si nutrition assessment - continuing education · 2015-05-07 · reflect nutritional status....

Nutrition Assessment

Accredited Continuing Professional Education Course

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Nutrition Assessment:Tools & Techniques

7th edition • Revised July 2011by Martha G. Acevedo, ms, rd

© 1993–2011 OnCourse Learning CorporationNo part of this course may be reproduced, duplicated or copied in any way without the written per-mission of the copyright holder. (See note on Page ii)

Edited by: Dale Ames Kline, MS, RD, CNSCCopyediting/proofreading: Rich Kline, Gwen Hulbert

Design: Courtney Naguib

Martha G. Acevedo, ms, rd is Director, Food & Nutrition of Guest Services at Tri-City Medical Center, Oceanside, Calif., where she has been Critical Care Dieti-tian, Clinical Resource Dietitian and Clinical Dietetics Coordinator. She supervises all nutrition support activities at this 377-bed hospital, including training and education for a staff of seven dietitians, techs and approximately 75 staff. Marty became a Certi-fied Nutrition Support Dietitian in 1990, and received the California Dietetic Assn. Practice Award for Excellence in Clinical Dietetics in 1998. Education: MS (biology, nutrition), University of Bridgeport (magna cum laude); BS (home economics, dietet-ics), University of Tennessee (magna cum laude).

Nutrition AssessmentTools and Techniques

7th Edition • Revised July 2011

by Martha G. Acevedo, ms, rd

Important - Read Before ProceedingEXPIRATION DATE: Students of all professions must submit this course for credit no later than May 31, 2016. Credit will not be awarded for this course after that date.

Course Code: RD100

This course approved for RD ........................10 CPEU DTR .....................10 CPEUCDM ......... 10 Clock hours

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Nutrition Assessment ii

How to Earn Continuing Education Credit

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Nutrition Assessment

Contents

iii

1 INTRODUCTION

3 CHAPTER ONE: Defnitions of Malnutrition • Acute Disease or Injury Related Malnutrition Chronic Disease Related Malnutrition • Characteristics of Malnutrition

11 CHAPTER TWO: Medical and Nutrition History Social Factors • Nutrition History Assessment Tools • Medical Factors

17 CHAPTER THREE: Clinical Assessment Clinical Inspection • Anthropometrics • Subjective Global Assessment • Prognostic Nutrition Index • Instant Nutrition Assessment

29 CHAPTER FOUR: Electrolytes and Acid-Base Balance Electrolytes: Sodium, Potassium, Chloride, Calcium, Phosphorus, Magnesium • Acid-Base Balance • Metabolic Acidosis • Anion Gap • Metabolic Alkalosis • Respiratory Acidosis/Alkalosis • Calcium • Phosphorus • Refeeding Syndrome • Magnesium

47 CHAPTER FIVE: Nutritional Assessment through Laboratory Values Creatinine-height Index • Protein Status Indicators: UUN, UNA, Albumin, Transferrin, Thyroxine-binding Prealbumin, Retinol-binding Protein • Immune Status Indicators • Other Laboratory Values: BUN, Creatinine, Liver Functions, Serum Lipids 59 CHAPTER SIX: Assessment of Nutritional Requirements Caloric Requirements: RQ, REE, Harris-Benedict Equation • Protein Requirements • Fluid Requirements • Vitamin Requirements: A, D, E, C, K, B1, B2, B6, B12, Niacin, Biotin, Folic Acid • Mineral Requirements: Zinc, Copper, Selenium, Iron • Nutritional Anemias

75 CHAPTER SEVEN: Nutritional Assessment in Disease States, Part I Pulmonary Disease • ARDS • Cancer • AIDS • Liver Disease • Renal Disease

101 CHAPTER EIGHT: Nutritional Assessment in Disease States, Part II Cardiac Disease Gastrointestinal Diseases Metabolic Stress and Sepsis Nutritional Assessment of Elderly Patients

123 APPENDICES Review Question Answers Food Frequency Form Activities of Daily Living Anthropometric Measurement Standards Instrumental Activities of Daily Living Recommended Daily Allowances Drug-nutrient Interactions Vitamin/Mineral Deficiencies Drug-related Nutritional Problems Physical Changes with Malnutrition Drugs Impacting Nutrient Metabolism Laboratory Test Checklist MetLife Height-Weight Tables/ Metabolic Assessment/Monitoring of TPN Age-Height-Weight Tables DRI Values for Energy Food Diary

145 Examination

Nutrition Assessment iv

Learning ObjectivesAt the conclusion of this course, the student will be able to:

1. Define and identify the different types of malnutrition.

2. Identify the components involved in obtaining a diet history and in the evaluation of a medical/surgical history.

3. Understand the physical symptoms of protein-calorie and vitamin/mineral malnutrition.

4. List the different types of anthropometrics and body composition studies.

5. Describe the components of the subjective global assessment.

6. Explain the relationships between nutritional status and various laboratory data.

7. Understand acid-base balance and its importance in assessing the appropri-ateness of nutrition support.

8. List and explain use of various protein status indicators in nutrition assess-ment.

9. List and explain use of various immune status indicators in nutrition assess-ment.

10. Describe various means by which nutritional requirements can be deter-mined and be able to calculate the needs of healthy people as well as acutely and chronically ill patients.

11. List the specific laboratory tests that should be used in the nutritional as-sessment of patients diagnosed with stress and sepsis, cancer, liver disease, pulmonary disease and diabetes.

12. Understand the changes in nutrition assessment and evaluation of nutrition requirements in the patient with chronic or acute disease.

13. List and explain the metabolic and physiologic changes that occur with ag-ing.

14. Discuss how the nutrition assessment of elderly patients differs from young-er patients.

Nutrition Assessment 1

Introduction

As many as 50 percent of our hospitalized patients may be malnourished or un-dernourished. Often a patient’s nutritional status will deteriorate during a hospital stay. In fact, the nutritional status of up to 69 percent of hospitalized patients declines during their hospital stay.

This malnutrition can increase the incidence of sepsis, cause poor wound healing and poor respiratory effort, and result in decreased absorption of nutrients. Morbidity associated with malnutrition has been estimated at 25 percent, while mortality due to malnutrition alone occurs in about 5 percent of cases.

Our inpatient population is sicker and at increased risk for malnutrition. Early nutritional assessment and appropriate intervention can prevent or delay the onset of malnutrition and its related complications.

Now, more than ever, nutritional assessment and intervention is not only appropri-ate, but often imperative in the home care setting. We will see more and more of our pa-tients as outpatients, in their homes, or in assisted living or skilled nursing facilities. The outpatient may well be at just as much risk for malnutrition as the hospitalized patient. However, because the patient is not hospitalized, the incidence of malnutrition may not be recognized.

This course will provide practical guidelines and references for the practitioner involved in the nutritional assessment of patients. Nutritional assessment is basically the same process in both the institutionalized and home care patient.

Initially, we’ll review the basics of nutritional assessment, define malnutrition, and review the means by which we can clinically assess our patient.

We’ll then move on to a more in-depth review of laboratory data and how it can


reflect nutritional status. We’ll review guidelines for the assessment of nutritional re-quirements and include ways to assess calorie and protein needs as well as vitamin and mineral requirements.

Finally, we’ll review the changes that occur, as related to nutritional status, with various stressed states, chronic illness and aging.

Case studies have been included to provide you with practical applications for what is discussed. Review questions are included at the end of each chapter, with the answers and discussion included at the end of the course. It will be to your benefit to attempt to complete these questions before reading the answers. They are not “extra” material; rather, they are an integral part of the course and will serve to illuminate the text material and facilitate completion of the post-examination.


Chapter One:Malnutrition in

Hospitalized Patients

More than three decades ago, the issue of malnutrition in hospitalized patients first came to the forefront. Charles Butterworth, in a landmark paper, noted that “malnutrition is a common accompaniment to the stress of illness among hospitalized patients. . . un-doubtedly contributing to increased mortality and morbidity“ (Butterworth, 1974).

Could not the same statement be accurately written today? Webster’s Dictionary defines malnutrition as “faulty or inadequate nutrition.“ Grant defines malnutrition as “under- or overnourishment due to lack or excess of food, want or excess of certain nec-essary elements in the diet, and/or abnormal assimilation“ (Grant, 1986).

The incidence of malnutrition in hospitalized patients has been estimated at one out of every five patients. The incidence increases to almost 50 percent in patients who have been hospitalized for a longer period, approximately 5 to 6 days (Hill, 1992). Other studies estimate the incidence of malnutrition in hospitals at between 30 to 55 percent (Robinson, et al., 1987; Nagel, 1993; Mowe and Bohmer, 1991). Malnutrition is recognized as a secondary diagnosis or “cc“ (complication/co-morbid condition) in coding via the inpatient prospective payment system. In 2007, malnutrition was recognized as impact-ing the acuity and severity of patients’ illnesses; reimbursement may be increased to compensate for the increased costs associated with the care of the patient.


Definitions of malnutritionThe American Dietetic Association and the American Society for Parenteral and

Enteral Nutrition have recently joined forces to propose the development of new defi-nitions for malnutrition. Rather than defining malnutrition as “marasmus“ (calorie malnutrition) and “kwashiorkor“ (protein malnutrition), definitions will refer to the conditions that contribute to the malnutrition: semi-starvation, systemic inflammatory response (SIRS) and inability to assimilate nutrients consumed.

Thus, starvation-related malnutrition refers to caloric depletion, as might occur in a patient with anorexia nervosa or a recent widow who’s suffering from depression and only wants a cup of tea and toast. SIRS malnutrition is often seen in acute disease, trauma or injury and occurs in individuals who were healthy prior to their illness. The inability to assimilate nutrients is most often seen in chronic disease.

semi-starvationDuring fasting and semi-starvation, the decrease in stores of protein occurs mostly

in the somatic and gut masses, while visceral protein stores are usually conserved. The patient becomes wasted and has diminished stores of fat, glycogen and muscle mass. However, enzymes, plasma proteins (such as albumin) and immune function appear to remain at normal levels. If starvation continues for an extended period, however, even these stores of protein will be used, as evidenced by decreased serum levels of albumin, prealbumin, and transferrin, and the person is at increased risk for infection and death as evidenced by decreased total lymphocyte counts (Gray and Kaminski, 1985).

With normal digestion, energy is usually stored as phosphates, fat and glycogen. These stores are used during normal periods of fasting. However, when fasting becomes starvation, the body adapts, through changes in hormonal interactions, to preserve as many of the body’s normal functions as possible (Gray and Kaminski, 1985).

Growth hormone, cortisol, and thyroxine may be elevated in starvation; insulin levels often remain normal, and TSH (thyroxine stimulating hormone) is reduced. These hormonal interactions allow for greater mobilization of fat from stores. The person who is starved will thus have diminished skinfold thickness (less than 3 mm) with a reduc-tion in arm circumference (less than 15 cm) (Butterworth and Weinsier, 1980).

In the hospital setting, simple starvation generally occurs in the patient receiving inadequate calories. He will appear starved, and his weight will be about 80 percent of ideal body weight. Serum protein levels such as albumin will likely be near normal. Changes in body cell mass and dietary intake correlate poorly with visceral protein such as albumin and prealbumin stores (Jensen, 2009).

We have all been exposed to pictures of third world residents with marasmus. Should we, as health care professionals, be concerned with starvation-related malnu-trition in our patients? How many patients have been left without oral intake, enteral feedings or total parenteral nutrition for an extended period? How many receive a liter


of D10 as their total nutritional support each day? How many of your patients have been on a “regular“ diet during their entire hospital stay but have eaten “30 percent“ and then been discharged 10 to 20 lb lighter?

Clearly, starvation-related malnutrition should be of concern to those of us respon-sible for providing nutritional care to our patients. Generally, the patient in the hospital who develops this type of malnutrition responds well to adequate feeding, which must take place over a period of time.

systemic inflammatory response synDrome (sirs)SIRS malnutrition may occur in the patient who has an increase in stressors, such

as surgery, sepsis, or trauma. The malnutrition may be due in part to the acute phase response and metabolic response that occurs when someone gets sick or injured.

During the acute phase response to illness, injury or acute inflammation the types and amounts of cytokines the body produces changes. Interleukin–1 (IL-1), interleukin–6 (IL-6), and tumor necrosis factor (TNF) all increase, causing a decrease in serum proteins like albumin, prealbumin, transferrin and retinol binding protein since protein is con-served in the somatic compartment (intracellular space), and synthesis is diminished. (Jensen, 2009). Albumin and other plasma protein levels fall quickly, immune function decreases as evidenced by low serum lymphocyte counts (Butterworth, 1974), and risk for morbidity and mortality increases.

The metabolic response during acute inflammation, injury or illness causes a po-tential increase of resting energy expenditure, and amino acids are shifted from muscles to the liver. Then, gluconeogenesis increases, third spacing occurs as extracellular fluids increase, and acute phase proteins are produced at the expense of serum albumin and visceral proteins (Jensen, 2009). Growth hormone is elevated to allow for protein synthe-sis and lipolysis (Munro and Crim, 1980). Glucagon, epinephrine, cortisol and catechol-amines are also increased (McClave, et al., 1992). Somatomedin, insulin and thyroxine levels decrease, but there is no change in cortisol and TSH levels.

These changes allow for greater protein synthesis than protein catabolism (Viteri and Torun, 1980). The body attempts to spare protein through recycling of amino ac-ids and a reduction in the turnover of amino acids and protein. The liver changes from producing albumin, transferrin and prealbumin to producing acute phase proteins like fibrinogen and C-reactive protein (McClave, et al., 1992). Clinically you see a drop in serum albumin.

The inflammatory response to injury and illness, mediated by cytokines, further contributes to malnutrition by causing anorexia (and resultant decrease intake of nutri-ents) and general malaise with deconditioning.

The chart on the next page compares the anthropometric and clinical changes seen in malnutrition due to semi-starvation and SIRS.


chronic Disease-relateD malnutritionIn chronic disease states with a concurrent inflammatory process, loss of muscle

mass and physical function occurs over time — even over months and years (Jensen, 2010). Muscle mass loss can be slowed or reversed with appropriate levels of nutrition. However, as in acute disease-related malnutrition, the degree of the inflammatory re-sponse may inhibit the success of nutrition intervention due to the altered cytokines and metabolic processes (Jensen, 2010).

With malnutrition, intestinal absorption will be impaired. Diminished production of bile and gastric and pancreatic reduces absorption of fats, sugars and protein. The ability to carry medications, minerals, hormones and other substances usually transport-ed through the blood on protein will be altered (Viteri and Torun, 1980).

characteristics of malnutritionSevere malnutrition is characterized by:• An inability or unwillingness to eat, resulting in more than 5 days of less than 50 percent of identified nutrient needs during acute illness and/or injury• Greater than 1 month of less than 50 percent of needs in the patient with a chronic condition or environmental or social issues • Unintended weight loss of varying degrees over periods of time is a characteristic of malnutrition, shown in the chart on the next page.

Clinical Changes in Malnutrition

Semi-Starvation Malnutrition

Normal: • serum albumin • serum transferrin • serum prealbumin • immune function Decreased: • muscle mass and strength • fat stores • thyroid-stimulating hormone • triceps skinfold • arm circumference Increased: • growth hormone

SIRS Malnutrition

Normal: • muscle mass and strength (initially) • fat stores (initially)

Decreased: • serum albumin, serum prealbumin • cortisol • somatomedin • insulin • total lymphocyte count • thyroxin • IL-6

Increased: • tumor necrosis factor, IL-1 • growth hormone • glucagon • epinephrine, catecholamines • cortisone • C-reactive protein, fibrinogen


Further criteria that can characterize the degree of malnutrition are measurement of hand grip strength; walking tests; testing of ability to climb stairs, maintain balance, and rise from a chair; and measurement of peak expiratory flow. These assessments can cor-relate with maintenance of muscle mass and nutrition status (ASPEN, 2011).

Non-severe (or moderate) malnutrition is characterized by an inability or unwill-ingness to eat more than 75 percent of identified needs for 7 days in acute injury or ill-ness, for 1 month with a chronic condition, and for 3 months with social or environmen-tal issues.

Nutrition status does not always improve during a hospital stay; in fact, it may worsen if the patient is not provided with adequate nutritional support. Butterworth listed several undesirable practices affecting nutrition status in his 1974 paper. Among them are: failure to record height and weight, prolonged use of glucose and saline intra-venous feedings, failure to observe patients’ food intake, withholding meals because of diagnostic tests, failure to recognize increased nutritional needs due to injury or illness, and delay of nutrition support until the patient is in an advanced state of depletion. Do any of these sound familiar?

Causes of Hospital Malnutrition

Failure to record height and weight or track weight lossProlonged glucose, saline IV feedingsFailure to observe food intakeWithholding meals because of testsUnrecognized increased needs due to injury or illnessDelayed or inadequate nutrition support

Loss of Total Body Weight Length of Time

More than 2 percent In one weekMore than 5 percent In one monthMore than 7.5 percent In 3 monthsMore than 10 percent In 6 monthsMore than 20 percent In 1 year

(Malone and White, 2011)

Unintended Weight Loss Criteria for Malnutrition


Who is at greatest risk for developing malnutrition before, during, or after hospital-ization? From a variety of sources, we can identify those at risk.

The patient may be underweight (at less than 80 percent of standard), overweight (greater than 120 percent of standard), or an alcoholic. Or the patient may have lost more than 10 percent of usual body weight over a six-month period or may have been without nutrition support and any oral intake for greater than five to seven days.

The patient who has greater than normal nutrient losses (from malabsorption, fistulas, dialysis, wounds, etc.) is at greater risk for developing protein malnutrition or protein-calorie malnutrition. Also at risk are patients with sepsis, trauma, major surgery, burns or fever, and those who receive medications such as steroids, immunosuppres-sants and antineoplastic agents (Butterworth and Weinsier, 1980).

Because malnutrition may be associated with greater mortality and morbidity, it is important to be able to identify patients who are malnourished. (These comorbidity fac-tors can be reversed with nutrition support in some cases [Grant, 1986].)

For instance, persons with protein-calorie malnutrition are at increased risk for in-fections because of the inability of the compromised immune system to resist or fight the infection. Lymphocyte function is compromised, and lymphocytes are less able to dif-ferentiate and mature. Antibodies may be either reduced in number or have diminished effectiveness. Phagocytes and macrophages may have altered or diminished function because of the malnutrition (Kline, 2008).

Perhaps if we identify the patient with malnutrition and treat with appropriate lev-els of nutrition support, we can improve the chances for recovery from associated infec-tions and improve the patient’s chances for a positive outcome from his illness or injury. The chart on the next page shows risk factors for malnutrition.

We’ve come a long way since 1974 when the “skeleton in the hospital closet“ was first identified. Our understanding of the contributing factors to malnutrition continues to improve. We know that serum albumin and visceral proteins are poor markers of nu-tritional status, particularly in acutely ill hospitalized patients and patients with chronic illnesses. We must rely on our clinical judgment to assess the presence of malnutrition: Look at the patient and talk to him or his family about his nutrient intake, and look for signs of wasting of muscle mass and loss of fat stores.

An evaluation of patients was repeated, using the same parameters as the ones used by Butterworth( Coats, et al, 1993). This study indicated that the incidence of mal-nutrition during hospitalization had decreased. However, if the patient was hospitalized for a longer period, he continued to be at risk — to the same degree as in 1974 — for the development of malnutrition. In fact, 45 percent of malnourished patients are hospital-ized longer than the average with an increased length of stay of 5.6 days as compared to the well nourished patient (Robinson et al, 1987; Chima, 1997; Correia and Waitzberg, 2003).


We have already briefly reviewed the means by which we can begin to assess our patients and clients for nutritional status. In later chapters, we will further discuss ways to physically evaluate our patients and tell how to interpret laboratory data and relate it to nutritional status. We will also discuss vitamin and mineral status and requirements, and the way nutritional status and analyze changes with different stressed states and chronic illnesses. The often-difficult assessment of the elderly population will also be discussed.

referencesButterworth CE. The skeleton in the hospital closet. Nutr Today, Mar/April 1974.Butterworth CE and Weinsier RL. Malnutrition in hospital patients: assessment and treatment. In:

Weight abnormalities• Underweight (< 80 % of standard) • Overweight (>120 % of standard) • Losses >10 % of usual weight

Impaired intake• No nutrition support• No oral intake > 5 - 7 days• Alcoholism • Anorexia/bulimia (eating disorder)• Anorexia/cachexia from disease• End stage liver disease

Abnormal losses • Malabsorption, fistulas, dialysis, wounds• Diarrhea (>500 mL >2 days)• Vomiting (> 5 days)• End stage renal disease

Increased needs • Sepsis, trauma, major surgery, burns or fever • Decubitus ulcers

Medication• Steroids, immunosuppressants, antineoplastic agents

Kovaceveic k, 1997

Risk Factors for Malnutrition


Modern Nutrition in Health and Disease, 6th ed. Goodhart RS and Shils ME, eds. Philadelphia: Lea & Febiger, 1980.

Chima CS et al. Relationship of nutritional status to length of stay, hospital costs, and discharge status of patients hospitalized in the medicine service. J Am Diet Assoc. 1997; 97: 975-978.

Coats KG, Morgan SL, Bartolucci AA, et al. Hospital-associated malnutrition: a reevaluation 12 years later. JADA, 1:27-33, 1993.

Correia MI, Waitzberg DL. The impact of malnutrition on morbidity, mortality, length of hospital stay and costs evaluated through a multivariate model analysis. Clinical Nutrition 2003; 22:235-239.

Grant JP. Nutritional assessment in clinical practice. Nutr Clin Prac, 1:1:3-11, Feb. 1986.Gray DS and Kaminski MV. Protein-calorie malnutrition. In: Hyperalimentation: A Guide for Clinicians.

Kaminski MV, ed. New York: Marcel Dekker, Inc., 1985.Hill GL. Body composition research: implications for the practice of clinical nutrition. JPEN, 16:3:197-

218, May-June 1992.Jensen GL, Bistrian B, et al. Malnutrition syndromes: a conundrum vs continuum. JPEN, 33:710-716,

2009.Jensen GL, Mirtallo J, et al. Adult starvation and disease-related malnutrition: a proposal for etiology-

based diagnosis in the clinical practice setting from the International Consensus Guideline Com-mittee. JPEN, 34(2):156-15, 2010.

Kline DA. Nutrition & Immunity, Part I Immune Components & Nutrients. 7th Ed. Ashland, OR Nutrition Dimension, 2008.

Kovacevick DS Boney BR, Braunschweig, et al. Nutrition risk classification: a reproducible and valid tool for nurses. Nutr Clin Prac, 12: 20-25, 1997.

Malone A and White JV. Revisiting “the skeleton“: new characteristics and criteria to define adult malnutrition. ASPEN, 2011.

McClave SA, Mitoraj TE, et al. Differentiating subtypes (hypoalbuminemic vs marasmic) of protein-calorie malnutrition; incidence and clinical significance in a university hospital setting. JPEN, 16:4:337-342: July-Aug, 1992.

Mowe M and Bohmer T. The prevalence of undiagnosed protein-calorie undernutrition in a population of hospitalized elderly patients. J Am Geriatr Soc, 39:1089-1092, 1991.

Munro HN and Crim MC. The proteins and amino acids. In: Modern Nutrition in Health and Disease, 6th ed. Goodhart RS and Shils ME, eds. Philadelphia: Lea & Febiger, 1980.

Nagel M. Nutrition screening: Identifying patients at risk for malnutrition. Nutr Clin Pract, 8:171-175, 1993.

Robinson G, Goldstein M, Levine GM. Impact of nutritional status on DRG length of stay. JPEN, 11:49-51, 1987.

Ukleja A et al. Nutrition care algorithm (Adapted from Standards for Specialized Nutrition Support: Adult Hospitalized Patients. Nutr Clin Pract, 25:403-414, 2010.

Viteri FE and Torun B. Protein-calorie malnutrition. In: Modern Nutrition in Health and Disease, 6th ed. Goodhart RS and Shils ME, eds. Philadelphia: Lea & Febiger, 1980.


Chapter Two:Medical and Nutrition History

Common sense tells you that the first step in performing a nutritional assess-ment should be the evaluation of a patient’s medical and nutrition history. Yet this basic, although admittedly sometimes complex, task is often overlooked, as we jump ahead to the evaluation of laboratory data, physical examination and anthropometric measure-ments. A simple review of a patient’s history of dietary intake and eating practices and his medical history can tell you many things about his potential for malnutrition and complications arising from malnutrition.

