selected Clinical Manifestations of HIV Infection and Treatment System Cardiac

Examples • Pericarditis/endocarditis • Pulmonary hypertension

Nutritional Implications Patients at risk for congestive heart failure and myocardial infarction may benefit from dietary modulation. (See Chapter 13)

• Coronary artery disease Neurologic

• Neuropathy • Dementia/altered mental status

Pain, weakness, and hypersensitivity to touch may impair appetite and capacity to exercise; impairment in cognitive function can interfere with self-care, including food-related activities.

Gastrointestinal tract and symptoms

• Rapid intestinal cell turnover; infection Immature enterocytes, reduction in intestinal enzyme production, and blockage of intestinal immune cells of intestinal surface can lead to malabsorption with or without diarrhea. Often a side effect of medication therapies; nausea, vomiting, abdominal pain, and diar• Nausea/vomiting rhea may lead to inadequate nutrient intake or nutrient losses and require both • Abdominal pain dietary and pharmacologic interventions. • Diarrhea

Hematologic

• Anemias

Anemias and related fatigue can impair physical capacity and the ability to maintain body composition.

Hepatic

• Hepatitis

Common coinfections and disorders with HIV may lead to dietary restrictions consistent with hepatic disease; intolerance to fat and deficiency of pancreatic hormones can result in malabsorption. (See Chapter 16)

• Biliary tract disorders Immune system

• Infiltration and destruction of immune The body’s response to infection is dependent on the severity of the infection or cell function and numbers trauma; repeated opportunistic events can lead to progressive wasting, particularly of body cell mass, and greater risk for morbidities and mortality. • Increased threat of opportunistic

Musculoskeletal

• Myopathy

Fatigue and muscle weakness limit the capacity to exercise and maintain body composition.

Oral

• Candidiasis

Oral pain, taste changes, and dry mouth can lead to a reduction in food intake and increased risk for weight loss.

events

• Herpes • Periodontal disease • Salivary gland disease Pulmonary

• Bacterial pneumonia • Kaposi’s sarcoma • Fungal pneumonia

Fever, fatigue, difficulty breathing, and persistent coughing may impair adequate food intake; pulmonary involvement may reduce exercise capacity and limit the ability to maintain nutritional status through exercise.

• Tuberculosis Renal

HIV-associated nephropathy (HIVAN)

Progression to end-stage renal disease is less common with ART, but can lead to significant dietary restrictions.(See Chapter 18)

Systemic

Inflammatory process as the body fights HIV infection

Catabolism of muscle stores and fluid shifts lead to subclinical wasting with or without weight loss; hormonal changes that occur with chronic inflammation can lead to alterations in nutrient metabolism.

malabsorption of nutrients.70,71 As malnutrition progresses, malabsorption continues, further contributing to health decline. Oral manifestations can be caused by fungal infection, viral infection, bacterial conditions, neoplastic problems, salivary gland disease, and other problems. Oral lesions can lead to mouth itching, pain, a burning sensation (especially when eating spicy or acidic foods), and taste changes.70,71 Neurologic disorders, such as neuropathy and dementia, can occur in HIV infection and treatment. Neuropathy is often peripheral and associated with pain, numbness, tingling, and burning sensations. This type of neuropathy may start with the feet and can spread. Peripheral neuropathy has been associated with a number of the antiretroviral therapies. Dementia and altered cognitive functions can be related to HIV infection, other infections, and nutrient deficiencies.69 Pulmonary disorders may occur both related to and unrelated to HIV infection. The CD4 cell count is related to the risk for the development of several types of pulmonary 694  Part 4  Nutrition Therapy

diseases. Pulmonary hypertension has been demonstrated in patients with HIV infection without AIDS-defining diagnoses. Some of the many symptoms associated with pulmonary problems, including persistent coughing, chest pain, fatigue, fever, and shortness of breath, may make it more difficult for the patient to maintain adequate food intake. Fortunately, antiretroviral (ARV) medications have significantly reduced AIDS-related pulmonary disorders.69 Cardiac manifestations may include infections and inflammation, cardiomyopathy, pulmonary hypertension, and coronary artery disease. Cardiomyopathy may be related to infectious agents, inflammation processes, and pharmacologic therapies. Much of the coronary artery disease risk is associated with medication interactions that increase blood lipid levels as well as the long-term comorbidities of cardiovascular diseases. Chronic inflammation, immune dysfunction, concomitant conditions (e.g., insulin resistance, diabetes, renal involvement, and hypertension), and