Dietitians learn about the concept of taking a nutrition history in their college classes and internships. How many practitioners, though, continue to obtain a detailed nutrition history from patients who are most at risk for malnutrition? Many of us obtain a nutrition history from those patients whom we instruct on a diabetic or other modified diet, but neglect to take a nutrition history from the at-risk, undernourished or malnour-ished patients we take care of each and every day.

So, to begin with the basics, how do we go about taking a nutrition history? What concepts are important to cover? How in-depth do we need to be in obtaining the his-tory? What about the patient who is unable to communicate, is on a ventilator, etc.?

These and other pertinent topics will be covered in this chapter.

Social factorSThe nutrition history should include some information about the patient’s social

history, since such factors as inadequate income, for example, can inhibit a patient’s abil-ity to buy enough or the right types of food.


Many people will not understand why a clinician needs to know about a patient’s financial status, and may resist revealing this information, so it must often be gleaned from other sources or interpreted using your best judgment. Many hospitals now have case management meetings wherein caregivers of all disciplines convene to review each patient and determine the best way to optimize the care given. These meetings can be invaluable tools.

Judging the importance of social factors can be difficult without a set of guidelines. Social scientists have identified certain daily living tasks and defined varying levels of competence in them. Two valuable assessment tools, of particular use with the elderly population, are Activities of Daily Living (ADL) and Instrumental Activities of Daily Living (IADL). Included in this course (Appendices #1 and #2) are checklists suitable for duplication for use in practice.

Evaluation of a person’s eating habits and the types of foods he eats can often give clues about his ability to supply himself with adequate nutrition. The person who lives alone, especially an elderly person, may also be at risk for altered or inadequate intake. How many of us can say we always cook dinner for ourselves when left for an evening alone? I’m sure I’m not alone in admitting that I’ve eaten only popcorn for dinner on occasion. How many of our elderly patients just don’t have the energy or don’t take the time to shop and/or prepare the right types of foods?

We need to consider more than calories and nutrients. Does the person have any disability that could prevent him from being able to prepare a meal? Is he an alcoholic or does he have a history of alcohol abuse? The person who abuses alcohol or other sub-

Social Factors Affecting Nutritional Status

Income

Eating habits – eating out, fast foods, processed foods

Living situation – lives alone, recent divorce, death, etc. – food storage/cooking/eating facilities – ADLs and IADLs

Physical limitations

Alcoholism/drug abuse

Smoking

Mental/emotional state – situational depression over illness – history of mental disease


stances may be at risk for nutrient deficiencies (e.g. thiamin and other B vitamins and protein-calorie malnutrition). Does the person smoke, thereby putting him at risk for vi-tamin C depletion? Does he eat alone? (He may well be at risk for malnutrition because he may not eat at all or may eat the wrong types of foods.) Can the person afford to buy fruits and vegetables?

How is the person’s appetite? Many hospitalized patients have poor appetites, either simply because they don’t feel well enough to eat or because of limitations caused by the disease or surgery that has placed them in the hospital.

How is the person’s dentition? Ill-fitting dentures or teeth that are in poor repair can keep the patient from being able to eat well and may place him at risk for malnutri-tion. As a person ages, salivary flow decreases, thereby making chewing and swallowing more difficult. Are there any other chewing or swallowing problems that inhibit ad-equate intake?

How varied is the person’s diet? Has he been using a liquid diet plan or another type of monotonous diet? Is the patient experiencing a loss of the sense of taste? This altered taste sensation can be caused by smoking, a disease process or infection, certain medications, chemotherapy, zinc depletion, etc. Who wants to eat when nothing tastes good? Terms that describe an altered sense of taste include ageusia (lack of or impaired sense of taste) and dysgeusia (perverted sense of taste).

Just as important is the sense of, or lack of sense of, smell. The senses of smell and taste are interrelated; alteration of either or both can drastically affect the quality and quantity of nutritional intake.

Does the person omit any major food groups, such as meat and animal products, from his diet, whether for cultural, religious or other personal reasons? How often does he eat away from home, at fast-food or other restaurants?

The patient who is in the hospital may be subjected to extended periods of no oral intake (NPO) status. The patient who has no intake for greater than three to five days may be placed at nutritional risk, depending upon other stressors, such as surgery or sepsis.

Prescribed and over-the-counter medications may have adverse interactions with food or nutrients, so the types of medication taken by the patient must be reviewed for the possibility of drug-nutrient interactions. Appendices #3, #4 and #5 list medications that affect taste, eating patterns, and/or nutrient utilization.

Does the person have any food intolerances or allergies that may hold a potential for nutrient depletion? The person who is intolerant to milk may be at risk for inad-equate calcium and other nutrients, for instance. Conversely, if the patient takes any vitamin or mineral supplements, we need to know if these supplements are balanced, or unbalanced so they place the person at risk for toxicity (e.g. vitamin A) or dependency (e.g. “rebound scurvy” from suddenly discontinuing large doses of vitamin C ).

Does the person follow a modified diet at home? Is this modified diet restrictive enough to place the person at nutritional risk if followed for an extended period of time (e.g. very low calorie diet, low residue or clear liquid diets)?


NutritioN hiStory aSSeSSmeNt toolSA simple evaluation of the patient’s recall of an average 24-hour intake, the frequen-

cy of intake of various foods, food diaries, or observation of percentage of meals taken or calorie counts of actual intake can be valuable in assessing the patient’s adequacy of nutritional intake.

Food frequency questionnaires, food diaries, and observation and documentation (calorie counts) of intake can also be helpful. Food frequency questionnaires should be accompanied by a “24-hour recall” to be most accurate.

Consideration of ethnic and cultural influences is important as well. Food diaries should cover at least three days, while seven days of recorded intake can be more valu-able. At least one weekend day should be included. Samples suitable for duplication and use in practice, are included as Appendices #7 and #8.

medical factorSThe patient’s medical history is equally as useful in completing a nutritional as-

sessment. Is there any history of weight change? An unplanned decrease or increase in weight of greater than 10 percent of usual body weight may signify nutritional risk. If usual body weight is 20 percent over or under ideal body weight, the patient may be at risk. Ideal body weight may be determined in a number of ways, including insurance height/weight tables (Appendix #6) and the Hammwi method.

To calculate ideal body weight using the Hammwi method, begin with a base weight of 106 lb for males, and add 6 lb for every inch of height above 5 feet; for females, begin with 100 lb, and add 5 lb for each inch above 5 feet in height.

Are there any medical problems that would affect or prohibit adequate nutrient intake? Does the patient have gastrointestinal symptoms, such as nausea, vomiting, diarrhea, or constipation? Pain associated with eating, such as indigestion, abdominal cramping, or sore mouth, can prohibit the ingestion of adequate types of foods.

Many medical diagnoses are associated with an increase in metabolic demand. Burns can drastically increase nutrient demands. Fever increases metabolic rate by 7 percent for each degree Fahrenheit (13 percent for each degree Celsius) above normal. Infection, sepsis, trauma, surgery, and endocrine diseases all have an impact on nutrient needs and, if intake is inadequate, can lead to malnutrition or, at the very least, dimin-ished nutrient stores.

Pregnancy can increase nutrient needs — especially in the latter stages — and fre-quent pregnancies over a short period of time have the potential of robbing the mother of important nutrient stores. Excessive nutrient losses should trigger further evaluation of nutritional status.

A fistula, abscess, or wound that is draining can result in increased fluid, protein and electrolyte losses, as well as the loss of minerals, such as zinc. Loss of protein into the urine or, in dialysis patients, into the dialysate can result in malnutrition.


Dialysis patients are very often malnourished because of the disease state, lack of appropriate intake, increased nutrient demand, and losses into the dialysate. Protein deficiency in patients with endstage renal disease increases their risk for morbidity and mortality.

A history of surgeries that involve resection of the gastrointestinal tract, liver, pan-creas, or gallbladder should trigger further evaluation of nutritional status. History of previous supplementation with enteral or parenteral feedings or with nutritional supple-ments indicates possible nutritional depletion.

The presence of chronic illnesses, such as diabetes mellitus, malabsorption, pancre-atitis, pulmonary disease, cancer, liver disease, and cardiac disease should act as a cue to the dietitian or health care practitioner for further investigation of nutritional status. All of these illnesses, as well as trauma, surgery, and critical illness, can cause altered or diminished nutrient stores. These illnesses can not only affect calorie and protein stores, but can also affect stores of micronutrients, such as vitamins and minerals.

Diseases or resections of the gastrointestinal tract can have a profound effect on the nutritional status of the patient, impacting calories, protein, vitamins, and minerals. Further discussion of these problems will occur in a later chapter.

Endocrine disorders, such as diabetes mellitus, can cause a loss of nutrients such as magnesium and chromium. Diseases of the kidney, liver, and cardiopulmonary system also affect all nutrient stores; these processes will be discussed in detail later.

Use of certain medications can increase nutrient demand, cause increased loss of nutrients, or diminish nutrient intake by causing anorexia and decreased absorption. Examples of these medications include steroids, chemotherapeutic agents, etc.

Clearly, a thorough review of a patient’s dietary and medical history is important in the initial stages of completing a nutritional assessment. Although not always easy to ob-tain, a diet history can provide valuable insight into the patient’s ability to cope and heal after discharge. Always use family members, friends, visiting nurses, and other caregiv-ers to provide information to assist you in the completion of a diet history. The medical and surgical history of a patient cannot be overlooked and is a valuable tool in providing you with an idea of what to look for in the nutritional assessment of your patient.

caSe StudyA 69-year-old obese woman is admitted to the ICU after falling from her chair at

home. She was found by a neighbor after she had been on the floor for more than two days. She is intubated and sedated, and thus is unable to communicate her nutrition or medical history. She has no apparent family members who are able to assist with provid-ing information to complete the assessment. Her neighbor relates that she goes grocery shopping for the patient and brings her food once or twice a week, and that the patient has not left her home for more than two years. Physical examination reveals a massive decubitus ulcer on her buttocks. She is also morbidly obese, weighing greater than 450 lb on her 5’7” frame. Fortunately, the patient is extubated by Day 2 of her stay and re-


veals that she is diabetic, wants “no sugar” but only “diet Pepsi and lots of ice.” Further questioning reveals that the patient consumed little more than diet soda and ice at home as well. Even though first glance might make one assume that the patient consumed an overabundance of calories, the completion of the nutrition history reveals that the pa-tient’s diet is severely deficient in protein, calories, vitamins, and minerals.

Use of a nutrition history is just one of many aspects in determining a patient’s nu-tritional status and should be considered just that — a portion of the assessment.

review queStioNS1. What components can be used to obtain a diet history?2. How do you calculate ideal body weight?3. What data from a medical history would trigger further investigation into nutritional

status?4. What are some of the aspects of a patient’s socioeconomic history that are important in

the assessment of a dietary history?

refereNceSBozzetti F. Nutritional assessment from the perspective of a clinician. JPEN 11:115S-121S, 1987.Grant A and DeHoog S: Nutritional Assessment and Support, 3rd ed. Grant & Dehoog pub., Seattle,

WA, 1985.Hopkins B. Assessment of nutritional status. In: Nutrition Support Dietetics. Shronts EP, ed. Silver

Spring, MD: ASPEN, 1989.Lang CE and Cashman MD. Nutritional status. In: Dietitian’s Handbook of Enteral and Parenteral

Nutrition. Skipper A, ed. Rockville, MD: Aspen Publishing Co., 1989.Practical Guide to Nutritional Care, Campbell SM, ed. University of Alabama, 1984.


Chapter Three:Clinical Assessment

How do you start a clinical assessment on a patient? Your best bet is to walk into the patient’s room and take a look at him. Sometimes, the incidence of malnutrition will be quite obvious to you. The patient may clearly be emaciated and may be described as being “skin and bones.”

On the other hand, he may not be emaciated but may have a markedly distended abdomen and edematous extremities, indicative of kwashiorkor (Lang and Cashman, 1989). Other patients may appear well-nourished (or not appear malnourished), but may, in fact, suffer from various forms of mal- or under-nutrition. Let’s review these physical signs of mal- or under-nutrition, which are summarized in Appendix #12.

Starting from the top, the person with protein-calorie malnutrition may have dry, easily pluckable, or sparse hair. By easily pluckable, we mean that a small amount of hair can be easily pulled from the head without much force and without causing pain (Grant and DeHoog, 1985; Hopkins, 1989). The hair may be thinner and straighter than normal for the individual or ethnic group. Changes in the usual hair color may occur with protein-calorie malnutrition or biotin depletion (Hammond, 1999).

The skin may become pale and dry with depletion of Vitamin A and essential fatty acids. Follicular hyperkeratosis (spinelike plaques around the mouths of hair follicles) also occurs with vitamin A and essential fatty acid deficiencies (Hammond, 1999). Dehydration may result in poor skin turgor. Poor wound healing and the presence of pressure ulcers may be linked to deficiencies of protein, vitamin C and zinc, but can also be related to friction and continual pressure.

Dermatitis can occur with niacin deficiency. Perifollicular petechiae (small hemor-rhagic spots on the skin around hair follicles) can occur with vitamin C and vitamin K deficiency. Nasolabial seborrhea occurs with niacin, riboflavin and vitamin B6 deficien-cies. Keep in mind that all of these skin changes can also occur because of other, non-nutritional, factors.


Let’s discuss why these skin changes occur with various vitamin deficiencies. Vi-tamin A deficiency results in abnormal function of mucus-secreting cells, leading to the problems with dry skin and plaquing around hair follicles (Olson, 1984).

Since vitamin C is essential for the formation of collagen, any deficiency may result in impaired syntheses of this substance, including the collagen in ground substance between cells (Jaffe, 1984). You’re likely already familiar with the symptoms of “classic” vitamin C deficiency: scurvy.

As vitamin K is essential for the formation of clotting factors in the blood, a defi-ciency of the vitamin could lead to increased bleeding time. Vitamin B6, riboflavin and niacin are all necessary for normal growth of cells; when these vitamins are deficient, new cells may not form as quickly and the result may be dry skin.

Next, let’s look at the patient’s eyes. Since vitamin A is essential for normal vision and for tissue differentiation, deficiencies of this vitamin will cause symptoms around the eyes. Xerophthalmia is a general term that includes xerosis, Bitot’s spots and changes in the cornea that include ulceration (Olson, 1984).

Xerosis is described as a cornea that is “dull, milky, hazy, or opaque” (Grant and DeHoog, 1985). Bitot’s spots are foamy spots, usually gray, yellow, or white, which ap-pear on the white portion of the eye. Keratomalacia may also be seen and is defined as a “softening of part or all of the cornea.” Night blindness is also associated with vitamin A deficiency (Hopkins, 1989; Olson, 1984). The corners of the eyes may also become cracked and red: this is known as angular palpebritis and is associated with riboflavin and niacin deficiency.

Let’s now move on down to the mouth. Angular stomatitis (cracks, redness and flaking at the corners) occurs with riboflavin, vitamin B6 and niacin deficiencies and may also be related to iron deficiency. Cheilosis (vertical cracks on the lips) is associated with vitamin B6, riboflavin and niacin deficiencies and can be explained by the same rationale used to explain nasolabial seborrhea. Obviously, these symptoms can occur because of other factors as well. These factors might include sun or wind exposure, herpetic lesions, or ill-fitting dentures, for example.

Now have the patient open his/her mouth. Bleeding and spongy gums can be as-sociated with vitamin C deficiency. A magenta tongue is a classic symptom of riboflavin deficiency, while a beefy red tongue (glossitis when also associated with symptoms of pain and atrophied taste buds) is a symptom of niacin, folate, riboflavin, iron, vitamin B12, pyridoxine and tryptophan deficiencies.

Koilonychia, an iron deficiency symptom, is described as “spooning” of the nails. This is just what it sounds like — the nails look like spoons.

Edema in the subcutaneous tissues, especially in lower extremities, can be an indica-tion of protein depletion or thiamin deficiency. Thiamin is involved in metabolism of car-bohydrate and some amino acids, while adequate protein stores are needed for adequate serum levels of albumin, necessary to maintain appropriate oncotic pressures. When albu-min levels are low, fluid shifts occur to normalize these pressures. Fluid shifts from inside the cell into the third space cause the outward symptom of edema.


Bowlegs or knock-knees can be associated with previous vitamin D and calcium deficiencies. Beading of the ribs is often related to vitamin D and calcium deficiencies, as well as protein-calorie malnutrition.

Cardiomegaly (enlarged heart) may be associated with thiamin deficiency (beriberi) and anemia. However, this symptom is usually non-nutritional. A patient with thiamin deficiency may be at risk for congestive heart failure.

We will further discuss assessment of vitamin/mineral deficiencies and require-ments and the reasons for these deficiencies in Chapter Six.

Anthropometrics or body composition studiesAnthropometry is defined by Heymsfield as a “technique in which simple mea-

suring instruments are used to describe human form” (Heymsfield and Casper, 1987). Most people think of anthropometrics as the measurement of subcutaneous fat and total body fat and measurement of skeletal protein mass. These measurements are obtained through measurement of triceps skinfold (TSF), subscapular and supra-iliac skinfold measurements, mid-arm circumference (MAC), mid-arm muscle circumference (MAMC), upper arm circumference (AMC) and arm muscle area (AMA).

triceps skinfold meAsurementsTriceps skinfold (TSF) measurements are obtained in the triceps or subscapular area

of the arm. Calipers which have been calibrated are necessary for accurate measurement. The choice of which arm to measure is debated, with some sources suggesting the use of the right arm while others suggest using the patient’s non-dominant arm. The choice you make should be followed consistently, especially when making sequential measurements on the same patient and when comparing data from patient to patient.

The patient should bend his elbow so that the arm is at a 45 degree angle, placing his hand across his stomach.

Measure the distance from the acromial process (the bony protrusion at the shoul-der-arm joint) to the olecranon process (the bone at the back of the elbow) and mark the midpoint on back of the patient’s arm. Next, have the patient let his arm drop naturally to his side. Grab a fold of fat and skin from the arm about one centimeter above the mid-point mark, making sure that no muscle has been included in the skinfold.

Measure the thickness of the skinfold by placing the pincers of the calipers over the mark. Take care to take each measurement three times, resting three seconds between each reading. Average the three measurements; record this figure.

The measurement of TSF is useful in determining the presence of obesity or calorie depletion. Comparison of measured TSF levels should be compared to established stan-dards with the following formula:

% of standard = (measurement obtained/standard) X 100


The TSF percentage of depletion is then classified as mild, 90 percent of standard; moderate, 60 to 90 percent; or severe, <60 percent (Hopkins, 1989). Tables of standard levels for TSF are included in Appendix #9.

mid-Arm circumferenceMid-arm circumference (MAC) is obtained by measuring the circumference of the

arm at midpoint and is used to determine MAMC and AMA with the following equa-tions:

MAMC(cm) = MAC(cm) - 3.14 TSF(cm) AMA(cm2) = MAC(cm)- 3.14 TSF(cm2 ) 4πComparison of measurements to standards is done in the same fashion as with TSF

and the characterizations of depletion are the same. Tables of standards are included in Appendix #9.

Before you go to the trouble of becoming an expert in the skills of obtaining anthro-pometrics, you should be familiar with the advantages and disadvantages of using them in assessing your patients. Advantages include that the measurements are simple and safe; are inexpensive; and can be used at the bedside (Heymsfield and Casper, 1987).

However, these advantages are countered by the disadvantages of the possibility of discrepancies of measurements, depending on the practitioner; poor calibration of the calipers; changes in tissue composition, especially in the elderly and critically ill; and the inability of the hospitalized patient to assume the necessary position to enable the measurements (Lang and Cashman, 1989; Hopkins, 1989).

Anthropometrics may be useful in the long-term care of patients and outpatients when the measurements can be taken and compared over a period of time. The measure-ments can be a good indicator of the patient’s changes in nutrition status. However, they are not always a good measure of nutrition status in acute care settings, because of the disadvantages discussed earlier.

other body composition meAsurement techniquesResearch continues in new methods of determining body composition through anthro-

pometrics. Ultrasonography, infrared interactance, magnetic resonance imaging (MRI) and computerized axial tomography (CAT) are a few of the new techniques being studied.

Computerized axial tomography allows the practitioner to clearly distinguish between the patient’s muscle, fat and bone, but cannot be regularly utilized for nutri-tion assessment because of the cost, exposure to radiation and possible need for sedation (Chiba, et al., 1989).

Ultrasonography, while providing a good measurement for assessment of fat and protein stores, is no better than less expensive measurements utilizing calipers (Chiba, et al., 1989).


Other studies have shown that techniques such as multiple isotope dilutions to as-sess nutrition status are useful and accurate. However, these studies are very complex and require specialized laboratories and personnel (Shizgal, 1987). In fact, Shizgal sug-gests that body composition measurements should be “limited to the research environ-ment . . . for investigational use.”

Examples of additional means by which to determine body composition include in vivo neutron activation analysis, potassium isotope dilution and total body potas-sium measurement. All of these methods, while useful, are expensive and not readily available in most clinical settings.

In vivo neutron activation analysis involves the measurement of isotopes of vari-ous elements in the body. These elements include nitrogen, carbon, chlorine, potassium and, to a lesser extent, calcium, sodium and phosphorus (Beddoe and Hill, 1985). The measurements obtained then enable the estimation of lean body mass and, thus, total body fat by using the formula: body weight – lean body mass = total body fat (Hop-kins, 1989).

Because potassium is almost always concentrated in the intracellular fluid, mea-surement of total body potassium can be used to judge body cell mass (by using the formula: measured total potassium (mEq) ÷ 68.1 (Beddoe and Hill, 1985). However, these measurements may be skewed because of metabolic stress, starvation and distur-bances in acid-base balance (Hopkins, 1989).

Potassium isotope dilution is a measurement of total exchangeable potassium and measures body cell mass as total exchangeable potassium X 8.33 (Hopkins, 1989). This measurement can also be skewed with the presence of the same processes mentioned in conjunction with total body potassium.

Other more non-invasive methods of determining body composition include whole body density, bioelectrical impedance and whole body conductivity.

To measure whole body density, the patient’s body fat is obtained by submerging the person in a water tank and determining residual lung volume. From this determi-nation, both fat mass and fat-free mass can be determined.

Whole body conductivity measures fat-free mass by measuring radio frequencies passed through the body. This method is affected by the presence of dehydration, fluid overload and electrolyte imbalances. Bioelectrical impedance is used more commonly than whole body conductivity and whole body density. An electrical current is passed through the body in order to measure total body fat and fat-free mass. This method is also limited in the presence of dehydration, fluid overload and electrolyte imbalances (Hopkins, 1989).

As stated earlier, it appears that the consensus among most nutrition support and assessment experts is that most methods of measurement of body composition are not very useful in the clinical setting and should be limited to use in research.

A more useful and much more readily available (sometimes!) anthropometric mea-surement is height and weight data. Height can be used to determine ideal body weight,


either through height/weight tables, i.e. Metropolitan Life Insurance Tables (see Appen-dix #6), or by using the Hammwi method referred to in Chapter Two:

Males: 106 lb for first 5 ft + 6 lb for each additional inch; Females: 100 lb for first 5 ft + 5 lb for each additional inch.

If the patient is unable to be measured in the conventional manner, arm span can be measured by having the patient extend his arms straight out to the side and then measuring from fingertip to fingertip. The measurement thus obtained is equal to the person’s height.

Knee height can also be utilized by measuring from under the heel of the foot to the middle of the knee joint. Calculations to determine estimated height are:

Males: height (cm)= 64.19 - (.04 x Age) + [2.02 x knee height (cm)]; Females: height (cm)= 84.88 - (.24 x Age) + [1.83 x knee height (cm)]

Body frame size can be determined by measuring wrist circumference or by mea-suring elbow breadth. Wrist circumference is measured by taking the smallest distance around the wrist; frame size is determined by height (cm) divided by wrist circumfer-ence (cm). Frame sizes are then compared to established standards, as shown below:

Elbow breadth is measured by taking the distance between the two prominent bones when the elbow is bent at 90 degrees. This measurement is then compared to es-tablished data, shown in the chart on the following page:

Large Medium Small

Men >10.4 10.4-9.6 <9.6

Women >10.9 10.9-9.9 <9.9

Frame Size Ranges


Once weight is determined through accurate measurement, the value should be compared to usual body weight and ideal body weight. A comparison of actual body weight to ideal body weight is done to assess the presence of and degree of malnutrition, using the formula below. Remember that weight may be affected by shifts in fluid status (i.e. IV fluids, diuretics, edema, ascites) (Shopbell, Hopkins, and Shronts, 2001).

Frame Size & Elbow Breadth

Height*5'2" to 5'3"5'4" to 5'7"5'8" to 5'11"6'0" to 6'3"6'4"

Height*4'10" to 4'11"5'0" to 5'3"5'4" to 5'7"5'8" to 5'11"6'0"

Elbow Breadth**2 1/4" to 21/2"2 1/4" to 21/2" 2 3/8" to 2 5/8"2 3/8" to 2 5/8"21/2" to 2 3/4"

Elbow Breadth**2 1/2" to 2 7/8"2 5/8" to 2 7/8" 2 3/4" to 3"2 3/4" to 3 1/8"2 7/8" to 3 1/4"

Men Women

*Height in one inch heels **Elbow breadth for medium frameMeasurements lower than those listed indicate small frame; higher measurements indicate large frame.

Assessing Malnutrition from Body Weight

Using Ideal Body Weight: actual body weight ideal body weight

Ratio assessment: <69% severe caloric depletion 70-79% moderate caloric depletion 80-90% mild caloric depletion >120% overweight >150% obese >200% morbidly obese

Using Usual Body Weight: actual body weight usual body weight

Ratio assessment: 85-95% mild malnutrition 75-84% moderate malnutrition <74% severe malnutrition

X 100 = ratio %

X 100 = ratio %


Of the two methods shown above, the second (usual body weight) is a more useful measurement and comparison in the critically or chronically ill patient (Hopkins, 1989). Unplanned weight loss of greater than 10 percent of usual body weight is usually con-sidered as moderate to severe caloric depletion.

body mAss indexAnother measurement comparing weight to height is the body mass index or BMI. BMI = Weight (kg) Height (m2)

Interpretation of the BMI is as follows (Hopkins, 1993):<15 Significant increase in morbidity16 to 17 Moderate malnutrition17 to 18.5 Mild malnutrition19 to 25 Appropriate weight (19 to 34 yr)21 to 27 Appropriate weight (>35 yr)>27.5 Obesity27.5 to 30 Mild Obesity30 to 40 Moderate obesity>40 Severe or morbid obesity

subjective globAl AssessmentOnce you have completed a review of the patient’s medical and dietary history and

assessed nutrition status by examining the patient’s physical condition, you can adapt this data for use in completing a subjective global assessment (SGA).

As described by Jeejeebhoy, et al., specifically, five criteria obtained in the history and physical are utilized in SGA. These include:

• Weight change history. Weight loss over the previous six months of less than 5 percent is considered minor, 5 to 10 percent weight loss is considered potentially significant and a weight loss of greater than 10 percent is definitely significant.

• Dietary intake change. Changes in dietary intake are described as normal or ab-normal; the length and degree of abnormal intake are also considered.

• Gastrointestinal symptoms. Any symptom (nausea, vomiting, diarrhea and an-orexia) lasting longer than two weeks is also noted.

• Functional ability is the patient’s energy level (i.e. bedridden, housebound, working).

• Illness and its effects. The metabolic demand placed on the body by the illness is characterized as no stress, low stress, moderate stress and high stress (Jeejeebhoy, et al., 1987).


Physical assessment of loss of subcutaneous fat, muscle wasting, ankle edema, sacral edema and ascites is also considered in the rating of the patient based on SGA. Physical assessment is characterized as: 0 = normal; 1+ = mild; 2+ = moderate; and 3+ = severe, referring to degree of loss of subcutaneous fat, muscle wasting, ankle and sacral edema and ascites (Lang and Cashman, 1989).

The SGA rating is then determined, utilizing subjective indices. Category A is “well-nourished;” Category B is “moderate or suspected malnutrition;” and Category C is “severe malnutrition” (Jeejeebhoy, et al., 1987).

The most emphasis is placed on weight changes, poor dietary intake, loss of sub-cutaneous tissue and muscle wasting. In fact, weight loss and the pattern of weight loss appears to be the most important component of SGA. Disadvantages to using the SGA techniques in assessing your patient might include the difference in one person’s assess-ment as compared to the next person’s assessment, because of the subjectivity. In begin-ning to use SGA, Jeejeebhoy suggests that we begin by performing assessments together as a group so as to attain a consensus and more consistency from practitioner to practi-tioner.

I feel that many of us use subjective global assessment without even knowing that is what we are doing. This type of assessment comes more easily with experience and exposure to a variety of patients, diseases and illnesses.

Criteria for History and Physical

*Weight change history: <5% weight loss over 6 mo. = minor depletion 5-10% weight loss over 6 mo. = potentially significant depletion >10% weight loss over 6 mo. = significant depletion

*Change in dietary intake: Normal vs. Abnormal Length of change _____________ Degree of change ___________

Gastrointestinal symptoms: (i.e. nausea, vomiting, diarrhea, anorexia) >2 wks

Functional ability of patient: bedridden housebound working

Metabolic demand: no stress low stress moderate stress high stress

Physical Assessment related to loss of subcutaneous fat*, muscle wasting*, ankle and sacral edema, and ascites. Depletion ratings are: 0 = normal 1+ = mild 2+ = moderate 3+ = severe

SGA rating (subjective): Category A = well-nourished Category B = moderate or suspected malnutrition Category C = severe malnutrition

*primary importance


prognostic nutrition indexSmith and Hartemink (1988) state that nutritional assessment has “traditionally had

various components: clinical, anthropometric, biochemical, immunologic and critical or-gan function.” From this data, a formula to increase the value of nutritional assessment in predicting patient outcome has been developed (Mullen, et al., 1979). The formula, known as the Prognostic Nutrition Index (PNI), is shown below.

As the risk percentage increases, the rate of complications in surgical patients also increases (Smith and Hartemink, 1988; Roy, Edwards, and Barr, 1985).

instAnt nutrition AssessmentAnother, less complicated, method to link nutritional assessment to prognosis is the

“instant nutrition assessment,” developed by Seltzer (Seltzer, et al., 1981). This method looks at albumin levels and total lymphocyte counts and considers the

significance of these levels in comparison to outcome. Serum albumin levels (Alb) >3.5 gm/dl associated with total lymphocyte counts (TLC) of >1500 mm3 are associated with fewer complications than Alb levels of <3.5 gm/dl with TLC levels either greater than or less than 1500 mm3. All of the patients in one study who had both low TLC and Alb developed complications.

As we have seen, clinical assessment includes evaluation of the patient’s physi-cal symptoms and status; anthropometrics, to include height and weight; a subjective assessment based on experience and keying in on amount and duration of weight loss; and, possibly, the development of a prediction for complications based on nutritional status.

The case study on the following page illustrates how clinical assessment can be used.

Prognostic Nutrition Index (PNI)

% risk = 158 – 16.6(ALB) – 0.78(TSF) – 0.2(TFN) – 5.8(DH) ALB = albumin (gm/dl) TSF = triceps skinfold (mm) TFN = transferrin (mg/dl) DH = delayed hypersensitivity (% positive reaction)

Risk assessment: Low <40% Intermediate 40 – 49% High >50 %


cAse studyA 74-year-old woman is admitted to the ICU. She is 5’8," weighs 158 lb and is classi-

fied as medium frame. Her hair is thinning and white. Her skin is flaky and dry. Ascites is noted in her abdomen.

Anthropometric measurements reveal no depletion when compared to standards. She does state that she has lost approximately 30 lb over the last three months, which is calculated to be 16 percent of her usual body weight. She was admitted for coronary artery bypass grafting and has been NPO for the past five days.

She is determined to be at nutritional risk because of the appearance of recent caloric depletion, as indicated by significant weight loss over the last three months and inadequate nutrient intake over the last few days, accompanied by altered nutrient and metabolic demands because of the stress of surgery. Protein depletion is also suspected because of the abdominal ascites and no history of alcohol abuse.

Nutrition support was recommended.

review questions1. What symptoms characterize protein-calorie malnutrition?2. What symptoms might indicate a thiamin depletion?3. What are the advantages and disadvantages of anthropometrics?4. What is the best comparison of weight values in critically ill patients?5. What are the components of a subjective global assessment?6. What parameters are used to develop the prognostic nutrition index?7. What lab values are used to complete an instant nutrition assessment?

referencesBeddoe AH and Hill GL: Clinical measurement of body composition using. In vivo neutron activation

analysis. JPEN 9:4: 504-520, 1985.Bozzetti F: Nutritional assessment from the perspective of a clinician. JPEN 11(5):115S-121S, 1987.Chiba T, Lloyd DA, Bowen A, et al.: Ultrasonography as a method of nutritional assessment. JPEN

13:5:529-534, 1989.Grant A and Dehoog S: Nutritional Assessment and Support, 3rd ed. Grant & Dehoog pub., Seattle,

WA, 1985.Hammond K. The nutritional dimension of physical assessment. Nutrition 15.412-417, 1999.Heymsfield SB and Casper K: Anthropometric assessment of the adult hospitalized patient. JPEN

11(5):36S-41S, 1987.Hopkins B: Assessment of nutritional status. In: Nutrition Support Dietetics. Shronts, EP, ed. ASPEN,

1989.Hopkins B: Assessment of nutritional status. In: Nutrition Support Dietetics Core Curriculum, 2nd ed.

Silver Spring, MD: ASPEN, 1993.Jaffe GM: Vitamin C. In: Handbook of Vitamins. Machlin LJ, ed. New York: Marcel Dekker, Inc., 1984.Jeejeebhoy KN, Detsky AS, et al.: What is subjective global assessment of nutritional status? JPEN

11:1:8-13, 1987.


Lang CE and Cashman MD: Nutritional status. In: Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A, ed. Rockville MD: Aspen Publishing Co., 1989.

Mullen J, Buzby G, Waldman T, et al.: Prediction of operative morbidity and mortality by preoperative nutritional assessment. Surg Forum 30:80-82, 1979.

Olson JA: Vitamin A. In: Handbook of Vitamins. Machlin LJ, ed. New York: Marcel Dekker, Inc., 1984.Roy LB, Edwards PA, Barr LH: The value of nutritional assessment in the surgical patient. JPEN

9:2:170-172, 1985.Seltzer MH, Fletcher HS, Slocum BA, et al.: Instant nutritional assessment in the intensive care unit.

JPEN 5:70-72, 1981.Shizgal HM: Nutritional assessment with body composition measurements. JPEN 11:5:42S-47S, 1987.Shopbell JM, Hopkins B, Shronts EP. Nutrition screening and assessment. In: The Science and Practice

of Nutrition Support: A Case-Based Core Curriculum. Gottschlich, MM, ed. Dubuque, IA, 2001. Smith RC and Hartemink R: Improvement of nutritional measures during preoperative parenteral

nutrition in patients selected by the prognostic nutritional index: a randomized controlled trial. JPEN 12:6:58-62, 1988.


Chapter Four:Electrolytes and

Acid-Base Balance

Of equal importance as diet and medical histories, physical examination, and anthropometrics is the interpretation of laboratory data. Laboratory data can tell you not only about the patient’s previous nutritional status, but can also tell you about the patient’s present status and whether or not he is receiving adequate nutrition support. In this chapter, we’ll discuss electrolytes and acid-base balance and their role in nutritional assessment of patients.

ElEctrolytEs

sodiumSodium is the primary element found in the extracellular fluid. Serum levels of so-

dium may not suggest the patient’s nutritional status, but can tell you about the patient’s fluid status. Total body sodium usually correlates well with serum sodium; however, this is not true when extracellular fluid levels increase.

As extracellular fluid levels increase, total body sodium levels increase as well (Paskin, 1989). Antidiuretic hormone secretion increases and acts to decrease glomerular filtration rate (GFR), causing better reabsorption of sodium and water in the kidneys (Watkin, 1980). However, serum sodium levels are often low due to the increased extra-cellular water.

Hyponatremia (normal levels are 135 to 145 mEq/L) occurs when there is dilution or fluid excess. This can occur in diseases such as renal failure, congestive heart failure, and liver disease. Dilutional hyponatremia can also occur in hospitalized patients who have been resuscitated with large amounts of hypotonic saline solutions after surgery or injury and in the hospitalized patient receiving IV solutions (Paskin, 1989).


When a patient has a condition where sodium is actually lost (i.e., diarrhea, fistulas, vomiting, and gastric suction), serum sodium levels will be lower than normal as well (Grant and DeHoog, 1985). Increased losses of sodium through urine can occur with SIADH (syndrome of inappropriate antidiuretic hormone), adrenocortical insufficiency (Addison’s disease), and diabetic acidosis. SIADH occurs often in the elderly popula-tion. Abnormal stimulation of antidiuretic hormone occurs with emotional stress, pain, stroke, pulmonary infections, and many drugs (Watkin, 1980).

Symptoms of hyponatremia include weakness, apathy, tachycardia (accelerated heart rate) and hypotension, nausea or vomiting, confusion, and delusion (McCormick, et al., 1985). Serum sodium levels also decrease in relation to elevations in serum glucose and BUN levels. Sodium levels will fall by 16 mEq/L with each 100 mg/dl increase in glucose; while for each 28 mg/dl increase in BUN levels, sodium levels will fall by 33 mEq/L. Correction of hyponatremia is usually directed at restricting fluids and sodium intake (since sodium may increase fluid retention).

Hyponatremia

CausesRenal failureCongestive heart failureLiver diseasePost-injury resuscitationGastrointestinal losses – diarrhea, vomiting, fistulas, nasogastric suctioningUrinary losses – SIADH, Addison’s disease, diabetic ketoacidosis

Symptoms WeaknessApathyNausea, vomitingConfusion, delusionTachycardiaHypotension

Hypernatremia

Symptoms Restlessness Tremors Coma Convulsions

Causes Dehydration Diabetes insipidusHyperglycemia-induced diuresis


Hypernatremia, on the other hand, occurs with dehydration and with diabetes in-sipidus. Hypernatremia can also occur when hyperglycemia causes diuresis (Green and Cress, 1993). Hypertonic enteral formula administration without adequate fluid intake can lead to elevated sodium levels.

Symptoms of hypernatremia include restlessness, tremors of the muscles, coma, and convulsions (Green and Cress, 1993). Elevated sodium levels can lead to edema, hy-pertension, and congestive heart failure (McCormick, et al., 1985). Correction of elevated sodium levels is accomplished with the provision of adequate fluid if the patient is dehy-drated.

PotassiumWhile sodium is the primary extracellular cation, potassium is the primary intra-

cellular cation. Potassium levels in the serum have no correlation with total body potas-sium (Paskin, 1989). Just as in the case of sodium, potassium is not an indicator of nutri-tional status, but should be considered as we care for our patients and assure that we are feeding them appropriately, whether through TPN (total parenteral nutrition), enteral nutrition, or oral intake.

The normal range of potassium is 3.5 to 5.0 mEq/L. Hypokalemia has several causes including gastrointestinal loss through vomiting, diarrhea, and nasogastric suctioning. Increased urinary loss due to potassium-wasting diuretics and mineralocor-ticoids contribute to low serum potassium. Other medications such as the antibiotic am-photericin B or the antineoplastic drug cisplatin have been noted to induce hypokalemia. Certain disease states such as renal disease result in potassium wasting. Intracellular shifts occur in alkalosis and refeeding syndrome, as potassium moves from the extracel-lular space to the intracellular space.

Hypokalemia

Symptoms IleusWeaknessArrhythmiasLethargyDehydration

CausesGastrointestinal losses – vomiting, diarrhea, nasogastric suctionUrinary losses – diuretics, mineralocorticoids, drugs, chronic renal diseaseSweatIntracellular shifts – alkalosis, refeeding syndrome


When cells have been destroyed (such as with trauma, surgery, etc.), potassium is lost as well. Symptoms of hypokalemia include altered smooth muscle function, ileus, weakness, lethargy, and dehydration (Randall, 1980).

Because ileus often precludes feeding through the gut of patients, it is important to note serum potassium levels when evaluating our patients. Once hypokalemia is cor-rected, the ileus may resolve, resulting in the ability to use the gut for nutrition. Cardiac arrhythmias can also occur from hypokalemia (Green and Cress, 1993). When nasogas-tric suction has been necessary, hypokalemic metabolic alkalosis may occur due to the losses of chloride, hydrogen ion, and potassium from the stomach (Randall, 1980). When potassium levels drop below 3.0 mEq/L, associated changes include the potential for in-crease in serum calcium levels and a high CO2 level. Glucose intolerance may also occur (Solomon and Kirby, 1990).

During repletion of nutrition deficiencies (or refeeding), potassium levels may fall if adequate potassium is not provided along with the other nutrients. As anabolism occurs and new cells are formed, potassium shifts from the serum into these cells. (McCormick, et al., 1985). The administration of dextrose and the subsequent increase in the release of insulin also causes a shift of potassium from the extracellular space to the intracellular space (Green and Cress, 1993). We’ll discuss refeeding syndrome further when we talk about phosphorus.

Repletion of potassium stores should be accomplished with administration of both potassium and chloride, especially when metabolic alkalosis has occurred.

Hyperkalemia is a potentially fatal condition which can lead to cardiac arrest. Other symptoms of elevated potassium levels are summarized below.

Hyperkalemia

CausesPotassium-sparing diureticsDehydrationDiabetic ketoacidosisRapid catabolism of proteinAcidosisPoor tissue perfusionRenal failure

SymptomsCardiac arrestWeaknessParesthesias


Causes of hyperkalemia include renal insufficiency, medications, (such as potas-sium-sparing diuretics like spironolactone), dehydration, diabetic ketoacidosis, severe infection or other instances when there is rapid catabolism of protein, and severe meta-bolic or respiratory acidosis and poor perfusion to tissues (Paskin, 1989).

Correction of the acidosis, reduction in the administration of potassium, and the ad-ministration of glucose intravenously (to shift the potassium into the cells) are all means by which hyperkalemia can be corrected. Kayexalate (a sodium-charged polystyrene sulfonate resin) can also be given to reduce potassium levels (Randall, 1980).

chloridEA deficiency in sodium usually results in a depletion of chloride. Losses of chloride

occur with nasogastric suction and vomiting; with diuretics; and in chronic renal disease and acute renal failure. With losses of chloride without adequate repletion, a metabolic alkalosis occurs. Hyperchloremia can occur with diabetes insipidus and brain stem in-jury and with excessive administration of chloride. Normal chloride levels are 95 to 107 mEq/L.

acid/basE balancELet’s take a moment here to review acid/base balance and the development of aci-

dosis and alkalosis. Acid/base balance is regulated through extracellular buffer systems, the kidneys, and the lungs. The kidney changes hydrogen ion excretion and bicarbon-ate reabsorption while the lungs change the rate and volume of ventilation (Whitmire, 1993b). In order to evaluate the presence of an acid-base disorder, we must have an understanding of normal electrolyte values and of normal blood gas values.

As part of metabolic monitoring, an understanding of acidosis and alkalosis is impor-tant, not so much as a part of the initial nutritional assessment of our patients, but more as a part of the ongoing reassessment that is necessary as we care for our patients and assure that we are feeding them correctly. This is helpful in nutrition support, especially TPN, and enables us to make suggestions regarding fluid and electrolyte therapy.

Hypochloremia/Hyperchloremia

Causes of Hypochloremia Nasogastric suctionVomitingDiuresisChronic renal diseaseAcute renal failure

Causes of HyperchloremiaDiabetes insipidusBrain stem injuryExcessive administration of chloride


There are four primary acid-base disturbances: metabolic acidosis, metabolic alkalo-sis, respiratory acidosis, and respiratory alkalosis.

What, exactly do we mean by acids and bases? Acids might include carbon dioxide (a volatile acid), which reacts with water to form H2CO3, which in turn dissociates to H+ ion and HCO3 (bicarbonate).

Other acids include sulfuric acid (from phospholipids, nucleic acids, phosphopro-teins and phosphoglycerides), and organic acids such as lactic acid. When referring to bases, we generally mean bicarbonate (HCO3).

mEtabolic acidosisMetabolic acidosis is characterized by an acid (or chloride) that is normal or in-

creased, with a decrease in base (or bicarbonate). The pH level of the blood falls, or become more acidic, thus the term acidosis. Normal pH level in the blood is 7.35 to 7.45 (Whitmire, 1993a). Potassium levels are increased because of a shift out of the intracel-lular fluid into the extracellular fluid to maintain appropriate osmotic pressures (Whit-mire, 1993b). The acidosis occurs due to hydrogen ion shifts from the extracellular fluid to the intracellular fluid.

Metabolic acidosis can occur with an increase in the production of acids in the body, such as in diabetic ketoacidosis; starvation; and hypermetabolism resulting from fever, sepsis, trauma, and surgery and with cellular hypoxia (i.e., lactic acidosis because of inadequate perfusion to tissues, pulmonary insufficiency, congestive heart failure, and shock) (Randall, 1980).

This type of acidosis can also be caused by a decrease in the excretion of hydrogen ion, as occurs in renal failure and decreased renal perfusion associated with shock, car-diac failure, and vascular disease.

Metabolic Acidosis

Characteristics Decreased bicarbonateNormal or increased chloride Decreased pHIncreased potassium

CausesDiabetic ketoacidosisStarvationHypermetabolismCellular hypoxiaRenal failureDecreased renal perfusionGastrointestinal losses of base – diarrhea, fistula, diuretics


Other causes of metabolic acidosis are a loss of base (or bicarbonate) through the gastrointestinal tract via diarrhea, fistulas, and diuretics, and with increased administra-tion of acid via parenteral or enteral routes (Randall, 1980; Whitmire, 1993a).

The body compensates for the metabolic acidosis via the lungs and the kidneys. The respiratory compensatory alkalosis occurs first and acts to increase ventilation to decrease plasma CO2 (pCO2) levels and increase pH levels. The kidneys follow by in-creasing ammonium ion production and conservation of bicarbonate (base) to bring the bicarbonate levels to near normal.

anion gaP

The determination of anion gap is useful when metabolic acidosis occurs. This de-termination allows us to better differentiate the cause of the acidosis and to provide the optimal treatment.

Anion gap can be determined by using the formula: sodium - (bicarbonate [HCO3] + chloride [Cl]), with normal range being eight to 16 mEq/L (McCormick, et al., 1985; Whitmire, 1993a).

An elevated anion gap (>16) can occur with diabetic ketoacidosis; lactic acidosis; ingestion of methanol, ethylene glycol (antifreeze), ethanol, or salicylates; dehydration; and with a decrease in unmeasured cations, as occurs with decreased levels of potas-sium, calcium, and magnesium (Randall, 1980; Whitmire, 1993a). This type of metabolic acidosis is also referred to as normochloremic metabolic acidosis. A decrease in anion gap to below normal levels can occur with hypoalbuminemia; elevated potassium, mag-nesium, and calcium; overhydration; and hyperlipidemia (Randall, 1980).

As dietitians, we need to recognize anion gaps in order to be able to assist in ade-quately correcting the problem. Generally, acid/base balance and anion gap calculations are most useful to dietitians who have an ability to impact the electrolytes the patient is receiving, such as patients on TPN.

Anion Gap

Increased anion gapLactic acidosisDehydrationIngestion of methanol,

ethanol, ethylene glycol, salicylates

Na – (HCO3 + Cl) Normal range 8-16 mEq/L

Decreased anion gapHypoalbuminemiaElevated potassium, magnesium,

and calciumOverhydrationHyperlipidemia


Hyperchloremic metabolic acidosis is a non-anion gap acidosis and occurs when the anion gap is less than 16 and is caused by a lower level of bicarbonate with an in-crease of chloride. Causes of this form of metabolic acidosis are shown below (Whitmire, 1993b). Clinical symptoms of metabolic acidosis include headache, nausea, vomiting, diarrhea, and convulsions (Green and Cress, 1993).

Treatment of metabolic acidosis should first focus on the cause of the acidosis. When chloride levels are elevated, chloride administration can be lowered. With normo-chloremic metabolic acidosis, acetate (a base) can be administered to replace bicarbonate losses, taking care to not overcorrect the problem. As the acidosis resolves, potassium will be shifted back into the cell; therefore, care should be taken to monitor potassium levels and correct accordingly (Whitmire, 1993a).

mEtabolic alkalosisMetabolic alkalosis is characterized by low or normal serum chloride levels with el-

evated bicarbonate levels and decreased potassium levels (due to the shift of potassium into the cell). Blood pH is elevated. It occurs when there are increased losses of chloride, which occurs with nasogastric suctioning without adequate replacement of chloride, with vomiting and with fistula drainage.

Metabolic alkalosis also occurs with administration of bicarbonate through antac-ids, blood transfusions (buffered with citrate), and Ringer’s lactate (during resuscita-tion). Significant losses of potassium can cause metabolic alkalosis. This can occur with potassium-wasting diuretics, gastrointestinal losses, inadequate potassium intake and renal tubular disease where potassium is wasted.