opportunistic conditions place a patient infected with HIV at a higher risk for cardiac disease. However, in addition to HIV infection, there are many other cofactors to consider such as smoking, drinking, and other risk factors. 69,70 Anemias are a common occurrence in chronic HIV infection, with a higher prevalence in more symptomatic phases of the disease. Anemia can be related to chronic disease, hormonal alterations, infections, and/or medications. Renal failure in the form of HIV-associated nephropathy (HIVAN) is associated with risk factors such as infection, certain medications, male gender, and black African ancestry. Tubular necrosis is associated with several medications commonly used in HIV-infected patients, such as acyclovir, tenofovir, adefovir, and cidofovir, among other nephrotoxic medications. Nephrolithiasis (formation of kidney stones) has been associated with indinavir, and adequate hydration is a key recommendation for its use.69 Volume depletion, which can occur in patients experiencing diarrhea related to infections or medication intolerance, increases the risk for renal involvement and hyponatremia, hypokalemia, and other imbalances. 69,70 AIDS-related wasting syndrome (AWS) was identified as an AIDS-defining diagnosis by the CDC in 1987. 72 The CDC’s definition states that weight loss of 10% without any known cause accompanied by fever or diarrhea for more than a month is AWS and qualifies for the diagnosis of AIDS. Wasting is less prevalent now than it was prior to the advent of combination antiretroviral therapies that can achieve low and undetectable viral loads. The potential effect of HIV on health is perhaps most clearly exhibited by a number of immunologic abnormalities that persist despite the suppression of HIV replication. The etiology of wasting may be related to hormonal deficiencies (testosterone or thyroid), the cytokine dysregulation often associated with chronic inflammation/infection, and metabolic demands of medications. It has been proposed that the immune system changes and persistent inflammation observed in AIDS-related wasting resemble those that occur with cachexia and in sarcopenia. Research has shown that the older HIV-infected population exhibits increased frailty, most likely related to loss of muscle mass.69

Medical Diagnosis Comprehensive testing recommendations include tests for early infection, anti-HIV antibodies using an enzyme immunoassay, and viral RNA levels. Available assays to identify early infection (within 2 weeks) evaluate p24 antigen levels and titers of viral RNA or DNA, which determine viral load. Antibody levels may increase progressively for about 3–5 months post exposure and then tend to retain a set point level. As the infection transitions from recent to established, the aggressiveness and affinity of HIV antibodies increase. Testing modifications have allowed for the differentiation in antibody titer and avidity to estimate whether an infection is established or recent.69 Combination ELISA testing for both antigen and antibodies allows for earlier diagnosis of HIV infection. Though early detection may be most important for blood donor agencies, it may also provide some clinical management advantages. Rapid HIV antibody tests of blood or oral fluid provide results within 10–20 minutes and can be performed

in clinician offices. The first rapid home-use HIV test kit was approved for self-testing by the Food and Drug Administration (FDA) in 2013. The results of initial testing should be confirmed with the Western blot test, which has a sensitivity of screening serologic tests of >99.9%.69 Current testing screens for two HIV subtypes: HIV 1, the primary subtype seen in the Americas, and HIV 2, which is endemic in western Africa. Definitive testing for newborns is difficult before the age of 6 months; because of the presence of maternal antibodies and the limited ability of the child’s immature immune system to produce antibodies, virologic rather than antibody testing is used. In addition to testing for the presence and levels of HIV in the blood, testing for HIV genetic material through genotype and phenotype assays can assist the process of choosing the most potentially effective therapies. A genotype assay is used to identify points in the DNA sequence of the virus genome that may be mutated and cause resistance to treatment. Phenotype assays are used to determine viral susceptibility to a particular drug. The prediction of virus susceptibility based on genotype and phenotype testing may assist in the effective use of medications and help to limit the exposure to medications and their associated toxicities when resistance is likely. The diagnosis of HIV infection as AIDS, according to the case definition set forth by the CDC, is a reportable disease in the United States and is broken down into classifications that provide a schematic for management of the disease. For individuals ≥18 years of age, diagnosis is made from results of a positive initial HIV antibody or combination antigen/ antibody test and a subsequent positive supplemental test.73 Staging after initial diagnosis is designated as stage 1–stage 3. See Table 22.13.

Treatment Treatment for chronic HIV infection includes antiretroviral medications, prevention of and treatment for opportunistic events, modulation of the altered hormonal milieu, and maintenance and restoration of nutritional status. Both the number of reported cases of HIV’s symptomatic manifestation as AIDS and the mortality rate have dropped significantly since the introduction of combination therapies. Prior to the

Table 22.13 CDC Clinical and Immune Cell Categories of HIV Infection for Individuals ≥6 years of age Stage

Laboratory Evidence

Stage 1

Laboratory confirmation of HIV infection and CD4+ T-lymphocyte count of ≥500 cells/μL or CD4+ T-lymphocyte percentage of ≥26

Stage 2

Laboratory confirmation of HIV infection and CD4+ T-lymphocyte count of 200–499 cells/μL or CD4+ T-lymphocyte percentage of 14–25

Stage 3 (AIDS)

Laboratory confirmation of HIV infection and CD4+ T-lymphocyte count of