This type of alkalosis occurs when the potassium level falls below 2 mEq/L. Alkalo-sis also occurs with overaggressive diuresis resulting in increased reabsorption of water and sodium; bicarbonate is reabsorbed along with the sodium.

Hyperchloremic Metabolic Acidosis

Fistulas Ostomy Excessive administration of chloride Diarrhea Renal tubular acidosis


The compensation by the body for metabolic alkalosis is through the lungs primar-ily; secondarily through the kidneys. The lungs reduce ventilation by slowing breath-ing and increasing pCO2 (a volatile acid) levels, thus lowering pH. Renal compensation follows with increased excretion of bicarbonate. Adequate electrolytes and water are necessary to prevent dehydration. (Randall, 1980; Whitmire, 1993a).

As with metabolic acidosis, treatment of metabolic alkalosis begins with treating the cause of the alkalosis. Alkalosis which has occurred because of nasogastric suction or diuretics can be treated with slow administration of chloride. When alkalosis has oc-curred because of both potassium and chloride loss, both potassium and chloride should be replaced.

rEsPiratory acidosis/alkalosisRespiratory acidosis is characterized by a fall in pH and an increase in pCO2 and

serum potassium levels.Causes of respiratory acidosis include retention of carbon dioxide because of chron-

ic obstructive pulmonary disease (COPD) or chronic obstructive airway disease (COAD), ARDS (adult respiratory distress syndrome), pneumothorax, pleural effusion, atelectasis, sleep apnea, asthma, inadequate mechanical ventilation, or anything that would cause hypoventilation (Randall, 1980; Whitmire, 1993b).

The body compensates for the respiratory acidosis through the kidneys with in-creased reabsorption of sodium and bicarbonate and increased excretion of chloride and hydrogen ion (Randall, 1980). This compensation, a metabolic alkalosis, results in a rise in bicarbonate levels.

As with the other acid-base disorders, treatment of respiratory acidosis is through addressing and treatment of the primary problem. Since metabolic alkalosis may become evident as a compensatory mechanism, care should be taken to correctly identify the primary acid-base disorder.

Metabolic Alkalosis

Characteristics Decreased or normal chlo-rideIncreased bicarbonateDecreased potassiumIncreased pH

CausesNasogastric suction, vomitingFistulaIncreased bicarbonate intake: antacids, blood transfusions, Ringer’s lactateSevere hypokalemiaOveraggressive diuresis


Since CO2 levels can be increased with overfeeding of calories, especially carbohy-drates (high CHO intake raises respiratory quotient and can cause CO2 retention), we should not overfeed patients with respiratory acidosis (Whitmire, 1993a) and should closely monitor patients with respiratory insufficiency when initiating feedings.

Respiratory alkalosis is characterized by an increase in pH and a decrease in pCO2 levels. This disorder is caused by increased ventilation and elimination of CO2. This can occur with apprehension and pain, sepsis, fever, head trauma, cerebral vascular acci-dents, mechanical hyperventilation, and salicylates.

Increased ventilation can also occur with pneumonia, hypoxemia, congestive heart failure, and pulmonary embolism. ARDS can also precipitate respiratory alkalosis because of the increased work of breathing caused by the hyperventilation. Compensa-tion for this type of alkalosis is via the kidneys with a metabolic acidosis. The kidneys increase excretion of bicarbonate, thus decreasing serum pH. Treatment of respiratory alkalosis should be directed at its primary cause.

Respiratory Alkalosis

Characteristics Increased pHDecreased pCO2

CausesIncreased ventilation related to:apprehension, pain, sepsis, fever, head trauma, CVA, salicylates, pneumonia, congestive heart failure, pulmonary edema, ARDS

Respiratory Acidosis

Characteristics Decreased pHIncreased pCO2

Increased potassium

CausesRetention of CO2 (COPD, COAD)Adult Respiratory Distress Syn-drome (ARDS)PneumothoraxPleural effusion AtelectasisSleep apneaAsthmaInadequate mechanical ventilation


To summarize, acid-base balance is achieved through the extracellular buffer sys-tem, the kidneys, and the lungs. Assessment of serum chloride, bicarbonate, and potas-sium, and pH and pCO2 obtained through blood gasses is necessary to determine the presence of any type of acid-base disorder.

Metabolic acidosis is characterized by low bicarbonate levels and increased potas-sium levels. The body compensates with a respiratory alkalosis by increasing ventilation, decreasing pCO2, and raising pH. Metabolic alkalosis is revealed by increased bicarbon-ate levels and decreased potassium and the body compensates with respiratory acidosis. The lungs reduce ventilation to increase pCO2 and lower pH.

Respiratory acidosis is characterized by a low pH and elevated pCO2 levels; the body compensates with metabolic alkalosis. Bicarbonate is reabsorbed more readily by the kidneys, thus increasing pH. Respiratory alkalosis has increased pH and decreased pCO2 levels; the body compensates with a metabolic acidosis, where the kidneys excrete more bicarbonate, lowering the pH toward normal.

calciumTrue calcium deficiencies are rarely seen (McCormick, et al., 1985). In fact, 99 per-

cent of calcium is stored in the bones and teeth. However, low serum levels of calcium can and do occur. Normal serum calcium levels range from 8.5 to 11.0 mg/dl (Grant and DeHoog, 1985).

Causes of hypocalcemia include vitamin D deficiency, hypoparathyroidism (be-cause of decreased resorption of calcium from the bones), renal tubular acidosis and nephrotic syndrome (because of increased excretion in the urine), malabsorption, and hypoalbuminemia (because calcium is carried bound to albumin), hypomagnesemia (because of the role magnesium plays in mineral homeostasis), and hyperphosphatemia (because of the calcium:phosphorus balance – usually 2:1).

Symptoms of hypocalcemia include irritability, confusion, tetany, seizures, conges-tive heart failure, and diarrhea. Calcium is found in the blood in two states — bound and ionized; when albumin and serum protein levels are decreased, the proportion of ionized calcium (the physiologically active form) increases.

Compensatory Mechanisms

Metabolic acidosis Respiratory alkalosis

Metabolic alkalosis Respiratory acidosis

Respiratory acidosis Metabolic alkalosis

Respiratory alkalosis Metabolic acidosis


Therefore, if you have a low serum albumin level and a low serum calcium level, the physiologically active calcium is neither bound nor measured, and will, in all prob-ability, be higher than the serum calcium level.

A better measurement of calcium in this circumstance is an ionized calcium. The following formula may also be utilized to give you a rough estimate of actual calcium levels, but may not be entirely accurate (Hopkins, 1993):

Adjusted calcium = [4 - Alb(gm/dl) x .8] + Ca(mg/dl)For example: If Alb is 2.0 and Ca is 7.9, then Adjusted calcium = [(4 - 2) x .8] + 7.9 = 1.6 + 7.9 = 9.5

Hypocalcemia can also result in osteomalacia in adults or rickets in children and can be treated with vitamin D and phosphate. Other forms of hypocalcemia should be treated with adequate calcium intake and correction of any magnesium deficiency. The new guidelines for adequate calcium intake appear below. Adults over 50, who often suffer bone loss due to aging, need 1200 mg/day.

Adequate Calcium Intake Guidelines

Lifestage Group New Calcium Goal (mg/day) 1-3 years 500 4-8 years 800 9-18 years 1300 19-50 years 1000 51+ years 1200 Pregnant or lactating ≤ 18 years 1300 19-50 years 1000

Hypocalcemia

CausesVitamin D deficiency HypoalbuminemiaHypoparathyroidism HypomagnesemiaRenal tubular acidosis HyperphosphatemiaNephrotic syndrome

SymptomsIrritability Congestive heart failureConfusion DiarrheaTetany


Hypercalcemia can be caused by neoplasm, renal insufficiency, excessive vitamin D, hyperthyroidism and calcium administration, prolonged immobilization and stress (resulting in bone resorption), and hyperparathyroidism. Symptoms include confusion, lethargy, anorexia, pancreatitis, nausea, hypophosphatemia, kidney stones, and constipa-tion. Treatment is attempted with restriction of calcium intake and rehydration, depend-ing upon the cause. In certain cases this is ineffective (as with neoplasms).

PhosPhorusWhereas potassium is the primary intracellular cation, phosphorus is the primary

intracellular anion. Phosphorus is of vital importance in the anabolism process and the creation of new cells. Phosphorus is necessary for many functions in the body; these include formation of high-energy phosphate bonds, erythrocyte formation, and the me-tabolism of carbohydrate, protein, and fat.

The RDA for phosphorus is 800 to 1200 mg/day. A normal level in the serum for adults is 2.0 to 4.5 mg/dl.

Hypophosphatemia can occur with diminished dietary intake or decreased absorp-tion, increased excretion (as in some renal disease), with the use of phosphate binders, in diabetic ketoacidosis, with alcoholism, in hyperventilation and respiratory alkalosis, and with inadequate supplementation during anabolism and refeeding.

Hypercalcemia

CausesNeoplasmRenal insufficiencyIncreased administration of vitamin D and calciumImmobilizationStressHyperparathyroidism

SymptomsConfusionLethargyAnorexiaPancreatitisKidney stonesConstipationHypophosphatemia


rEfEEding syndromEWhen a patient is starved, he loses lean body mass, water, and minerals. When we

begin to refeed these patients, especially with dextrose or other carbohydrate calories, the release of insulin is initiated. These circumstances stimulate the uptake of glucose, phosphorus, water, and other nutrients into the cells. This, accompanied by depletion of phosphorus during starvation, can result in severe extracellular hypophosphatemia. (Solomon and Kirby, 1990).

We recall from our biochemistry classes that phosphorus is a vital part of the pro-cess of anabolism and of carbohydrate metabolism. The depletion of phosphorus associ-ated with refeeding, anabolism, and increased metabolism can result in many serious complications.

These complications include cardiac (arrhythmia, congestive heart failure), neuro-muscular (paralysis, confusion, coma, lethargy, paresthesias, rhabdomyolysis, seizures), hematologic (anemia, thrombocytopenia, decreased platelet function), and respiratory (acute ventilatory failure) (Solomon and Kirby, 1990).

Refeeding Syndrome

Risk Factors:MalnutritionAlcoholismChronic weight lossHyperglycemiaAnorexia nervosaStress, inadequate feeding

Hypophosphatemia

Causes Decreased intake or absorptionIncreased excretionPhosphate bindersDiabetic ketoacidosisAlcohol abuseRefeeding syndrome


Several researchers have concluded that patients at greatest risk for hypophospha-temia with refeeding are those “with alcoholism, chronic weight loss, and hyperglyce-mia,” as well as those patients who are not fed seven to 10 days when under stress and those with anorexia nervosa. Care should be taken to monitor phosphorus levels before and during refeeding. Phosphorus should be supplemented as needed to correct defi-ciencies (Solomon and Kirby, 1990).

We’ve already discussed potassium and refeeding, but, as a review, starvation causes depletion of body potassium and magnesium. As refeeding occurs, potassium is shifted into the newly formed cells (anabolism) so blood levels fall. Supplementation to correct this depletion should follow. Other nutrients that are impacted by refeeding the malnourished patient are magnesium and thiamin. Since magnesium is found intracellu-larly and is a vital part of enzyme systems used in metabolism, serum magnesium levels also fall during refeeding. Magnesium levels should be monitored and supplementation ordered with low levels.

Since thiamin is important in carbohydrate metabolism and deficiency may exist in starved — especially alcoholic starved — individuals, Solomon and Kirby postulate that thiamin deficiency may be contributory in refeeding syndrome. It makes sense to pro-vide adequate thiamin, and possibly to supplement additional thiamin, in the starved patient who is being refed.

To avoid refeeding syndrome, we should monitor and correct abnormal levels of minerals, especially phosphorus, potassium, and magnesium. Delivery of nutrition support should be started slowly and increased gradually. Patients should never be overfed.

Hyperphosphatemia is usually associated with renal insufficiency, but can be found with excessive supplementation of phosphorus. Symptoms include listlessness, confu-sion, hypertension, and cardiac arrhythmias. Treatment is to reduce supplementation or treat the underlying renal disease.

Hyperphosphatemia

CausesRenal insufficiencyExcessive administration

SymptomsListlessnessConfusionHypertensionArrhythmias


magnEsiumAs we stated earlier, magnesium is primarily found intracellularly. We know that

magnesium plays a vital role in protein and carbohydrate metabolism and is necessary for normal metabolism of calcium and potassium. Recommended daily intake is 280 to 350 mg/day.

Hypomagnesemia can occur with losses through the gastrointestinal tract (vom-iting, diarrhea, fistulas) inadequate intake, losses through the urine (with diuretics, diabetic ketoacidosis) with alcoholism and acute renal failure, and with administration of drugs such as amphotericin B and cisplatin, and during refeeding with inadequate supplementation of magnesium (McCormick, et al., 1985; Green and Cress, 1993).

Hypermagnesemia

CausesRenal insufficiencyExcessive administration

SymptomsLethargyHypotensionCardiac arrhythmias Cardiac arrestRespiratory depression

CausesGastrointestinal losses – vomiting, diarrhea, fistulaInadequate intakeUrinary losses – diuretics, diabetic ketoacidosis AlcoholismAcute renal failureDrugsRefeeding syndrome

Laboratory FindingsAnorexiaParesthesiasCardiac arrhythmiasHypokalemiaHypocalcemia

Hypomagnesemia


Deficiency symptoms and laboratory findings include anorexia, paresthesia, trem-ors, confusion, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. Treat-ment of hypomagnesemia is accomplished with appropriate supplementation.

Hypermagnesemia (greater than 3 mEq/L) occurs with renal insufficiency and oversupplementation of magnesium. Symptoms of hypermagnesemia include lethargy, hypotension, cardiac arrhythmias and, possibly, cardiac arrest, and respiratory depres-sion. Treatment is accomplished by reducing magnesium supplementation, taking care to check for magnesium-containing antacids.

While monitoring of electrolytes (sodium, potassium, calcium, phosphorus, and magnesium) may not tell us much about the nutritional status of our patients, it can help us to optimize their nutritional care. Monitoring can also tell us about medical condi-tions that may lead to nutritional depletion so we can get a head start on preventing or treating these nutritional deficiencies.

casE studyLS is a 55-year-old male who is admitted to the ICU following surgery to repair his

ruptured abdominal aortic aneurysm. He is 5’9" and weighs 130 lb. You learn from his son that he typically drinks at least a six-pack of beer a day and has had erratic eating habits before admission. You note that he has an ileus and has been noted to have occa-sional arrhythmias.

He’s being fed with a standard TPN formula through a central line. His needs of 1500 to 1800 kcal/day and 60 to 90 gm protein/day are being met with the TPN. How-ever, you note that his labs have come back as follows:

Alb: 2.5 Ca: 6.5 Na: 120 K: 2.5 Phos: 1.7 Mg: 1.5

Let’s evaluate the problem with this patient. The sodium could be low because of the fluid resuscitation associated with his major surgery, or it could be related to exces-sive fluid provided by the TPN.

What about the albumin and calcium? We’ll discuss this further in the next chapter, but calcium is bound to albumin for transport, so it is affected by low serum albumin levels. An ionized calcium would likely show that calcium levels are, in fact, normal. Albumin is decreased with stress, surgery, overhydration, but a low serum level could also be caused by inadequate intake by the patient prior to admission (note his history of alcohol abuse, erratic intake, and below IBW).

Now, what about the low potassium, phosphorus, and magnesium levels? In this malnourished patient, these low levels are likely caused by refeeding syndrome and inadequate parenteral supplementation of potassium, phosphorus, and magnesium.


rEviEw quEstions1. Give three reasons why a sodium level on a patient might be 120 mEq/L.2. What electrolyte might become elevated if a hypertonic enteral formula is given with-

out adequate fluid?3. What can lead to losses of potassium from the body?4. What nutrients may become depleted in the extracellular fluid during refeeding?5. What changes occur with an anion gap metabolic acidosis? Why does this disorder

occur?6. How does the body compensate for respiratory acidosis?7. Your patient comes in with respiratory distress. He is 6' and weighs 168 lb and is 69

years of age. His albumin level is 2.4, serum glucose is 189, potassium is 3.0, cal-cium is 7.5. Is this a true hypocalcemia?

rEfErEncEsGrant A and DeHoog S: Nutritional Assessment and Support, 3rd ed. Grant and DeHoog pub., Seattle,

WA, 1985.Green K and Cress MJ: Metabolic complications of parenteral nutrition. Supp Line XV:1:5-9, 1993.Hopkins B: Assessment of nutritional status in: Nutrition Support Dietetics, 2nd ed. Gottschlich MM,

Matarese LE, and Shronts EP, eds. Silver Spring, MD: ASPEN, 1993.McCormick DC, Knutsen CV, Griffin RE, et al.: Pharmaceutical aspects of parenteral nutrition. In: Hy-

peralimentation: A Guide for Clinicians. Kaminski MV, ed. New York: Marcel Dekker, Inc., 1985.Paskin DL: Fluid, electrolyte, and acid-base balance. In: Dietitian’s Handbook of Enteral and Parenteral

Nutrition. Skipper A, ed. Rockville, MD: Aspen Publ., 1989. Randall HT: Water, electrolytes, and acid-base balance. In: Modern Nutrition in Health and Disease.

Goodhart RS and Shils ME, eds. Philadelphia: Lea & Febiger, 1980.Solomon SM and Kirby DF: The refeeding syndrome: a review. JPEN 14:1:90-97, 1990.Watkin DM: Nutrition for the aging and the aged. In: Modern Nutrition in Health and Disease. Good-

hart RS and Shils ME, eds. Philadelphia: Lea & Febiger, 1980.Whitmire SJ: Acid-base balance revisited: application to formulation of TPN recommendations. Supp

Line XV:1:5-9, 1993a.Whitmire SJ: Acid/base balance and fluid-electrolyte balance. ASPEN 17th Clinical Congress (program

manual 365-369), 1993b.


Chapter Five:Nutritional Assessment

through Laboratory Values

In addition to the evaluation of serum electrolytes, the evaluation of other labora-tory values can provide valuable information on the nutritional status of the patient and whether the nutritional care and support you are providing is adequate. In this chapter, we will look at laboratory values that can give you an indication of the patient’s protein status, immune function, and general health.

Creatinine-height index (Chi)Creatinine-height index (CHI) is used to determine body composition. Creatinine

is a by-product of the metabolism of creatine; creatine is mainly found in the muscles of the body. Measurement of urinary creatinine can indirectly reflect lean body mass. The ratio of urinary creatinine to expected creatinine excretion (based on sex and height of the patient) is used to assess the degree of muscle depletion.

Values of expected creatinine excretion are: for women — 18 mg creatinine/kg IBW and for men — 23 mg creatinine/kg IBW (Grant, 1986). Expected creatinine excretion lev-els are given in Appendix #12. A value of 60 to 80 percent of expected excretion suggests moderate protein depletion, while <60 percent suggests severe protein depletion.

Because of the many limitations in determining CHI, many authors suggest that it should not be utilized as a measurement of nutritional status. Twenty-four hour urine collections are difficult to obtain accurately. Standards for CHI were based on young healthy men and women and creatinine excretion decreases with age. Standard CHI val-ues are based on medium frame only. Creatinine excretion may be influenced by dietary intake. Therefore, I do not recommend the use of CHI in assessment of protein status.

Next, we’ll look at some indicators of protein status.


Urinary Urea nitrogen (UUn)During stress, protein metabolism is altered and the body becomes hypermetabolic.

Amino acids are shunted toward formation of acute phase proteins and this, along with the physiologic response to stress, can lead to a loss of nitrogen, primarily in the urine. Nitrogen balance can be utilized as a measure of the amount of stress the patient is under (for instance, a multiple trauma patient usually has a very high nitrogen output), and can be used to assess the adequacy of nutrition support (Candio, Hoffman, and Lucke, 1991).

Simply put, nitrogen balance is a measure of the difference between nitrogen intake and nitrogen excreted. A positive nitrogen balance indicates anabolism, while a negative nitrogen balance suggests catabolism (Grant, 1986; Candio, Hoffman, and Lucke, 1991; Konstantinides, et al., 1991). Nitrogen intake is determined by calculating the amount of protein ingested parenterally, enterally, or orally. This amount of protein is then divided by 6.25 gm nitrogen to determine nitrogen intake orally or enterally; parenteral protein intake is divided by 6.06 gm nitrogen because of the different nitrogen contents of vari-ous parenteral amino acids (Compher, 1993).

Creatinine-height Index % Cr excretion = Actual 24 hr Cr excretion Expected 24 hr Cr excretion Expected 24 hr Cr excr for women = 18 mg/kg IBW Expected 24 hr Cr excr for men = 23 mg/kg IBW

% CHI = Actual 24 hr Cr excretion Expected 24 hr Cr excretion Normal =100% 60-80% = moderate depletion < 60% = severe depletion

X 100

X 100

Nitrogen Balance

Nitrogen balance = protein intake (gm) – (UUN X 1.2) + 2 to 4 6.25*

>0 = anabolism (goal of +2 to +4) <0 = catabolism

*use 6.06 if patient is fed via TPN


The determination of the amount of nitrogen excreted is a more cumbersome proce-dure. A urine collection is necessary; traditionally, this collection has been for 24 hours. Because a 24-hour collection is inconvenient and potentially inaccurate, some authors have suggested that shorter collection times may reveal better and more accurate results (Candio, Hoffman, and Lucke, 1991). They found that a 12-hour urine collection was a satisfactory estimate of a 24-hour collection when the 12-hour urinary urea nitrogen level is doubled.

This determination came with the additional recommendations of a urine collection from noon to midnight, a constant infusion of parenteral nutrition, and that the patient be NPO without enteral feedings. For other enterally or orally fed patients, a 24-hour urine collection is necessary (Candio, Hoffman, and Lucke, 1991).

Urinary urea nitrogen (UUN) represents 80 to 90 percent of total urinary nitrogen. Thus, a correction of the UUN by increasing it by 20 percent is necessary to account for nonurea urinary nitrogen losses (Konstantinides, et al., 1991; Freed, 1985). Insensible losses from the skin, breath, and stool account for an additional 2 to 4 gm of nitrogen; this must be factored in to the equation when determining nitrogen balance.

However, in the hospitalized patient under stress or with disease, the 20 percent correction for UUN is not accurate. This discrepancy may be caused by altered liver function with stress or by the stress response where the body attempts to conserve lean body mass (Konstantinides, et al., 1991). We should consider the UUN as an estimate of nitrogen lost in the urine, rather as an absolute number. UUN is not valid in renal insuf-ficiency.

Urinary nitrogen appearanCe (Una)In the patient with altered renal function or on dialysis, we must adjust nitrogen

balance by looking at the changes in blood urea nitrogen (BUN). Measurements of weight and BUN are done over one to three days and during interdialytic intervals (Hopkins, 1993; Tayek, 1988). The formula to determine urinary nitrogen appearance (UNA) is:

(BUNf - BUNi) x 0.6BW + (BWf - BWi) x BUNfwhere i = initial, f = final, BUN = Blood Urea Nitrogen (gm/liter), and BW = body

weight (kilograms).

This figure is then added to the previously determined UUN.

To summarize, nitrogen balance can be determined with a 24-hour urine collec-tion (possibly, a 12-hour urine collection in carefully controlled situations) to determine UUN. UUN is then adjusted upward by 20 percent to account for nonurea urinary nitrogen losses. Nitrogen intake from various sources, including parenteral, enteral, and oral, is determined by dividing grams of protein by 6.25 for enteral and oral intake and by 6.06 for parenteral intake.


For the patient with renal insufficiency, a UNA is calculated and added to the UUN. Nitrogen balance is then determined by subtracting nitrogen out (adding 2 to 4 gm for insensible losses) from nitrogen in.

Results of nitrogen balance studies can be interpreted as follows: positive nitrogen balance indicates anabolism; generally a goal is set for a positive balance of 2 to 4 gm N/day. A negative balance indicates catabolism.

protein statUs indiCatorsThe assessment of visceral protein status can be accomplished through the evalu-

ation of serum protein values, including albumin, transferrin, thyroxine-binding preal-bumin, and retinol-binding protein. As we will see, some of these parameters are better assessment tools than others.

albUminSerum albumin comprises 50 percent of all serum proteins. However, its half-life

of 21 days makes it a less-than-optimal indicator of acute changes in nutritional status. (Half-life is the time required by the body to metabolize one-half the amount of the chemical or substance. In assessing a patient, always keep in mind the half-life in ad-dressing the adequacy of renourishing a patient.)

Albumin has many functions in the body. Plasma oncotic pressure is maintained by albumin. Albumin also acts as a transport mechanism for calcium, magnesium, zinc, bilirubin, fatty acids, enzymes, hormones, and drugs (i.e. anticoagulants and antibiotics).

Albumin is an important factor in wound healing because it transports amino acids and fatty acids necessary for healing to the wound, as well as allows for adequate on-cotic pressure for the delivery of nutrients to the wound site (Bozetti, 1987).

Albumin, because of its long half-life, is considered to be a poor marker of nutri-tional status, especially in the critically ill patient. It may be a better marker when used sequentially in the recovering patient or the outpatient receiving periodic and long-term assessments. However, serum albumin levels are considered a good marker for morbid-ity in hospitalized patients.

Protein Depletion

Albumin Transferrin Prealbumin Mild: 2 .8 to 3.5 gm/dL 150 to 200 mg/dL 10 to 15 mg/dLModerate: 2.1 to 2.7 gm/dL 100 to 150 mg/dL 5 to10 mg/dLSevere: < 2.1 gm/dL <100 mg/dL <5 mg/dL


Nutritional factors that can cause depleted albumin levels include inadequate protein intake, malnutrition, and malabsorption. Many non-nutritional factors can affect serum albumin levels; these include overhydration, which can occur in surgery, with re-suscitation, and with bedrest. Bedrest causes an increase in plasma volume; this increase is associated with an equal reduction in serum albumin levels (Tayek, 1988).

Nephrotic syndrome can result in excessive losses of protein; 72 percent of the protein lost in the urine is albumin (Bozzetti, 1987). Burns and other skin injuries can cause losses of albumin, since 20 percent of the body’s albumin is stored in the skin. Liver disease can inhibit albumin synthesis, with a resultant decrease in serum albu-min levels.

Other non-nutritional factors affecting albumin levels are: acute stress (because of the shift by the liver to making acute phase proteins instead of albumin), eclamp-sia, infection, and trauma. Normal serum values for albumin are 3.5 to 5.0 gm/100 ml; mild depletion is characterized as 2.8 to 3.5 gm/100 ml; moderate depletion as 2.1 to 2.7 gm/100 ml; and severe depletion as < 2.1 gm/100 ml.

Albumin synthesis can be stimulated by a reduction in oncotic pressure, with an-tibiotic treatment, with glucocorticoid therapy, and with amino acid administration. A serum albumin level greater than 5.0 gm/100 ml would indicate dehydration.

transferrinA somewhat better measurement of protein status is transferrin, which has a half-

life of eight to 10 days. Transferrin is more sensitive to changes in nutrition status. Trans-ferrin can be profoundly influenced by iron deficiency, since it is the transporter of iron in the blood.

Elevated levels of transferrin can occur with iron deficiency, pregnancy, dehydra-tion, and with chronic blood loss. Transferrin is depleted with liver disease, pernicious anemia, infection, uremia, nephrotic syndrome, iron overload, overhydration, and with inadequate protein intake (Hopkins, 1993; Grant and DeHoog, 1985).

Transferrin can be estimated by measuring total iron binding capacity (TIBC) levels in patients who are not obviously malnourished. While a constant and proportional

Non-nutritional Factors Affecting Albumin

Hydration status Nephrotic syndromeLiver diseaseAcute stressEclampsia

InfectionTraumaSurgeryBurns


relationship does exist between transferrin and TIBC, this relationship may vary from laboratory to laboratory.

The formula used to derive transferrin from TIBC should be standardized for each individual institution, based on actual measurement of transferrin and TIBC levels. Ex-amples of some practitioners’ formulas are:

Blackburn: Transferrin = (0.8 x TIBC) - 43 Heymsfield: Transferrin = (0.9 x TIBC) - 4.5 Grant: Transferrin = (0.87 x TIBC) + 10

Mild depletion is characterized by transferrin levels of 150 to 200 mg/dl; moderate depletion as 100 to 150 mg/dl; and severe depletion as <100 mg/dl. Transferrin appears to reflect changes in nitrogen balance and can be used as an assessment of nutritional status and of how effective nutritional support is.

thyroxine-binding prealbUminPrealbumin, with its shorter half-life of two to three days, appears to be a more

accurate marker of acute changes in nutritional status and of response to nutritional support (Tuten, et al., 1985). Prealbumin (also known as transthyretin) acts to serve as a transport for thyroxine and for retinol-binding protein. Synthesis of prealbumin is im-pacted by changes of response to nutrition therapy (Ingenbleek and Young, 1994; Smith, et al., 1975; Shetty, et al., 1979).

Factors Affecting Transferrin

Iron deficiency PregnancyIron deficiencyBlood lossInfection

Liver diseaseUremiaNephrotic syndromeIncreased iron storesHydration status

Non-nutritional Factors Affecting Prealbumin

Renal diseaseLiver disease

StressSurgeryInfection Dialysis


Prealbumin levels can be decreased with malnutrition, inadequate protein intake, acute stress states, surgery, renal disease with dialysis, liver disease, and infection. Lev-els can be increased with renal disease without dialysis.

Normal prealbumin levels are 15.7 to 29.6 mg/dl. Mild depletion is characterized as 10 to 15 mg/dl; moderate as 5 to 10 mg/dl; and severe depletion as <5 mg/dl. Because of its short half-life and relatively inexpensive cost, prealbumin is considered a good marker of nutritional status.

However, Fletcher, et al., found good correlation between transferrin and pre-albu-min and recommend routine transferrin levels as opposed to routine prealbumin levels (Fletcher, Little, and Guest, 1987).

Tests for albumin, transferrin and prealbumin, while not always readily available, are not cost prohibitive. It may be difficult to persuade a facility to purchase the equip-ment necessary to perform prealbumin testing. You might be able to make a good case by studying the impact of appropriate nutrition support on patient length of stay in the ICU and/or hospital and show how the test may save money by decreasing length of stay.

However, if the only test you have available is serum albumin, you can monitor your patient’s nutrition progress with nitrogen balance studies.

retinol-binding proteinRetinol-binding protein’s short half-life of only 12 hours makes it a highly sensitive

indicator of acute changes in protein status. Retinol-binding protein forms a complex with prealbumin and responds to nutritional changes much the same as prealbumin. It can’t be used as an assessment tool in renal failure because it is filtered through and metabolized by the kidney (Hopkins, 1989).

Normal levels are 2.6 to 7.6 mg/dl. Diminished levels of retinol-binding protein can be found in liver disease (hepatitis, cirrhosis), stress, surgery, with vitamin A deficiency, and with chronic illness. Retinol-binding protein is not commonly used as an assessment tool outside of teaching institutions and research facilities at the present time and is cost prohibitive for most institutions.

immUne statUs indiCatorsMalnutrition can have a profound effect on a person’s immune status. With protein-

calorie malnutrition, the immune system is unable to resist infection. The lymph system, comprised primarily of the thymus, bone marrow, lymph ves-

sels and nodes, spleen, tonsils, appendix, and Peyer’s patches, becomes unable to per-form its normal functions during malnutrition (Kline, 2002).

T cells mature in the thymus gland and are developed, along with B cells in the bone marrow. The bone marrow also produces macrophages. The other lymph organs store the T cells and B cells for use as needed during an infection. During malnutri-tion, T cell function is markedly diminished, while B cell and macrophage functions are


decreased as well (Chandra, 1988). Lymphocytes are unable to differentiate and mature and the total number of T cells is decreased.

Gamma globulin production decreases, sometimes significantly; complement levels are also depressed. Complement is defined as a series of serum proteins activated by the antigen-antibody complex in a sequential cascade, which ultimately leads to destruction of the antigen-antibody complex (Shronts, 1993).

Macrophages and neutrophils are less able to kill invading antigens. The mac-rophages are unable to function effectively and, as a result, antibodies are less able to recognize antigens. The altered macrophage functions, along with the decrease in T cells and T helper cells, are manifested clinically by a decrease in the delayed hyper-sensitivity reaction.

Delayed hypersensitivity skin tests can also be decreased with deficiencies of zinc, iron, pyridoxine, pantothenic acid, folate, vitamin B12, vitamin A, vitamin C, and thiamin (Chandra, 1988).

In a delayed hypersensitivity skin test, the patient is injected with test extracts, con-taining Candida, purified protein derivative (PPD), trichophyton and mumps antigens. A healthy immune system would respond to the antigen and produce a localized reac-tion (induration) around the injection site within one to two days.

Anergy is defined as a lack of any immune response; relative anergy occurs with only one positive response to the antigen. A person is considered reactive if a reaction

Alterations of Immunity in PCM

Humoral Immunity• B cell count may be normal• Antibody count may be normal or increased• Serum Ig A normal• Secretory Ig A decreased• Antigen-antibody affinity decreased

Other Changes• Abnormal antigen processing by macrophages• Bactericidal activity decreased• Decreased lysozyme production• Decreased production of complement

General Changes• Increased rate of infection• Increased morbidity & mortality• Organs atrophied• Decrease in thymus-produced hormones• Decreased cytokine production (lymphokines & monokines)

Cell Mediated Immunity• Delayed hypersensitivity• Decreased T cell counts • Decreased proliferation of lymphocytes• Decreased chemotaxis of cells• Decreased phagocytosis


occurs to at least two antigens. The usefulness of delayed hypersensitivity skin testing in nutritional assessment is limited because of the lack of uniformity in testing, age, and the effects of disease on immune status, i.e., cancer, immunosuppressive diseases, liver disease, and renal failure (Dominioni and Dionigi, 1987).

As stated earlier, T cells and B cells (lymphocytes) are depleted with alterations in immune status associated with malnutrition. One of the most reliable immunologic mea-surements of nutritional status is the blood lymphocyte count (Dominioni and Dionigi, 1987). Total lymphocyte count can be determined by the percent of lymphocytes and the white blood cell count, shown below (Cerra, 1984):

TLC levels can also be decreased with cancer, surgery, with steroid and immuno-suppressive therapy, and with inherited and acquired immune deficiency states. TLC levels may be elevated with infection (i.e., tuberculosis, measles, chicken pox, mononu-cleosis), multiple myeloma and leukemia.

other laboratory valUes

blood Urea nitrogen (bUn)Blood urea nitrogen (BUN) levels are not often used alone as an indicator of nutri-

tional status. However, you should be familiar with the factors that can cause changes in the BUN level. Of course, we all know that BUN becomes elevated in renal insufficiency and renal disease.

Other factors that can cause an elevated BUN include protein catabolism, as associ-ated with starvation and stress, dehydration, and gastrointestinal bleeding. BUN levels may be depleted or decreased with liver failure, pregnancy, nephrotic syndrome, and with malabsorption. BUN levels may also rise in conjunction with delivery of high pro-tein intake parenterally, enterally, or orally. Normal BUN levels are 10 to 20 mg/dl.

CreatinineSerum creatinine levels are primarily a marker of renal function. Elevated levels

(normal is 0.7 to 1.5 mg/dl) are associated with renal insufficiency and with endocrine disorders such as gigantism and acromegaly.

Total Lymphocyte Count% lymphocytes

100 TLC = white blood count/mm3 X

1500 to 1800 = mild depletion900 to 1500 = moderate depletion < 900 = severe depletion


Cholesterol and triglyCeridesSerum cholesterol levels can drop in the malnourished or undernourished patient;

levels can also become depleted in end-stage liver disease. Elevated levels occur with lipid metabolism disorders and with excessive dietary intake and can be a risk factor for coronary artery disease and peripheral vascular disease.

Triglycerides can be elevated with poorly controlled diabetes mellitus, with various lipid metabolism disorders and with improper dietary intake (i.e., excessive intake of simple carbohydrates and alcohol) as well as with obesity. Triglycerides can also become elevated with the administration of intravenous lipids and can indicate an intolerance to fat or a familial hyperlipidemia. Extended periods of elevated triglyceride levels may lead to pancreatitis.

liver fUnCtion testsLiver function tests include alkaline phosphatase, the transaminases (SGOT and

SGPT), GGT, and bilirubin. Although elevated values usually indicate some sort of liver disease, the elevation can also be associated with nutrition support.

The administration of total parenteral nutrition (TPN) can cause intrahepatic cho-lestasis and fatty liver. The cause of cholestasis remains unclear but seems to be associat-ed with the administration of TPN and disuse of the gastrointestinal tract, with resultant impairment of bile flow from the gallbladder.

Cholestasis can also occur with overfeeding of calories, especially with the over-feeding of carbohydrate calories. Cholestasis is evidenced by an increase in serum alkaline phosphatase and in serum total bilirubin. To avoid the occurrence of cholestasis, we should not overfeed our patients, and should use the gastrointestinal tract whenever possible.

Fatty liver disease can occur with overfeeding of carbohydrate calories, overfeeding in general, and with deficiencies of carnitine and essential fatty acids. Fatty liver is di-agnosed with liver biopsy, but is suspected with elevated liver function tests within one to two weeks of initiation of parenteral nutrition therapy. An analogy for the develop-ment of fatty liver related to overfeeding is paté. Paté is derived from the livers of ducks which have been purposefully overfed. To avoid the development of fatty liver associ-ated with TPN, we should not overfeed, especially with carbohydrate calories.

We’ve seen that biochemical or laboratory assessment of nutritional status can be helpful. We’ve also seen that many of the parameters we utilize for nutritional assess-ment are potentially flawed because of the non-nutritional factors influencing them. With time and experience, along with the use of a physical and dietary assessment, subjective global assessment, and review of the medical history, you will be able to sort through all of the information available to effectively assess your patient’s nutritional status.


Case stUdyYour patient is an 80-year-old female who is admitted to the medical-surgical floor

after surgery to repair her fractured hip. She is 5’4" and weighs 90 lb with a small frame. You notice dryness and flakiness of her skin and there is obvious wasting of fat and muscle stores. She’s a little confused and states that she’s not hungry and would just like a little chicken noodle soup and crackers.

You note the following abnormal lab values: Alb 2.4; Transferrin 120; Prealbumin 8; TLC 1200. You decide that the patient is moderately protein depleted and is moderately calorically depleted as well, since she is at 83 percent of her ideal body weight.

Because her oral intake is inadequate, enteral feedings are initiated, but are not tol-erated as the patient has high gastric residuals and substantial diarrhea. Her physician is concerned about the possibility of aspiration because the patient is growing more and more confused and may be unable to protect her airway.

The decision is made to stop oral feedings and initiate TPN, which she tolerates at a volume which provides 2200 kcal and 60 gm protein. You calculate her needs to be 1300 to 1500 kcal and 45 to 60 gm protein/day and suggest that her caloric level be decreased. The physician, though, feels that the patient needs to gain weight and leaves the TPN at the current level.

Ten days later, you note that the lab values reflect that the liver function tests are elevated. You know that overfeeding, especially of carbohydrate calories, can cause cholestasis and elevated liver function tests. You also know that disuse of the gastroin-testinal tract can also cause cholestasis. You recommend that low volume enteral feed-ings or a restart of oral feedings be allowed and suggest, again, that the caloric level be decreased. The physician decides to cut the TPN in half and to restart the oral feedings.

The patient is less confused and manages to gradually increase her PO intake to about 800 kcal and 35 gm protein. The physician discontinues TPN and you continue to help the patient to increase her PO intake. Her albumin level has remained around 2.5, but you note improvement in transferrin and TLC levels. The liver function tests have progressively decreased as PO intake increased.

review qUestions1. Give reasons why you would or wouldn’t use CHI as an assessment tool.2. Your patient has a calorie count revealing intake of 950 calories and 20 gm protein. He

is also receiving a tube feeding that provides 1440 calories and 52 gm protein. UUN reveals a level of 9. What is N (nitrogen) in? What is N (nitrogen) out? What is the nitrogen balance?

3. Is albumin a good nutritional marker in the acutely ill hospitalized patient?4. Why would prealbumin be a better marker of nutritional status than transferrin and

albumin?5. Define anergy.6. What nutritional factors may contribute to cholestasis?


RefeRencesBozzetti F: Nutritional assessment from the perspective of a clinician. JPEN 11(5):115S-121S, 1987.Candio JA, Hoffman MJ, and Lucke JF: Estimation of nitrogen excretion based on abbreviated urinary

collections in patients on continuous parenteral nutrition. JPEN 15(2)148-151, 1991.Cerra FB: Pocket Manual of Surgical Nutrition. St. Louis: CV Mosby Co, 1984.Chandra RK: Immunity and Infection. In: Nutrition and Metabolism in Patient Care. Kinney JM,

Jeejeebhoy KN, Hill GL, and Owen OE, eds. Philadelphia: WB Saunders Co., 1988.Church JM and Hill GL: Assessing the efficacy of intravenous nutrition in general surgical patients: dy-

namic nutritional assessment with plasma proteins. JPEN 11(2):135-139, 1987.Compher C: Calorimetry, body composition, nitrogen balance, labs. Unpublished address at ASPEN

17th Clinical Congress, San Diego, 1993.Dominioni L and Dionigi R: Immunological function and nutritional assessment. JPEN 11(5):70S-72S,

1987.Fletcher JP, Little JM, and Guest PKL: A comparison of serum transferrin and serum prealbumin as

nutritional parameters. JPEN 11(2):144-147, 1987.Freed BA: Tools and techniques for the metabolic support nutritionist. In: Hyperalimentation: A Guide

for Clinicians. Kaminski MV, ed. New York: Marcel Dekker, Inc., 1985.Glassman RG: Nutrition assessment: a critical review. Topics in Clinical Nutrition 1:4:16-27, 1986.Grant A and DeHoog S: Nutritional Assessment and Support, 3rd ed. Grant and DeHoog publ., Seattle

WA, 1985.Grant JP: Nutritional assessment in clinical practice. Nutr in Clin Prac 1(1):3-11, 1986.Hopkins B: Assessment of nutritional status. In: Nutrition Support Dietetics. Shronts EP, ed. Silver

Spring, MD: ASPEN, 1993.Ingenbleek Y and Young V. Transthyretin (prealbumin) in health and disease: nutritional implications.

Ann Rev Nutr 14:495-533, 1994.Kline DA: Nutrition & Immunity: Part I: Immune Components and Nutrients, 5th ed. Ashland, OR:

Nutrition Dimension, 2002.Konstantinides FN, Konstantinides NN, Li JD, et al.: Urinary urea nitrogen: too insensitive for calculat-

ing nitrogen balance studies in surgical clinical nutrition. JPEN 15(2):189-193, 1991.Kopple JD: Uses and limitations of the balance technique. JPEN 11(5):79S-85S, 1987.Shetty PS, Jung RT, Watrasiewicz KE, et al.: Rapid-turnover transport proteins: an index of subclinical

protein-energy malnutrition. Lancet 10:230-232, 1979.Shronts EP: Overview of Immunology. Unpublished address to ASPEN 17th Clinical Congress, San

Diego, 1993.Smith FR, Suskine R, Thanangkul O, et al.: Plasma vitamin A, retinol-binding protein and prealbumin

concentrations in protein-calorie malnutrition, III: response to varying dietary treatments. Am J Clin Nutr 28:732-738, 1975.

Tayek JA: Albumin synthesis and nutritional assessment. Nutr Clin Prac 3(6):219-221, 1988.Tuten MB, Wogt S, Dasse F, et al.: Utilization of prealbumin as a nutritional parameter. JPEN 9:6:709-

711, 1985.


Chapter Six:Assessment of

Nutritional Requirements

Now that we have determined the nutritional status of our patients, what comes next? Knowing the nutritional status of the patient is all well and good, but if we do not adequately and appropriately nourish that patient, we will not help the patient to achieve or maintain improved nutritional status.

There are a number of different methods to determine caloric and protein require-ments; we will discuss some of these in this chapter. We will also discuss vitamin and mineral needs and the role they play in the patient’s recovery.

CaloriC requirementsA number of different methods can be utilized to determine caloric requirements.

These methods can include actual measurement of basal metabolism, measurements of gas exchanges to estimate resting energy expenditure, and the use of formulas to esti-mate basal energy expenditure (BEE) and resting energy expenditure (REE).

The actual measurement of basal expenditure with direct calorimetry is usually cost — and convenience — prohibitive and may be limited to the research setting. Indirect calorimetry, on the other hand, has been useful in the clinical setting in providing a measurement of caloric expenditure by measuring oxygen consumption, carbon dioxide production, and minute ventilation. The development of metabolic measurement carts has made indirect calorimetry much easier and quicker to perform.

Indirect calorimetry can be performed by one of two methods: the open-circuit method or the closed-circuit method. The open-circuit method, which is more accurate, allows the patient to breathe room air. With the open-circuit system, the actual volume of the gas expired is measured and the fractions that are oxygen and carbon dioxide are measured. From these numbers, oxygen consumption and carbon dioxide production


are calculated. Energy expenditure is then determined. The open-circuit system as-sumes that there is no oxygen or carbon dioxide pooling in the body and no other gasses pass across the lung membrane. The closed-circuit method, which is easier to perform, requires that the patient breathe from a controlled air system (Ireton-Jones, 1992). The controlled air system allows us to know volume and oxygen concentration.

How is oxygen consumption determined? Oxygen consumption is defined as the milliliters of oxygen utilized in one minute. The following formula is utilized to deter-mine oxygen (O2) consumption: O2 consumption = (volume inspired/minute X FIO2) - (volume expired X FEO2), where FIO2 is the fractional concentration of O2 in inspired gas and FEO2 is the fractional concentration of O2 in expired gas.

What about measurement of carbon dioxide (CO2) production? CO2 production is defined as the milliliters of CO2 produced in one minute and can be determined by the following equation: CO2 production = expired minute volume (FECO2 - FICO2), where FECO2 is the fractional concentration of CO2 in expired gas and FICO2 is the fractional concentration of CO2 in inspired gas.

Measurement of the oxygen consumption tells us about energy expenditure, while measuring both oxygen consumption and carbon dioxide production tells us what types of nutrients are being utilized for that energy.

Metabolic measurement carts measure oxygen consumption and carbon dioxide production. In preparation for the measurements using the metabolic cart, the patient should be kept at a “steady state.” A steady state has been described as keeping the patient NPO for greater than two hours (if TPN or enteral feedings are being utilized, infusion should be at a constant rate); the room must be quiet and thermoneutral; and there should be no use of skeletal muscles (Ireton-Jones, 1992; Compher, 1993).

Open-circuit systems are most commonly utilized. Because of the use of open-cir-cuit systems, some patients are not candidates for metabolic cart measurements. Patients who cannot remove their supplemental oxygen to breathe room air and those intubated patients who are on high pressure support or whose measured oxygen levels are low would not be candidates for metabolic cart measurements (Compher, 1993).

Continuous 24-hour metabolic monitors are also available and may reflect actual energy expenditure and respiratory quotient. No equations are necessary because the monitor reflects the actual requirements of the patient.

respiratory quotient (rq)Metabolic carts also have the capability to determine respiratory quotient (RQ). RQ

is important in the determination of whether the patient is being nourished with the ap-propriate mix of nutrients. RQ is defined as the ratio of carbon dioxide produced (VCO2) to the oxygen consumed (VO2). RQ can give an indication of the type of substrate (fat, protein, carbohydrate) being utilized for energy (Ireton-Jones, 1992).


Oxidation of specific substrates results in very specific RQ values, ranging from 0.7 to 1.0. Fat synthesis is thought to occur when RQ exceeds 1.0, but an RQ greater than 1.0 also occurs with excessive carbohydrate or total calorie intake (Ireton-Jones, 1992; Schwartz, 1993). Abnormally low RQ values can occur with inadequate nutri-ent intake or with inaccurate measurements of carbon dioxide production and oxygen consumption.

resting energy expenditureThe Weir equation, below, is used to determine resting energy expenditure (REE).

(Ireton-Jones, 1992; Compher, 1993): REE = 1.44 X [(3.9 x VO2) + (1.1 X CO2)] For repletion = 1.5 X REEFor maintenance = 1.3 X REE

Adjustment of the REE is made since the measurement was made at a steady state of rest. In addition, calories may be needed for repletion. The factor for repletion is 1.5 X REE and for maintenance is 1.3 X REE (Compher, 1993).

Comparison of REE to predicted basal energy expenditure can be done to give a reference point.

Many factors can influence metabolic rate. Situations that can increase metabolic rate include: activity, posturing (a phenomenon that occurs in brain injured patients and has to do with involuntary reflexing of extremities), hyperthermia, disease states, dialysis, hyperthyroidism, and surgery. Factors that can decrease metabolic rate include: muscle relaxants, sleeping, starvation, narcotics, hypothermia, and hypothyroidism. Metabolic monitoring is not appropriate for all patients, especially those with conditions that inhibit accurate gas measurement. Examples of conditions prohibiting metabolic monitoring include:

• those patients with chest tubes or tracheal cuffs with significant leaks• those patients receiving more than 80 percent oxygen• those patients undergoing dialysis

Respiratory Quotient

carbon dioxide production oxygen consumption

Oxidation of fat = 0.7 Oxidation of protein = 0.8 Oxidation of carbohydrate = 1.0 Mixed substrate = 0.85

RQ =


Since indirect calorimetry and metabolic measurement carts are not available at all institutions, other methods of estimating caloric requirements must be employed. These include: use of the Harris-Benedict equation; use of suggested calories per kilo-gram as specified for a given disease or stress state; and the use of other equations that are available. In 2002, a DRI for energy was established for the first time and is included in Appendix # 10. Note that the DRI is very general, not accounting for age and other individual variables.

Harris-BenediCt equationHarris and Benedict developed an equation in 1919 that allows us to estimate basal

energy expenditure, utilizing sex, weight, height, and age. The basic equation is shown below, with stress factors that are applied to the derived BEE to determine caloric needs. These factors allow us to take into account the increased demands placed on the patient by increased activity or stress.

An adaptation of the Harris-Benedict equation has been done by Carol Ireton-Jones. The equation may be more suitable for hospitalized patients as it takes into account the presence of trauma, burn, and whether or not the patient is intubated (Ireton-Jones, et al., 1992; Hopkins, 1993).

Caloric requirements can also be determined by using guidelines for kilocalories/kg body weight. Generally, I use actual weight, unless the patient’s weight is greater than 20 percent of ideal body weight. If the patient is obese, I use an adjusted body weight to take into consideration that lean body mass is less proportionate in the obese patient than the normal weight person and use ideal body weight if patient is obese. Utilize actual weight if the patient is underweight.

Harris-Benedict Equation

Males: 66.5 + [13.75 x weight(kg)] + [5 x height(cm)] – (6.76 x age) Females: 655 + [9.56 x weight(kg)] + [1.85 x height(cm)] – (4.68 x age)

Stress Factors* Starvation BEE Elective Surgery BEE X 1.3 Multiple Trauma** BEE X 1.3 – 1.5 Sepsis (early) BEE X 1.3 – 1.5 Sepsis (late)** BEE X 1.3 – 1.5

*Activity factors are included in these stress factors**These stress factors are lower than those commonly used, but reflect the latest recommendations.


To determine caloric requirements, the actual or adjusted body weight is then mul-tiplied by a stress factor. We once estimated these factors at higher levels, but have since found that we may have overestimated our patients’ nutrient requirements and that overfeeding can have deleterious effects.

In general, recommendations are: the non-stressed patient who is undernourished requires a level of 20 kcal/kg; while patients under stress due to surgery, sepsis, etc. require approximately 25 to 30 kcal/kg (Shronts and Lacy, 1993).

Another method of determining REE is through the use of the Fick method. This method utilizes cardiac output, hemoglobin levels, and arterial and mixed venous oxy-gen concentrations from a pulmonary artery catheter (Sawyer, et al., 1988; Williams and Fuenning, 1991; Smithies, et al., 1991; Cobean, et al., 1992; Brandi, et al., 1992; Kearney, et al., 1992; Mink, et al., 1995; Flancbaum, et al., 1999).

Energy Expenditures for Hospitalized Patients

EEE = 1784 – 11A + 5W + 244G + 239T + 804B (ventilator-dependent patients)

EEE = 629 – 11A + 25W – 609O(spontaneously breathing patients)

A: age in yearsW: weight in kgG: gender (male = 1, female = 0)V: ventilator support (present = 1, absent = 0)T: trauma (present = 1, absent = 0)B: burn (present = 1, absent = 0)O: obesity >30% above IBW (present = 1, absent = 0)

Fick EquationREE = CO x Hb (SaO2 - SvO2) 95.18

CO = cardiac output (L/min) Hb = hemoblobin level (mg/L) SaO2 = oxygen saturation of arterial blood SvO2 = oxygen saturation of mixed venous blood


Some studies suggest that there is a high correlation between the REE data obtained from the Fick equation with data determined with indirect calorimetry; other studies (Mink, et al., 1995; Flancbaum, et al., 1999) found poor correlation. The Fick equation may underestimate REE (Cobean, et al., 1992; Brandi, et al., 1992). The variables associated with use of the Fick equation may account for the variation between REE suggested by this equation and that determined by indirect calorimetry.

protein requirementsProtein requirements can be determined in a number of ways, as well. As we have

previously discussed, protein requirements can be determined through the use of nitro-gen balance studies, with urinary nitrogen appearance, and with urea kinetic modeling.

Protein requirements can also be determined by using a specific factor and mul-tiplying it by the patient’s weight or adjusted body weight in kilograms. The recom-mended daily allowance (RDA) for protein is 0.8 gm/kg. This requirement, of course, changes with specific disease states and stress states. We’ll discuss requirements in the next chapter when we discuss nutritional assessment in specific disease states.

In general, the patient who is starved but not stressed requires a protein intake of 1.0 gm protein/kg/day, while the patient who is highly stressed requires approximately 1.5 to 2.0 gm protein/kg/day (Shronts and Lacy, 1993).

Protein requirements can also be determined by figuring appropriate nonprotein-calorie to nitrogen ratios. Generally, for the nonstressed patient, the calorie to nitrogen ration should be 150:1. This figure changes with specific diseases (i.e., it will be higher with renal disease). Stressed patients require a calorie to nitrogen ratio of 80 to 100:1.5 (Shronts and Lacy, 1993).

We’ll discuss specific nutrient requirements (fat, protein, and carbohydrate) as they relate to specific diseases in the next chapter. The nonstressed patient should receive less than 30 percent calories from fat and should receive about 20 percent calories from protein, with the remainder of the caloric intake from carbohydrate.

Appendix #10 includes the DRI's for total fat, Ω-3 and Ω-6 fatty acids, fiber, carbo-hydrate and protein for healthy people (IOM, 2004).

Fluid requirementsFluid requirements are recommended at 20 to 40 ml/kg/day or 1 to 1.5 ml/kcal

consumed.

Vitamin-mineral requirementsWe’re all familiar with the recommended daily allowances (RDA) and Daily Refer-

ence Intakes (DRI) for vitamins and minerals. These levels are listed in Appendix #10 and are generally considered accurate and adequate for the general healthy population. However, in the clinical setting, vitamin deficiencies can and do occur. Requirements for vitamins and minerals change with stress and with certain diseases.


In this section, we’ll discuss requirements for vitamins and minerals, deficiency symptoms, their roles in wound healing, and vitamin toxicity symptoms. Appendix #11 summarizes the symptoms and causes of vitamin and mineral deficiencies.

True vitamin deficiencies do not often occur in the United States, except when there has been a history of inadequate intake and when the patient has been subjected to stressors that increase the need for certain nutrients. Let’s start with the fat-soluble vitamins, A, D, E, and K.

• Vitamin A, especially in the form of retinoids and beta carotene, has attracted a great deal of attention in the area of cancer prevention. We should be aware that some of our patients may overdo their supplementation, believing that “more is better.” Vitamin A can become toxic if supplemented in large amounts and when the storage capacity of the liver is exceeded. Vitamin A can also become toxic in patients with chronic renal failure.

Symptoms of Vitamin A toxicity include headache, dizziness, nausea, and vomit-ing. Chronic toxicity can be reflected as changes in the skin, skeletal system, and central nervous system (Hopkins, 1993; Rapp, 1993).

Vitamin A deficiency symptoms include vision changes, especially in regards to the ability to adapt to darkness. Vitamin A deficiency can also lead to male sterility and changes in cellular growth. Vitamin A levels can become deficient in those patients with malabsorption, especially of fat; with biliary insufficiency; and in those patients who in-crease their excretion of vitamin A, such as those with infections and cancer (Grant and DeHoog, 1985).

The RDA for vitamin A is 600 to 1300 mcg or RE (retinol equivalent)/day. Docu-mented deficiency states of vitamin A can be treated with 37,500 to 45,000 RE/day (Hop-kins, 1993). Deficiency can be documented with serum vitamin A levels, with retinol-binding protein levels, and with serum carotene levels (Hopkins, 1993; Olson, 1984).

Increased needs for vitamin A can occur with wound healing because of the role vitamin A plays in cellular growth and differentiation.

• Vitamin D has an established RDA of 5 to 15 mcg or 200 to 600 IU/day. Defi-ciencies can occur with fat malabsorption and when requirements are increased; as for example, in liver and renal disease (Grant and DeHoog, 1985). Deficiency symptoms in-clude skeletal changes, such as rickets, spine curvature, osteomalacia, and hypocalcemia (Hopkins, 1993; Grant and DeHoog, 1985; Miller and Norman, 1984).

If excessive vitamin D is administered, toxicity symptoms, such as hypercalcemia, bone and soft tissue calcification, anorexia, nausea, and polyuria may occur (Olson, 1984; Miller and Norman, 1984).

Vitamin D can be synthesized by the body if exposed to sunlight; this source of the vitamin should be considered when determining if any supplemental vitamin D should be given.

What’s interesting is that it has long been known that people living in northern climates have a higher incidence of cancer and chronic diseases, such as heart disease, hypertension, diabetes, multiple sclerosis and cancer. The winter sunlight is not strong


enough to produce vitamin D, so circulating levels of 25(OH)D3 are reduced. Unless the body has adequate stores, a deficiency occurs. Dietary sources of vitamin D are limited to cod liver oil, fatty fish and fortified foods such as milk, cereal and orange juice and do not contribute measurably to raising vitamin D levels (Heaney, 2003).

Heaney and colleagues (2003) conducted one of the first studies to measure the relationship of vitamin D intake to serum levels of 25(OH)D3. The results were astonish-ing, in that it took 3000 to 5000 IU/day of vitamin D to maintain normal serum levels of 25(OH)D3 in the range of 30 to 40 ng/ml (78 to 100 nMol/L) (Note: “ng” = nanograms). In the winter, approximately 80 percent of vitamin D needs were met from body stores. Consider that the DRI for vitamin D is 200 to 600 IU/day, depending upon age and gen-der, well below the amount needed to maintain serum levels. The upper tolerance level is 2000 IU/day (IOM, 1997), well below the amount needed by the study subjects .

Hollis (2004) is presently conducting a study supplementing lactating women with either 2000 or 4000 IU vitamin D/day. The preliminary data shows that circulating levels of 25(OH)D3 do increase in both the mother and the breastfed infant, without any harm.

The incidence of vitamin D deficiency is rising in the US, that includes infants who are solely breastfed, young adults and adults living in northern states, African Ameri-cans, and the elderly (Heaney, 2003; Hollis, 2004). Some studies estimate 30 to 42 percent of those in high risk groups can be deficient (Holick, 2004). As we age, the skin is less able to produce vitamin D, decreasing the amount of 25(OH)D3 in the blood.

Supplementing vitamin D in the winter may be necessary and even in the summer months, for those individuals who are not exposed to adequate sunlight.

It now appears that the DRI for vitamin D is inadequate for all population groups, including pregnant and lactating women, and is the vitamin most in need of reassessment in light of new research since the DRI was set (Heaney, 2003; Hollis 2004; Weaver, 2004).

• Vitamin E’s established RDA is 11 to 19 mg/day. Deficiency states can be deter-mined with erythrocyte hemolysis tests and measurement of serum tocopherol esters (Hopkins, 1993; Machlin, 1984). Vitamin E plays a role as a free radical scavenger and acts to prevent the production of peroxides in the body. Deficiency of vitamin E has been seen in premature and low-birth-weight infants and manifests itself as a hemolytic ane-mia. Deficiency in adults is not common, but could occur with fat malabsorption.

Vitamin E is generally considered nontoxic, but excessive doses of vitamin E can interfere with vitamin K functions and can lead to prolonged clotting times. Vitamin E has also been shown to play a beneficial role in wound healing, especially in the preven-tion of scarring.

• The RDA for vitamin K ranges from 60 to 120 mcg/day. Deficiency states rarely occur but can be caused by fat malabsorption, liver disease, and with drug therapy. Vitamin K deficiency could conceivably occur in the patient on TPN without supplemen-tation and whose gut is not functional (vitamin K is also synthesized by gut bacteria). Deficiency is manifested by increased clotting times, resulting in excessive bruising and bleeding.


• Vitamin C plays an important role in the formation of collagen, which is impor-tant in wound healing (Jaffe, 1984). It can also play a role in inhibiting free radical reac-tions. Vitamin C also acts to increase the levels of immunoglobulins and antibodies, as well as to increase the mobility of white blood cells in stimulating the immune system. Increased metabolism of vitamin C occurs with smoking, while stress (whether emotion-al or environmental) can lower serum vitamin C levels. Vitamin C also helps to regulate cholesterol metabolism (Gottschlich, 1989).

Deficiency of vitamin C is manifested as scurvy — a syndrome with symptoms of anemia, hemorrhagic disorders, gingivitis, weakness, and irritability. Depletion of vitamin C stores can occur with alcoholism, inadequate intake, stressed states, and with smoking. A rebound scurvy can occur in people who have taken megadoses of vitamin C and suddenly reduce their intake.

Large doses of vitamin C can cause diarrhea, nausea, and vomiting, and can in-terfere with glucosuria tests. The RDA for vitamin C is 45 to 120 mg/day, while the AMA recommends supplementation with as much as 100 mg/day in the patient who is stressed or receiving TPN.

• Thiamin (B1) is important in the metabolism of energy and carbohydrate and plays a role in nerve transmission (Gottschlich, 1989; Gubler, 1984). Deficiencies of thiamin are manifested by loss of appetite, neurological symptoms, and cardiac involve-ment. Deficiency is classified as beriberi and can be common in persons in the Orient or in immigrants from the Orient whose primary intake is unfortified rice. Thiamin defi-ciency also occurs in alcoholism, where the intake of “empty” calories does not often include thiamin.

Thiamin status can be assessed with measurement of erythrocyte transketolase activity. Toxicity is rarely seen. The RDA for thiamin is 1.0 to 1.4 mg/day.

• Riboflavin (B2) is important in metabolism as well. Deficiencies of vitamin B2 are manifested as angular stomatitis, seborrheic dermatitis, cheilosis and impaired wound healing (Gottschlich, 1989; Cooperman and Lopez, 1984). Deficiency can occur with inad-equate intake, increased needs, stress, surgery, burns, chronic illness, and malabsorption. Toxicity in humans has not been reported. The RDA for riboflavin is 1.3 to 1.6 mg/day.

• Niacin deficiency is recognized by the “four D’s”: diarrhea, dermatitis, dementia, and death, and is called pellagra. The tongue can become scarlet red and there is angular stomatitis and cheilosis. Anemia occurs as well. Niacin deficiency rarely occurs in the United States at present, but may occur with inadequate intake or supplementation with TPN, chronic diarrhea, cancer, and with increased requirements (i.e., pregnancy and lactation) (Grant and DeHoog, 1985; Hankes, 1984).

Niacin is integrally involved in metabolism and needs may be increased with stress and hypermetabolic states. The RDA for niacin is 16 to 18 mg/day, but therapeutic dos-ages can be given for the healing of broken blood vessels, as a vasodilator, and in lower-ing serum cholesterol levels. High dosages are not without side effects: these include flushing, nausea, vomiting, and diarrhea (Gottschlich, 1989; Hankes, 1984).


• Pyridoxine (B6) acts as a coenzyme in many metabolic reactions. Deficiency rarely occurs, but symptoms include a hypochromic microcytic anemia, weight loss, depres-sion, and confusion. Deficiencies can occur in patients with renal and liver diseases, alco-holism, pregnancy, in the elderly, and with stress (Driskell, 1984). The RDA for pyridox-ine is 1.3 to 2.0 mg/day. Toxicity has been seen with varying levels of megadoses, from a low of 50 mg/day to upwards of 500 mg/day.

• Biotin. Most of the needed biotin is produced by bacteria in the normally func-tioning gut. In 2001, an Adequate Intake for biotin was established, with a range of intake 25 to 35 mcg/day, based on age and gender (IOM, 2001). Biotin has proven to be an important vitamin to supplement in patients on long-term TPN and/or antibiotic therapy. Symptoms of biotin deficiency include anorexia, vomiting, nausea, scaly derma-titis or rashes, and alopecia. No toxicity symptoms have been observed. Biotin should be supplemented in the patient on TPN (Bonjour, 1984).

• Folic acid is vitally important in amino acid and nucleotide metabolism. It is important in the maintenance of red blood cells and in protein metabolism. Folic acid deficiency is not uncommon and may occur with inadequate intake, especially in the elderly; with malabsorption; with increased needs and insufficient supplementation (as in pregnancy); with alcoholism; and with therapies with anticonvulsants, oral contracep-tives, and other drugs (Brody, Shand, and Stokstad, 1984).

Symptoms of folate deficiency include macrocytic anemia, stomatitis, glossitis, and gastrointestinal disorders. Immune function is depressed. The anemia associated with folate deficiency is similar to the anemia associated with vitamin B12 deficiency.

Folate status can be determined with the measurement of urinary formiminoglu-tamic acid (FIGLU) or with measurement of serum folic acid levels. The RDA for folic acid is 400 to 600 mcg/day; however, higher dosages from 400 mcg to 1 mg/day have been recommended for therapeutic reasons (Hopkins, 1993; Gottschlich, 1989; Brody, Shand, and Stokstad, 1984).

Toxic levels of folate are not known and toxicity is generally not seen. However, supplementation of large amounts of folic acid is not recommended because it may mask the incidence of vitamin B12 deficiency.

• Vitamin B12 is important in the metabolism of carbohydrate, protein, and fat, as well as in cellular reproduction. With an RDA of 2.4 to 2.8 mcg/day, vitamin B12 is usu-ally ingested in adequate amounts by most people. However, people on a purely veg-etarian diet and those people who lack intrinsic factor (whether because of gastrectomy or other reasons) can become B12 deficient. Malabsorption of B12 can also occur with sprue, ileal resection, parasite infestations, and with drug therapy (i.e., neomycin, colchicine, ethanol, potassium chloride, etc.).

Deficiency of vitamin B12 is manifested by pernicious anemia, megaloblastic anemia, poor appetite, weight loss, and neurological changes, such as spinal cord degradation and peripheral neuropathy. Toxicity of vitamin B12 has not been shown (Gottschlich, 1989; Ellenbogen, 1984).


minerals• Zinc is a vital nutrient that plays a role in many of the enzyme reactions neces-

sary for metabolism. It also plays a role in wound healing by promoting protein synthe-sis, replication of cells, and in collagen formation. If a person becomes zinc deficient, his immune status will be impacted adversely as well.

Zinc deficiency occurs frequently in alcoholics; with long-term total parenteral nutri-tion support with inadequate zinc supplementation; and can occur with malabsorption, diarrhea, fistulas, and burns. Inadequate intake of zinc can also cause deficiency.

Needs for zinc are increased during pregnancy and after trauma or burns (this makes sense because of the role zinc plays in cell replication and protein synthesis). Symptoms of zinc deficiency include impaired wound healing, alterations in taste and smell, hair loss, dermatitis, alterations in immune function, apathy, depression and, in advanced cases, growth failure (Hopkins, 1993; Gottschlich, 1989).

Zinc status can be assessed with serum zinc levels; however, these levels may be in-accurate. Measurement of zinc in hair and nails may also be helpful. The RDA for zinc is 15 mg/day, but intake may need to be higher if hypermetabolic conditions or excessive losses exist. The recommendation for supplemental zinc in burn patients and in patients with decubiti is two times the RDA.

• Copper. No current recommendations for the intake of copper exist, but it ap-pears that an intake of 890 to 1,300 mcg/day is adequate. Copper is essential for the formation of collagen and in the scavenging of free radicals. Among its many other func-tions, copper plays a role in metabolism of cholesterol and glucose, in phospholipid and prostaglandin production, and in an effective immune system. While deficiency is rare, it can occur with nephrosis, Wilson’s disease, malabsorption, and after burns.

Symptoms of copper deficiency include microcytic anemia, changes in skeletal min-eralization, poor wound healing, alterations in immune function and neutropenia, and impaired glucose tolerance. Status of copper can be assessed with ceruloplasmin levels or with serum copper levels (less accurate).

• Selenium is an important nutrient in metabolism. Selenium acts to protect cells from damage by hydroperoxides. Selenium levels may be reduced with inadequate in-take, increased losses (as occurs with malabsorption), and with increased needs. Serum selenium is a good indicator of selenium status.

Symptoms of selenium deficiency include muscle tenderness, cardiomyopathy, and growth retardation. In 2001, an AI for selenium was set at 40 to 60 mcg/day, based on age and gender (IOM, 2001). Supplementation may be necessary in long-term TPN but there is no consensus on exact requirements. If you are following a patient on long-term TPN, you should periodically check selenium levels.

• Iron is an essential nutrient involved in the transport of oxygen and in oxidation of various nutrients. Iron is frequently deficient, because of inadequate intake, malab-sorption, and excessive losses. The RDA for iron is 15 to 18 mg/day for women, 8 mg/day for teenage boys, and 8 mg/day for men and women over 51 years of age.


Deficiency can be detected with ferritin levels, serum iron levels, and with serum total iron binding capacity levels. Symptoms of iron deficiency include iron deficiency anemia (a hypochromic, microcytic anemia), cheilosis, glossitis, and koilonychia.

nutritional anemiasLet’s talk a little here about nutritional anemias. Iron deficiency anemia is quite com-

mon, especially in women of childbearing age, infants and children, and in those patients who have had excessive losses (i.e., blood losses during hip replacement surgery). Megalo-blastic anemias associated with B12 and folate deficiency are also not uncommon and may be caused by inadequate intake, alterations in metabolism, and with increased losses (Lang and Cashman, 1989).

Diagnostic tests for anemias start with measurement of hemoglobin concentration, hematocrit, and red blood cell count. Normal hemoglobin levels range from 12 to 16 gm/dl for women and 14 to 18 gm/dl for men. Hemoglobin levels are decreased in all anemias.

Normal hematocrit levels range from 37 to 47 percent in women and from 42 to 52 percent in men. Hematocrit levels are decreased in anemias caused by iron deficiency, deficiencies in B12 and folate, and with the anemias of chronic disease and chronic infec-tion.

Taken a step further, the red blood cells are further measured to determine mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpus-cular hemoglobin concentration (MCHC). Differentiation of the types of anemias can be accomplished by looking at MCV, MCH and MCHC. MCV levels are elevated with deficiencies of folate and B12, but are decreased with iron deficiency. MCV reflects the size of the red blood cells.

Microcytic cells are small while macrocytic cells are large. MCV is determined by multiplying the hematocrit by 10, then dividing by the RBC. MCH levels that are lower than normal indicate hypochromia and signify iron deficiency. MCHC is calculated by multiplying hemoglobin by 100, then dividing by the hematocrit. It reflects the amount of hemoglobin in a red blood cell (Grant and DeHoog, 1985). The chart below summa-rizes various types of anemia.

Anemias

MCV MCHC Type of cellsIron deficiency decr decr microcytic, hypochromicB12 deficiency incr norm megaloblastic, macrocyticFolate deficiency incr norm megaloblastic, macrocyticChronic disease norm norm normocytic, normochromicChronic infection decr norm normocytic/microcytic and normochromic/ hypochromic


Other indicators of a nutritional anemia include measurement of serum iron and ferritin levels and of transferrin levels. As stated earlier, serum ferritin levels are a good marker of iron status; ferritin levels may also be decreased in folate deficiency.

Serum iron levels are a good indicator of iron deficiency as well; serum iron levels may even be increased in folate and B12 deficiency. Transferrin levels will be increased in iron deficiency, but may be increased, decreased, or normal in B12 and folate deficiency (Hopkins, 1993).

To sum up, megaloblastic, macrocytic (large cells) anemia, as evidenced by an increase in MCV, is associated with B12 or folate deficiency. A microcytic, hypochromic anemia (small cell, little color), as evidenced by a decrease in MCV and MCHC, indicates iron deficiency.

The anemia seen with chronic disease is evidenced by a normocytic, normochromic anemia, while anemia of chronic infection is reflected by normochromic or hypochromic and normocytic or microcytic cells (Hopkins, 1993). The chart below summarizes the various types of anemia.

summaryAs you can see, assessment of nutrient requirements involves more than just analy-

sis of caloric and protein requirements. It also involves provision of the right mix of nutrients, depending upon the disease state or metabolic process the patient is experi-encing. We’ll discuss the appropriate mix of nutrients with different disease states in the next chapter. Assessment also includes evaluation of vitamin and mineral stores, to assess for deficiency or excessive intake.

Case study #1ND is a 73-year-old male who presents to you in the outpatient clinic for nutritional

counseling. He complains that he has lost 25 lb since his subtotal gastrectomy three months before. He complains that he feels tired much of the time and that he has a very poor appetite. He states that he has had some symptoms of “dumping,” but these symp-toms have lessened recently and he continues to follow a small frequent feedings diet. He is 6' and weighs 160 lb and is of medium build.

Calculation of his caloric needs indicate that he should have an intake of 1800 to 2200 kcal/day and 72 to 90 gm protein/day. His diet history reveals intake of approxi-mately 1200 kcal/day and approximately 50 gm protein/day. He takes a multivitamin supplement, containing 100 percent of the RDA for vitamins, daily.

Review of the CBC reveals a megaloblastic, macrocytic anemia. We then suspect a deficiency of folate or vitamin B12. We know that he is likely taking in adequate folate and B12 through his diet and vitamin supplement. Upon further questioning, we learn that he does not receive injections of vitamin B12. We know that he would be at risk for B12 deple-tion if the area of the stomach where intrinsic factor is produced was removed. Symptoms of B12 deficiency include poor appetite, weight loss, and megaloblastic, macrocytic anemia.


Recommendations are made for B12 injections and the patient is instructed on ways to increase his caloric and protein intake.

Case study #2BT is a 43-year-old female who is 5’5" and weighs 150 lb. She is admitted to the

hospital after a bout of the flu with dehydration. She states that she has lost 10 lb and complains of nausea, vomiting, and diarrhea. Her appetite is poor, she states, because nothing smells or tastes appetizing. She complains of a sore mouth and wants mostly liquids to drink. Her diet history prior to the current illness reveals that she eats tea and a doughnut for breakfast, usually skips lunch or eats french fries for lunch, and some-times eats cottage cheese and canned fruit for dinner. She snacks on pretzels or popcorn after work as she enjoys a cocktail.

Further questioning reveals that the cocktail often turns into three or four. Since alcohol abuse is suspected, and we know that alcoholism can cause depletion of stores of folate, thiamin, B6, and zinc, lab tests are ordered. The CBC reveals a megaloblastic, mac-rocytic anemia. Further lab tests are not readily available since BT wants to check out of the hospital and refuses further blood draws. Supplementation of folic acid and thiamin, as well as zinc, is recommended. This recommendation is made because of the type of anemia; the inadequacy of the intake revealed by diet history; the history of alcohol abuse; her poor appetite and sore mouth accompanied by weight loss; and her complaint of an alteration in taste and smell.

reView questions1. Your patient is 5’3", weighs 170 lb, and is 63 years old. She is admitted to the ICU,intubated, with pancreatitis after a cholecystectomy. What are her caloric andprotein needs?2. What vitamin and/or mineral deficiencies are associated with malabsorption?3. What vitamin and/or mineral deficiencies can be associated with alcoholism?4. What vitamin and/or mineral deficiencies are associated with gastrectomy?

reFerenCes___________ IOM (Institute of Medicine) Food and Nutrition Board, Dietary Reference Intakes for

calcium, phosphorus, magnesium, vitamin D and fluoride. National Academy Press, Washington DC, 1997.

___________ IOM (Institute of Medicine) Food and Nutrition Board, Dietary Reference Intakes for thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, biotin, and choline. National Academy Press, Washington DC, 1998.

________ Institute of Medicine (IOM). Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press, Washington D.C., 2000.

________ Institute of Medicine (IOM). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington D.C., 2001.


________Institute of Medicine (IOM) Food and Nutrition Board, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. 2002.

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tients? JPEN, 19S:22S, 1995.Olson JA. Vitamin A. In: Handbook of Vitamins. Machlin LJ, ed. New York: Marcel Dekker, Inc., 1984.


Rapp RP. Vitamins: Clinical Use vs. Abuse. Unpublished lecture presented at ASPEN 17th Congress, San Diego, 1993.

Sawyer M, Rolandelli R, Novick W, et al. Measurement of resting energy expenditure (REE) in the ICU using pulmonary artery catheters. JPEN, 12:5S, 1988.

Schwartz DB. Pulmonary failure. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese LE, and Shronts EP, eds. Silver Spring, MD: ASPEN, 1993.

Shronts EP and Lacy JA. Metabolic support. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese LE, and Shronts EP, eds. Silver Spring, MD: ASPEN, 1993.

Smithies MN, Royston B, Makita K, et al. Comparison of oxygen consumption measurements: Indirect calorimetry versus the reversed Fick method. Crit Care Med, 19:1401-1406, 1991.

Weaver CM, Fleet JC. Vitamin D requirements: current and future. Am J Clin Nutr, 80(s):1735S-9S, 2004.Williams RR and Fuenning CR. Circulatory indirect calorimetry in the critically ill. JPEN, 15:509-512,

1991.


Chapter Seven:Nutritional Assessment

in Disease States, Part I

The stress of serious illness impacts nutritional status greatly. In this chapter, we’ll cite specific kinds of stressed patients, and discuss how their illnesses change the way we assess their nutritional status.

Pulmonary diseaseThe person with pulmonary disease is often at risk for malnutrition, because of the

higher metabolic requirements that accompany the increased work of breathing; dimin-ished intake; and, to a lesser extent, the inability or diminished ability to shop for and prepare meals. Malnutrition also has a profound effect on the function of the lungs and diaphragm.

As many as 40 percent of the patients who have chronic obstructive pulmonary dis-ease (COPD) have lost 10 percent or more of their body weight (Weissman and Askanazi, 1985). This weight loss may be related to the increased work of breathing associated with pulmonary disease. Malnutrition in patients with COPD is estimated from 19 to 74 percent of cases (Schols, et al., 1989; Laaban, et al., 1993).

The normal, healthy individual uses 36 to 72 kcal/day for breathing, while the patient with COPD may utilize 430 to 720 kcal/day just to breathe (Wilson, Rogers, and Hoffman, 1985). Why does this occur? The COPD patient often has increased resistance in his airways and the efficiency of the respiratory muscles is diminished (Miller, 1986).

The patient with COPD or other respiratory diseases may also experience weight loss because he/she is unable to shop for or prepare meals due to the shortness of breath and fatigue. It’s difficult for a patient with severe pulmonary disease to eat and breathe at the same time. He or she may be unable to eat as much because of ulcer disease and/or abdominal discomfort related to bronchodilators or corticosteroids


(Schwartz, 1989). The patient may well be hypermetabolic, with increased needs — as much as 10 to 25 percent over predicted resting energy expenditure (Rothkopf, et al., 1989).

Once the patient with pulmonary disease becomes malnourished, his lung func-tion and efficiency is impacted even further. Prolonged fasting causes a decreased respiratory rate, tidal volume, and a decreased metabolic rate (Benedict, 1915). Muscle mass, including respiratory muscle mass, decreases. The diaphragm, intercostal muscles, and accessory muscles of respiration lose both mass and strength, causing a decrease in the maximal inspiratory pressure and expiratory strength (a measure of the amount of air the lungs can move in and out with a breath) (Miller, 1986; Benedict, 1915; Schwartz, 1993).

Other malnutrition-associated changes in lung function include a decrease in vital capacity and a decrease in minute ventilation. Immune function is also impacted, as evi-denced by a decrease in the rate of surfactant production, a decrease in immunoglobulin levels, and a decrease in the development of new cells in the epithelial lining. Why are these changes important?

Surfactant acts to reduce the surface tension within the lungs and prevents alveolar collapse. A diminished production of surfactant could lead to atelectasis and, potentially, pneumonia, because of increased surface tension, stiffer pulmonary tissues, and reduced surface area for air exchange (Wilson, Rogers and Hoffman, 1985; Schwartz, 1993). Re-plenishment of cells in the epithelial lining is important in fighting off infection. Macro-phages in the lining defend against the invasion of foreign materials and bacteria. If the number of macrophages decreases, immune function is compromised.

Clearly, the nutritionally compromised patient is placed at risk for pulmonary infections. We’ve discussed the effects of decreased surfactant and diminished immune response. Another area that impacts immune function is alteration in the antioxidant protective mechanisms (Schwartz, 1989). Deficiencies of the sulfur-containing amino acids, copper, selenium, iron, and vitamins can all lead to the decrease in protection from free radicals.

Effects of Malnutrition

Minute ventilation Response to hypoxia Immune Response Affects pulmonary metabolism

Respiratory rate Tidal volume Muscle mass Muscle strength Vital capacity


The COPD patient with emphysema appears to have a greater incidence of deple-tion of protein stores, as well as caloric stores. In assessing the patient with chronic lung disease, we should compare current weight with usual weight. We should also take a complete diet history to assess the adequacy of nutrient intake, determine the ability of the patient to shop for and prepare meals, and determine the presence of any gastroin-testinal symptoms that may inhibit intake. A review of laboratory values, including albu-min, transferrin, prealbumin, and total lymphocyte count, and an evaluation of nitrogen balance to assess if actual intake is adequate may also be helpful.

So, how do we assess the patient’s nutrient requirements? We’ve determined that energy expenditure is sometimes markedly increased in the patient with pulmonary disease. The best determination for actual needs is through indirect calorimetry, utilizing a metabolic cart (see Chapter Six). However, if a metabolic cart is unavailable, nutrient requirements can be predicted using factors. For maintenance needs, a factor of 1.2 to 2.0 X REE or 25 to 30 kcal/kg is used (McCarthy and Deal, 2002).

How should these calories be divided among substrates? As we discussed in Chapter Six, various substrates have varying effects on respiratory quotient. The patient who is a carbon dioxide retainer may do better with a higher concentration of fat calories in his intake, so that RQ will be lower, and the work of breathing will be eased. Recom-mendations for a mixed intake of 50 percent carbohydrate and 50 percent fat (of non-protein-calories) have been made (Rothkopf, et al., 1989; Schwartz, 1993; and Kinney and Askanazi, 1984).

Protein intake is recommended as: 1.0 to 1.5 gm protein/kg/day (McCarthy and Deal, 2002). We should be aware that a high protein intake can increase minute ventila-tion and increase oxygen consumption. If respiratory distress does occur with a high protein intake, protein intake should be decreased to the lower level in the ranges pro-vided. (Miller, 1986; Rothkopf, et al., 1989; Schwartz, 1993).

Adequate vitamin and mineral intake is essential for pulmonary patients. Provision of amounts as recommended in the RDA appears to be adequate. Because low serum phosphorus alters oxygen transport and appears to reduce the strength of the dia-phragm, adequate phosphorus should be provided.

Pulmonary Patient Pertinent Lab Values

albumin total lymphocyte count transferrin nitrogen balance prealbumin


ardsARDS is an acronym for Adult Respiratory Distress Syndrome and is characterized

by “severe acute lung injury resulting in acute hypoxemic respiratory failure” (Bernard, et al., 1994). ARDS may occur with sepsis, aspiration, pneumonia, trauma, burns, massive blood transfusions, transplantation, and pulmonary edema (after seizure or intracerebral bleed) (Hogg, et al., 2001). The inflammatory response associated with ARDS alters lung function and metabolism. Calorie and protein requirements are similar to those of the septic patient, i.e. 25 to 30 kcal/kg and 1.5 to 2.0 gm protein/kg. Care should be taken to avoid overfeeding to reduce the incidence of excessive carbohydrate production.

Levels of phosphorus, magnesium, and potassium should be closely monitored. Phosphorus is a critical component of oxygen transport and diaphragm contraction (Schwartz, 1998; Freund, 1991). Magnesium levels may decrease with utilization of di-uretics and with hypokalemia (Ireton-Jones, 1998).

Case study: Pulmonary diseaseJM is a 60-year-old male who presented with a GI bleed, COPD, pneumonia, and a

history of alcohol abuse. He weighed 81 kg upon admission, was 6’4" and had a serum albumin level of 1.6 gm/dL. His usual weight was stated at 90 kg. Ideal body weight was assessed to be 83 to 102 kg. He was determined to be at 90 percent of his usual body weight.

His fat stores appeared wasted. Assessment of dietary history wasn’t possible be-cause of the patient’s mental status and the absence of family. He developed acute renal failure during his stay (this altered calculation of his protein requirements). Nitrogen balance studies were not possible because of the renal failure.

His needs were calculated to be 2200 to 2600 kcal/day (30 to 35 kcal/kg) and 90 to 135 gm/day (1.0 to 1.5 gm/kg/day). The patient began to show symptoms of retaining carbon dioxide, with increased work of breathing and high pCO2 levels. The percentage of calories from fat was increased in his intake to 50 percent and pCO2 levels and work of breathing decreased. Slowly, his serum albumin levels increased, with support. He was also given supplemental thiamin because of the history of alcohol abuse.

Calories ProteinMaintenance 1.0 - 1.2 x REE 1.0 - 1.5 gm/kg/d ay 25 - 35 kcal/kg

Repletion 1.4 - 1.6 x REE 1.5 - 2.0 gm/kg/day(Anabolism) 35 - 45 kcal/kg

Nutrient Requirements for Pulmonary Patients


Case study #2: Pulmonary diseaseEW is a 69-year-old male admitted with the diagnosis of exacerbation of chronic

obstructive pulmonary disease and left lower lobe pneumonia. He relates that he has smoked two packs of cigarettes per day for the last 55 years. He has lived in his car for the last 10 years and is estranged from his family. Shortly after admission, he is intu-bated. His admitting weight is 40.5 kg; no height is available, but he appears thin. His medications include sliding scale insulin, Solumedrol, and gentamicin. Admitting labs include: Alb 2.4; BUN 39; Cr 1.2; Hgb 14.4; and WBC 22.1. Enteral feedings are started and initially provide 720 cc, 864 kcal, and 38 gm protein. His needs are assessed at 1100 to 1300 kcal/day (remember not to overfeed) and 40 to 60 gm protein per day. His en-teral feedings are later increased to 1728 kcal and 76 gm protein; he appears to tolerate the increased nutrients and even reflects weight gain to 43.7 kg; however, his albumin is now 1.9. His pulmonary status is improving and, barring further complications, he appears to be on the road to recovery. EW was determined to be at severe nutritional risk with his apparent low weight for height, his low albumin, and his diagnosis. After extubation, perhaps we can learn more about his dietary habits and attempt to assist him in changing some of his habits to improve his nutritional status.

CanCerCancer, diagnosed in greater than one million Americans each year, and its related

therapies can cause a myriad of nutritional problems. The patient with cancer may appear visibly malnourished; on the other hand, the patient may exhibit no outward symptoms of malnutrition, but upon examination of laboratory values, it becomes clear that he is indeed malnourished. Cancer is a wasting disease and many metabolic chang-es occur when cancer is present in the body. Malnutrition is more prevalent in cancers involving the gastrointestinal tract (63 to 87 percent of patients with pancreatic or gastric cancers exhibit weight loss). Patients diagnosed with non-Hodgkins lymphoma and cancers of the colon, prostate, and lung exhibit weight loss in 48 to 61 percent of cases. And those patients diagnosed with breast cancer, favorable outcome non-Hodgkin's lymphoma, acute lymphocytic leukemia, and sarcoma are less likely to realize weight loss (Dewys, 1980).

Cancer causes marked changes in protein metabolism. Whole-body protein turn-over is increased by as much as 32 percent and there is an increase in the rate of protein synthesis in the liver (Bloch, 1993). Skeletal muscle begins to break down as it is synthe-sized more slowly. Cori cycle activity, also known as “futile cycling,” is the breakdown of muscle glycogen, with formation of lactic acid, which enters the bloodstream, is converted to liver glycogen, which in turn breaks down into glucose, which is carried to muscles where it is reconverted to muscle glycogen. There is also altered glucose met-abolism, resulting in glucose intolerance and insulin resistance. Cachexia occurs related to increased lipolysis and decreased lipogenesis, resulting in decreased adipose tissue (Dewys, 1980; Barber, 1999; Argiles and Lopez-Soriano, 2000).


This cycle increases by as much as 20 percent in the cancer patient, contributing to the progressive weight loss so often seen with cancer patients (Bloch, 1993; Maillet, 1987; Kehoe and Daly, 1985). Energy expenditure is not consistent in the cancer patients. Ap-proximately 33 percent are hypometabolic, 33 percent have energy needs that are near normal, and the remaining 33 percent are hypermetabolic.

Anorexia is common among patients with cancer. Early satiety is a frequent com-plaint; this can be caused by tumor production of neurotransmitters, increased release of serotonin, and increased levels of free fatty acids. All occur with various types of cancer. Changes in taste and smell are common and can, obviously, affect intake of adequate amounts of foods.

Therapies to treat cancer include surgery, radiation therapy, and chemotherapy. All of these therapies can impact nutritional status. Head and neck surgeries can be associated with inability to swallow or chew and a change in taste and smell (Bloch, 1993; Burgess, 1989). Esophageal resection can cause difficulty in eating, malab-sorption, decreased gastric motility, and diarrhea. Fistulas are not uncommon after esophageal resection. Gastrectomy can lead to dumping syndrome, hypoglycemia, malabsorption, iron deficiency anemia, B12 deficiency, and deficiencies of calcium and fat-soluble vitamins.

Head and Neck Inability to chew Inability to swallow Changes in sense of taste and smell

Esophagectomy Difficulty eating Malabsorption Decreased motility Aspiration Fistulas Dysphagia

Gastrectomy Nausea and vomiting Dumping syndrome Hypoglycemia Malabsorption Iron deficiency anemia B12 deficiency Deficiency of fat-soluble vitamins Deficiency of calcium

Small bowel resection Diarrhea Rapid transit Malabsorption B12 deficiency Deficiency of fat-soluble vitamins Calcium deficiency Magnesium deficiency Electrolyte disturbances

Colon resection Loss of bile Diarrhea Bacterial overgrowth

Pancreatectomy Malabsorption of fats Malabsorption of protein Malabsorption of fat-soluble vitamins Diabetes mellitus

Nutritional Problems of Surgery


Resection of the small bowel can cause a multitude of nutritional problems. Diar-rhea, rapid transit, malabsorption, and deficiencies of B12, fat-soluble vitamins, calcium, magnesium, and electrolytes can occur. Resection of the colon can lead to loss of bile, deficiency of B12, and bacterial overgrowth. Pancreatectomy often leads to malabsorption of fats, protein, fat-soluble vitamins, and minerals.

Knowledge of what occurs nutritionally with each of these surgeries is important in the assessment of the patient and should trigger you to look for symptoms of associated deficiencies. Radiation therapy can cause nausea, vomiting, diarrhea, and malabsorp-tion. Changes in the senses of taste and smell are common. Stomatitis, mucositis, and decreased salivation may occur, causing difficulty in chewing and swallowing. Strictures and fistulas can also occur.

Chemotherapy can cause many deleterious side effects that can impact nutritional intake and nutritional status. Anorexia, nausea, vomiting, diarrhea, and weight loss are not uncommon. Many chemotherapeutic agents can cause changes in the metabolism of nutrients, and some can cause deficiencies of vitamins and minerals (methotrexate — fo-late and calcium; cisplatin — zinc). Inflammation and discomfort of the mouth, esopha-gus, stomach, and colon are common.

Kouba (1989) defines as goals of nutrition support in the patients with cancer the abil-ity “to achieve and maintain desirable weight and to prevent or correct nutritional imbal-ances and deficiencies.” Assessment of the cancer patient is much the same as that of any other patient. Patients with cancer quite often will exhibit weight loss. Total lymphocyte count may not be a good indicator of nutritional status in patients with cancer because it can be affected by the cancer itself or by chemotherapy or radiation therapy.

During the nutritional assessment, actual weight should be compared against ideal body weight. A weight loss of 20 percent of usual body weight is considered significant, while a weight loss of 10 percent of usual body weight should trigger close monitoring of nutritional intake and consideration for nutrition support. Assessment of nutrient requirements is much the same as for the patient without cancer. Caloric and protein requirements are shown below.

Nutrient Requirements — Patients with CancerCaloric requirements

Sedentary patients: 20 to 25 kcal/kg Weight gain or anabolism: 30 to 35 kcal/kg Hypermetabolic or malabsorption: 35 kcal/kg

Protein requirements Maintenance 0.8 to 1.0 gm/kg/day Repletion or with protein wasting 1.5 to 2.5 gm/kg/day


We should remember that many of the therapies for cancer can cause depletion of vitamin and mineral stores. The tumors themselves can also cause deficiencies of vita-mins and minerals. Any losses should be replaced and repletion should be accomplished if deficiency occurs. Vitamin and mineral supplementation should be considered if the patient’s intake is inadequate or if surgery, radiation, or chemotherapy causes depletion of stores.

Case study: CanCerKI was admitted to the hospital with metastatic gastric cancer and a small bowel ob-

struction. He had been on home TPN via a Groshong catheter, but had a 25 lb weight loss over the previous three months. He was 5’3" tall and weighed 130 lb. His only abnormal laboratory values were a phosphorus of 4.3, a glucose of 165, and an albumin of 2.7. His needs were established to be 1500 to 1800 kcal/day and 70 to 90 gm protein/day.

While he was within his range for ideal body weight, the 25 lb weight loss was of concern, especially since he was on home TPN. His low albumin was likely related to the increased needs related to his diagnosis. Also, as cancer progresses, the tumor may start to utilize more and more of the patient’s protein stores. At this point, the cancer may be “winning.” KI tolerated his TPN well but showed no improvement in weight or labora-tory data during his hospital stay.

Case study #2: CanCerMB is a 34-year-old male with T-cell lymphoma who is admitted for chemotherapy.

Although his weight has recently been stable, he noted progressive weight gain when his chemotherapy was altered. His weight is 175 lb at 5’11" (within IBW range); no labs are ordered or available from this or previous hospitalizations. He relates 100 percent intake on his regular diet but wants to continue to drink his “Isosource HN” that he was drinking at home since he no longer instills the feeding via his gastrostomy tube. He tells us that he has regained the thirty pounds he had lost early in his chemotherapy regimen. MB appears well-nourished and able to meet his nutrient requirements.

aidsAIDS is caused by the human immunodeficiency virus (HIV) that infects and kills

specific immune cells, causing abnormal immune function and increasing susceptibility to infection and cancer. Forty million people in the world have HIV/AIDS and it is esti-mated that three million have died in 2001 (Joint United Nations Programme on HIV/AIDS, 2001).

HIV is classified as a retrovirus. It is distinguished by the presence of reverse transcriptase, an enzyme that allows the RNA of the virus to make its own DNA by us-ing genetic material from the host cell. The virus binds to a glycoprotein receptor, CD4, on the surface of a cell, then penetrates into the cell. Once infected, the cell no longer functions properly, even if it is not actively replicating. At the time of activation, the cell


produces more viruses, filling until it bursts, releasing more viruses. Cells that have the CD4 receptor (and which therefore can become infected) include CD4 T lymphocytes (T helper cells), macrophages and monocytes, some B cells, and dendritic cells of the germi-nal centers (part of the nervous system).

There are numerous tests that can determine the status of the immune system in HIV positive and AIDS patients, including tests to measure the absolute number of CD4 cells, the percentage of lymphocytes that are CD4 cells and the ratio of CD4 to CD8 cells (suppressor or cytotoxic cells). The normal ratio is 2 CD4 cells to 1 CD8 cell. In HIV that ratio is reversed to 1 to 2.

While these tests indicate the number of cells, they do not give any indication of how well the cells can function. Preferentially, HIV destroys the CD4 T lymphocyte. As the CD4 count goes down, the types of opportunistic infections increase in severity, as shown in the chart below (Fauci, et al., 1996).

New diagnostic tests measure HIV RNA — the genetic material of the virus — in the plasma of infected patients, which indicates the activity of the virus. This test is referred to as measuring the “viral load” of a patient. Some HIV RNA tests can detect as few as 20 copies of the virus in the blood. Valuable information regarding the progres-sion of the disease and effectiveness of antiretroviral therapies can be learned by mea-suring the amount of virus in the body.

Studies also suggest that viral load is a good indicator of survival. Mellors, et al. (1996) divided 181 subjects into two groups based on plasma HIV RNA levels: those with more than 10,000 copies/mL and those with less than 10,000 copies/mL. After 10 years, the survival rate in the group with over 10,000 copies/mL was 30 percent com-pared with a 70 percent survival rate in the group with less than 10,000 copies/mL. Patients with the lowest viral loads, less than 4500 copies/mL were considerably less likely to develop AIDS.

At the time of initial infection, viral loads can differ dramatically from individual to individual. Some may have a viral load of 10,000 copies/mL while others may have 100,000 copies/mL or higher. Once antiretroviral therapy is begun, levels are measured to determine how well patients respond and when a therapy may no longer be effective.

varicella-zoster virus, bacterial infectionsoral candidiasisPneumocystis cariniicytomegalovirus (CMV)Mycobacterium avium complex (MAC)

<350<250<200<100<50

CD4 & Risk of Opportunistic Infections

CD4+ cells/mm3 Opportunistic infections


The good news is that in developed countries, the devastating progression of AIDS is mitigated in part by effective treatment, supported by a generally high level of nutri-tional health. Those individuals receiving highly active antiretroviral therapy (HAART), common in the US, have fewer opportunistic infections, increased quality of life and longer life expectancy (Kotler, 2004). Patients receiving HAART do have nutritional problems that need intervention, such as nutritional deficiencies, metabolic abnormali-ties, weight loss and weight gain, body composition changes, diarrhea and GI distur-bances. In addition, HAART has other side effects, such as lipodystrophy, alterations in serum lipids, and metabolic abnormalities that increase the risk for cardiovascular disease and diabetes (Samaras, 2007).

Some of those metabolic abnormalities include: increased total and LDL cholesterol; increased triglycerides; decreased HDL cholesterol; insulin resistance; increased serum glucose; increased C-reactive protein and inflammation; increased leptin and decreased adiponectin.

As soon as someone is diagnosed as HIV+, nutrition assessment and counseling should begin. The goal is to get the individual paying attention to diet when still feel-ing well, so he is eating optimally, maximizing reserves, giving the immune system adequate nutrition and minimizing weight loss. Supplementation can begin early in the disease, to maximize stores of nutrients and keep levels normal for as long as possible.

malnutrition and aidsAs our knowledge of HIV advances, so does our understanding of the importance

of nutritional status in HIV+ and AIDS patients. Nutritional status is an independent predictor of survival; preliminary data indicates nutritional status may be a predictor of hospitalizations and quality of life (Guenter and Muurahainen, 1995).

Why are HIV positive patients at risk for malnutrition? These patients often have increased metabolic rates, decreased intake, malabsorption, and altered digestion related to a multitude of opportunistic infections. Malnutrition and tissue-wasting is correlated with the timing of death in these patients when 66 percent of total body mass or 54 per-cent of lean body mass is lost (Kotler, et al., 1989).

The Centers for Disease Control (CDC) describes the wasting syndrome associated with AIDS as greater than 10 percent unintentional weight loss in the presence of diar-rhea or fever for more than 30 days that is not attributable to other disease processes (Centers for Disease Control, 1992). Eighty percent of AIDS patients develop the syn-drome at some point during their illness (Trujillo, et al., 1992). Persons infected with HIV often have progressive involuntary weight loss early on; the weight loss increases in magnitude with the progression of the disease (Raiten, 1990). This weight loss is primar-ily associated with malabsorption and gastrointestinal tract infections, as well as altera-tions in nutrient intake. Changes in body composition may occur as well; thus it may be helpful to utilize various body composition measurements; (i.e. bioimpedance), (Fields-Gardner, 1995).


The weight loss correlates quite significantly with death and diminished quality of life. Muscle wasting that occurs not only affects extremities, but also can result in atrophy of the heart and lungs, thus compromising cardiac and respiratory function. Protein and lipid metabolism becomes abnormal. Weight gain with supplementation typically results in increased fat stores and diminished restoration of lean body mass (Macallan, 1999).

The weight loss associated with AIDS may manifest itself in two ways: slow and progressive or rapid and episodic (Macallan, et al., 1993; Macallan, 1999). The slow weight loss generally occurs with diminished nutrient intake and GI discomfort, diar-rhea, etc. The rapid weight loss may be followed by weight gain and is associated with acute exacerbations of infection. Acute infections can also cause a decrease in serum protein levels.

Weight loss associated with diminished intake can be related to the disease process and/or to the medications provided to the patient. The presence of infection causes an increase in cytokines, tumor necrosis factor, interleukin-1, and interferons. All of these can cause anorexia (Grunfeld and Palladino, 1990). Other causes of the anorexia associat-ed with AIDS include painful lesions in the mouth and esophagus; nausea and vomiting; early satiety; diarrhea (Kotler, et al., 1990); altered taste sensation and dysphagia (Bell, et al., 1998). We should not forget the role that psychosocial factors and financial problems can play in the person with any chronic disease, but especially AIDS. These patients may not have the money or desire to shop for, prepare and eat food.

Malabsorption can occur with any of the opportunistic infections, which occur when the CD4+ T helper counts goes below 200/mm3 and is a sign that the HIV infection has progressed to AIDS (Kotler, 2004). Many of these infections cause profound diarrhea and malabsorption, with subsequent weight loss and malnutrition. Existing malnutrition (hypoalbuminemia) can also cause diarrhea and altered or diminished absorption capac-ity in the small bowel. This further compromises the patient and a cycle of malnutrition – diarrhea – further malnutrition can occur.

The patient with AIDS may experience both hypometabolism and hypermetabo-lism during the course of his disease (Fields-Gardner, 1995). However, REE is gener-ally increased even when the patient is stable without infection (Dworkin, et al., 1990; Hommes, et al., 1991; Rakower, et al., 1989). Thus it may be difficult to estimate energy requirements for this group of patients. As with other patients, measurement of needs with a metabolic monitor or cart may be helpful as compared to estimation of needs with various equations. However, Hickey (1991) suggests that requirements can be estimated with either of the following formulas:

35 to 40 kcal/kg/day and 1.0 to 1.5 gm protein/kg/day OrREE = Harris Benedict equation* X activity factor** X injury factor + 500

* adjusted for sex ** Activity factor: sedentary = 1.2; ambulatory = 1.3; fever = 1.13 X each degree >37C


Protein requirements are approximately 1 gm/kg/day when the patient is stable and 1.5 gm/kg/day when infection is present.

Deficiencies of many vitamins and minerals occur with AIDS. Folate and vitamin B12 deficiencies often occur. These deficiencies may be associated with decreased intake and/or with decreased absorption, related to diarrhea and lower gastrin levels. B6 levels may be low in the AIDS patient. The fat-soluble vitamins (A, D, E, and K) may be defi-cient: remember that we can lose these vitamins with diarrhea, especially steatorrhea.

Low serum zinc levels may be related to life style or to the progression of the dis-ease with malabsorption and diarrhea (Raiten, 1990). We should examine zinc status, whatever the cause, because zinc deficiency can cause changes in immune function, changes in taste and anorexia. Selenium levels may become depleted as well (Dworkin, et al., 1986, 1989). Supplementation of various nutrients, including vitamins A, E, C, and B12 as well as selenium and zinc has been suggested. However, megadoses are not recom-mended; toxicity has been demonstrated with high doses of vitamin A (Olson, 1988), zinc (Fosmire, 1990), and selenium (Levander, 1988; Olstead, et al., 1989).

How can we assist the patient with AIDS? If a client is taking HAART, with pro-tease inhibitors, it is important to screen for lipodystrophy and metabolic abnormali-ties. Changes in fat distribution due to lipodystrophy should be screened for by taking measurements of the arm, thighs and waist and monitoring BMI and lean body mass. Laboratory tests to screen for lipids, cholesterol and glucose tolerance are also appropri-ate. The sooner these are discovered, the sooner interventions can begin.

If a patient is not on HAART, we need to treat or reverse malnutrition. High calorie and high protein oral supplements can be utilized to slow or reverse the weight loss that occurs. Enteral and parenteral feedings can be of use as well. Utilization of formulas con-taining MCT oil and/or peptide formulas may be beneficial. We should attempt to help the patient maintain adequate intake of both macro- and micronutrients.

Nutritional screening, similar to that done with any other patient, should occur soon after diagnosis so that appropriate nutrition interventions can be implemented. We should examine any report of weight loss and look for the potential causes, which may include inadequate intake, early satiety, drug nutrient interactions, anorexia, diarrhea and malabsorption, and hypermetabolic states (Raiten, 1990). We can then assist the pa-tient with various interventions that can help him/her to improve intake. Because many of the infections complicating the patient’s health are opportunistic, we should educate the patient on various food safety issues.

liver diseaseThe liver is an essential organ, necessary for detoxification of the blood, carbohy-

drate metabolism, lipid metabolism, protein synthesis, and secretion of bile (Fox, 1987). Most nutrients must pass through the liver, where they are stored, used for energy, or processed into other substances. All essential amino acids, except for branched-chain


amino acids, are metabolized in the liver (Munro and Crim, 1980). The primary meta-bolic organ for fats and carbohydrates is the liver.

Any disease of the liver will have an impact on nutritional status. Careful nutri-tional assessment of the patient with liver disease is important so that the appropriate nutritional care plan can be developed.

Liver disease and damage can occur with viral infections, such as the various forms of hepatitis, Epstein-Barr, and cytomegalovirus; ischemic damage after trauma or sur-gery; abuse of alcohol and drugs; autoimmune diseases; and cancer (Shronts and Fish, 1993). All of these illnesses can lead to cirrhosis, an irreversible change in liver cells.

As liver disease worsens and the patient develops hepatic insufficiency, ascites and edema can occur, causing decreased appetite, cachexia, and weight loss. The portal hypertension that occurs, along with severe hypoalbuminemia, can cause malabsorp-tion and steatorrhea. This steatorrhea can cause increased losses of fat-soluble vitamins, calcium, magnesium and zinc (Shronts and Fish, 1993).

The injured or diseased liver is often unable to maintain normal carbohydrate metabolism. Hypoglycemia can occur in acute liver failure, while hyperglycemia occurs with chronic liver disease.

Absorption of fat is dependent upon the normal production and secretion of bile salts; the diseased liver may be unable to produce bile. Without normal fat metabolism, short-chain fatty acids accumulate in the liver, leading to “fatty liver” (Visocan, 1989).

Metabolism of protein is significantly altered in the diseased liver. Formation of nonessential amino acids and albumin, fibrinogen, prothrombin, and urea, among other things, is inhibited. As protein metabolism progressively worsens, the sequelae of pro-gressive liver dysfunction continue, with a decrease in urea production and increased serum ammonia levels. An increase in aromatic amino acids (because of a decrease in their breakdown) and a decrease in branched-chain amino acids (because of an increase

Metabolic Alterations with Liver Disease

hypoglycemia (in acute) fat malabsorptionhyperglycemia (in chronic) fatty liverdecreased protein synthesis decreased serum albumindecreased fibrinogen levels decreased prothrombin levelsdecreased production of urea increased ammonia levelsincreased aromatic amino acids decreased BCAAincreased liver function tests fat-soluble vitamin deficiencythiamin deficiency B6 deficiencyfolate deficiency niacin deficiencyiron deficiency copper deficiencymanganese deficiency zinc deficiency


in their use for energy) occurs, causing production of “false neurotransmitters.” These eventually cause confusion and a decreased level of consciousness (Shronts and Fish, 1993; Hiyama and Fischer, 1988; Levinsky and Spiro, 1985).

Laboratory values are altered with hepatic insufficiency. Bilirubin, aspartate amino-transferase (SGOT), alanine aminotransferase (SGPT), and alkaline phosphatase levels will increase. Serum albumin is often lower than normal and may be significantly decreased.

The lowered serum albumin is important to remember because of albumin’s roles in maintaining oncotic pressure and in transporting other substances. Other transport proteins synthesized by the liver include retinol-binding protein and thyroxine-binding prealbumin. These levels may also fall. Diminished levels of albumin, retinol-binding protein and prealbumin may or may not reflect nutritional status as well as declining liver function. Ammonia levels may or may not be elevated because of the liver’s inabil-ity to convert ammonia to urea.

The patient with liver disease is at risk for malnutrition because of the malabsorp-tion that occurs. Intake is often poor, especially if the liver disease is associated with alcohol abuse. In fact, malnutrition was found in 88 to 100 percent of patients hospital-ized with cirrhosis.

Nutritional assessment of patients with liver disease is often difficult because of their altered mental status, changes in laboratory values caused by the liver disease, and ascites associated with this condition. As with other diseases, evaluation of recent weight change is important as is assessment of adequacy of nutrient intake.

Questions should be asked regarding any gastrointestinal symptoms, such as diar-rhea. Because of the fluid shifts associated with ascites and treatment for fluid overload, anthropometrics may not be valid.

Laboratory values, as noted, are difficult to assess in relation to nutritional status. Fluid status, use of steroids, malabsorption, liver disease itself, and the stress associated with the liver disease and treatment all play a role in the levels of albumin, transferrin, thyroxine-binding prealbumin, and retinol-binding protein.

Other indicators of nutritional status, including total lymphocyte count, are af-fected not only by nutritional status, but also by the disease process itself. We should be aware of vitamin/mineral deficiencies that can occur with liver disease and with alco-hol abuse. Look for deficiencies of fat-soluble vitamins, thiamin, pyridoxine, folate, and niacin. Low levels of iron, copper, manganese, and zinc have been reported in patients with liver disease. The nutrient requirements of the patient with liver disease are shown on the following page.

Caloric requirements are estimated to be 22 to 25 kcal/kg/day, utilizing 25 to 40 percent calories as fat (Pomposelli and Burns, 2002). Protein requirements are estimated at; for hepatitis: 0.8 to 1.0 gm protein/kg/day; for cirrhosis without encephalopathy: 1.5 gm protein/kg/day; and for cirrhosis with encephalopathy: 0.5 to 0.7 gm protein/kg/day. As encephalopathy improves, protein intake can be increased by 0.2 gm/kg/day to as much as 1.2 to 1.5 gm/kg/day.


Vitamin and mineral supplementation may be necessary, but should be closely monitored. While increased losses of fat-soluble vitamins can and do occur, the liver also stores these vitamins. With the liver’s inability to metabolize or transport these vitamins, toxicity can occur. Supplementation should be carefully administered and closely monitored.

Case study: liver diseaseBF is a 62-year-old man admitted with a history of alcoholic liver disease (a his-

tory of 6 beers/day with additional wine since the age of 14), cirrhosis and a pancreatic pseudocyst. He also had esophageal varices and portal hypertension. A splenorenal shunt and a portacaval shunt were placed after he suffered a gastrointestinal bleed. He weighed 155 lb and was 5’8" tall.

BF’s needs were assessed to be 2100 to 2500 kcal/day and 55 to 70 gm protein/day, initially. This was based on 30 to 35 kcal/kg and 0.8 to 1.0 gm protein/kg. His albumin level was 3.4 and amylase was 1677; glucose was 272 and liver function tests were near normal. He developed atelectasis and ascites and was diagnosed with Clostridium dif-ficile colitis after workup for the cause of his diarrhea.

With the TPN ordered, he received 2200 kcal and 54 gm protein. His course stabi-lized and calories were increased to 2800 kcal/day. Lab values generally remained stable except for a fall in albumin to 2.5, likely related to inadequate protein intake accompa-nied by bedrest. Two weeks later, he was started on a clear liquid diet and protein intake was increased to 72 gm protein/day. IV albumin was given and his albumin rose to 3.0.

Liver function tests slowly started to rise, indicating that perhaps his liver function was deteriorating further (calories had been decreased to 2230 kcal/day with 72 gm pro-tein/day). Liquids were not tolerated well. Serum albumin levels remained stable, as did other laboratory values over the next three weeks. His weight remained relatively stable as well, at 68 kg.

Caloric & Protein Requirements: Liver Disease

Caloric Requirements: 22 - 25 kcal/kg/day

Protein Requirements: hepatitis: 0.8 - 1.0 gm/kg/day cirrhosis, no encephalopathy: 0.8 - 1.5 gm/kg/day cirrhosis with encephalopathy*: 0.5 - 0.7 gm/kg/day

*Recommendations are to begin with 40-50 gm of protein/day, decreasing down to 20 gm/day until the patient improves.


One week later, he developed worsening liver failure, which was accompanied by renal failure, sepsis, and intubation. His albumin levels fell to 2.0 and cholesterol and triglycerides were 62 and 122, respectively. BUN was 84 and creatinine was 3.4. Liver function tests actually started to fall as liver function continued to deteriorate. After no progress was seen over the next two weeks, the decision was made to withdraw support and keep the patient comfortable.

Case study #2: liver diseaseWB is a 63-year-old male with COPD, hypertension, cardiomyopathy secondary

to alcohol abuse, cirrhosis, esophageal varices, and emphysema. He is 5’10" and weighs 77.4 kg (within the range for IBW). His medications include prednisone, lasix, theodur, digoxin, potassium, and inhalers. He stopped smoking and drinking alcohol six months ago. His labs were normal except for a potassium of 5.6, BUN of 16, creatinine of 2.0, and cholesterol of 220. He is placed on a low salt diet and is eating 80 to 100 percent of his meals. His needs are assessed to be 1900 to 2300 kcal/day and 75 gm protein/day (until we determine if he can tolerate a higher level of protein). He is at moderate nutritional risk because of his multiple medical problems; he may also be in need of vitamin supple-mentation with his history of alcohol abuse.

renal diseaseThe patient with renal disease is often at risk for nutritional depletion. Because of

the alterations in renal function, many metabolic abnormalities occur. These may in-clude fluid retention; elevated serum potassium, magnesium, phosphorus, BUN, and creatinine; and decreased serum calcium. You’ll recall that BUN and creatinine levels can reflect catabolism of protein stores. BUN and creatinine levels can fall below their usual level with low protein intake and malnutrition (Matarese, 1993). The chart below reviews protein assessment in renal disease.

Because edema and fluid shifts are common in the pre-dialysis and dialyzed pa-tient, determination of a “dry” weight may be difficult. “Dry” weight can be determined at the end of dialysis and is defined as the weight at the end of dialysis. Weight should be evaluated as a comparison of usual weight to ideal body weight.

Changes in weight are often due to fluid shifts and changes, so once this baseline weight is established, weight should be monitored daily in the hospitalized patient. Weight gain of greater than 1/2 to 1 kg/day generally reflects fluid gain rather than an increase in lean body mass. Anthropometric measurements in the renal patient are often invalid as well, because of the edema.


Evaluation of the patient, utilizing a visual overview, is important in the nutritional assessment of this particular group of patients. Wasting of muscle mass and depletion of fat stores may be obvious. A complete dietary history is important to evaluate the ad-equacy of caloric and protein intake.

The dietary history can also provide valuable information about the patient’s intake of potassium, sodium, phosphorus, and fluid (Matarese, 1993; Liftman, 1989). Questions should also be asked about the use of vitamin/mineral supplements and about what types of medications are used.

Other components of the dietary history are important as well; these include evalua-tion of ability to chew and swallow, ability to procure and prepare meals, and evaluation of appetite and the presence of any gastrointestinal symptoms.

Laboratory values are sometimes difficult to evaluate in the patient with renal dis-ease. Serum albumin, with its half-life of 21 days, is also profoundly affected by changes in fluid status. Levels can be elevated with dehydration but depleted in fluid overload. Albumin levels may also become depleted with chronic losses associated with nephrotic syndrome and with chronic poor intake.

Protein Parameters

Albumin Affected by fluid shifts Increased protein losses w/nephrotic syndrome May be supplemented during dialysis Long half-life

Transferrin Better indicator in renal disease Less impacted by fluid shifts Increased with iron deficiency

Prealbumin Increased in renal disease

Retinol-binding protein Increased in renal disease


Albumin is, not uncommonly, given during dialysis in the patient who may have dif-ficulty tolerating the dialysis and changes in fluid. This administration, as well as adminis-tration of whole blood and plasma, can cause a transient elevation in serum albumin.

Transferrin may be a more accurate indicator of nutritional status because of its half-life of eight days. Transferrin levels are impacted by hydration status, but to a lesser degree than albumin levels. Transferrin levels are affected by many of the same factors as albumin levels; these include surgery and sepsis.

Transferrin levels are also increased with iron deficiency, a common problem among renal patients. Treatment of this anemia with recombinant human erythropoietin neces-sitates assessment of iron stores, including serum transferrin, total iron binding capacity (TIBC), serum iron, and ferritin.

Thyroxine-binding prealbumin may become elevated in renal disease because the diseased kidney is unable to break it down as effectively as the healthy kidney. Retinol-binding protein is filtered and metabolized by the kidney and serum levels are often elevated in the patient with renal disease.

Glucose levels can increase if the patient is noncompliant with his diet (many renal disease patients are also diabetics). Elevated levels can also be present with infection and end-stage renal disease because of uremia. Alkaline phosphatase increases with the bone disease associated with renal disease. Electrolyte levels are often skewed and require close monitoring and correction.

Calcium levels may decrease because of the end-stage renal disease, but also be-cause of elevated phosphorus levels (remember that calcium and phosphorus maintain a balance intra- and extra-cellularly). A patient who is vitamin D deficient or deficient in magnesium will also have low calcium levels. Both phosphorus and magnesium increase with progressive renal failure and levels should be monitored.

Laboratory Values with Renal Disease

Glucose Increased w/dietary noncompliance Increased w/infection Increased w/uremia

Alkaline phosphatase Increased w/renal bone disease

Electrolyte levels Increased or decreased

Calcium Decreased because of elevated phosphorus or decreased vitamin D

Phosphorus Increased


Evaluation of protein intake and protein status can be accomplished with determina-tion of protein catabolic rate and with urea kinetic modeling. Nitrogen balance studies are difficult to obtain and are made invalid because of the accumulation of fluid and the end products of catabolism in the patient with renal failure. For that reason, urea kinetic model-ing was developed in the 1970s; this can be used to assess protein and nitrogen balance.

Protein catabolic rate (PCR) is done to determine the amount of protein catabolized in a day’s time; this number is then compared to the protein intake and nitrogen balance is determined (Davis, 1991). Before PCR is determined, urea nitrogen generation rate (GUN) must first be figured. GUN is determined by multiplying the residual urea clear-ance by the BUN. The residual urea clearance (KrU) is determined by evaluating urinary urea nitrogen in comparison to changes in BUN with dialysis (Matarese, 1993; Davis, 1991; Murray, 1986). The chart below shows the calculation of KrU.

So, what do we do with this figure of residual urea clearance? KrU can be plugged in to the urea kinetic modeling equations for those patients who still produce urine; i.e. the non-dialyzed patient. For the dialyzed patient, urea kinetic modeling can be deter-mined whether or not the patient is producing urine.

Figuring total body water is necessary to determine urea nitrogen generation rate (GUN). The distribution of urea in the body correlates well to total body water. To deter-mine total body water, a nomogram can be used to determine body surface area. Anoth-er method is to estimate total body water (TBW) by using 58 percent of lean body weight for men and 55 percent of lean body weight for women (Davis, 1991). This figure is then used in the determination of urea nitrogen generation rate (GUN). This calculation var-ies with the patient status and is reflected in the table on the following page.

KrU = UUN x UV BUN t

KrU = residual urea clearance (ml/min)UUN = urinary urea nitrogen (mg/ml)

BUN = mean BUN = BUN1 + BUN2 (mg/ml) 2UV = urine volume (ml)t = time of urine collection (minutes)BUN1 = post-dialysis BUN (mg/ml) or first BUN measuredBUN2 = pre-dialysis BUN (mg/ml) or second BUN meaured

Calculation of Residual Urea Clearance (KrU)


nitrogen balanCeNitrogen balance can be determined, utilizing protein catabolic rate (PCR) and com-

paring it with nitrogen intake, as shown below.

Nitrogen balance = Nitrogen intake – [PCR + (2-4gm)] 6.25

Nitrogen balance gives an indication of the amount of protein being utilized by the patient and can indicate the level of protein intake required. Other methods to determine protein requirements in various forms of renal failure are shown in the following table (Matarese, 1993):

For the patient who is nutritionally stable and not dialyzed: a. Calculate KrU: KrU = UUN x Uv BUN t b. Calculate GUN: GUN = BUN x KrU c. Calculate PCR: PCR = (GUN + 1.2) (9.35)

For the patient who is nutritionally unstable but not dialyzed: a. Calculate KrU: KrU = UUN x Uv BUN t b. Calculate GUN: GUN = (BUN2 - BUN1)(Vu) + (KrU x BUN ) O c. Calculate PCR: PCR = (GUN + 1.2) (9.35)

For the dialyzed patient who is anuric (does not produce urine) a. Calculate GUN: GUN = (Vu2 x BUN2) - (Vu1 x BUN1) O b. Calculate PCR: PCR = (GUN + 1.2) (9.35)

For the dialyzed patient who has nitrogen losses in urine: a. Calculate KrU: KrU = UUN x Uv BUN t b. Calculate GUN GUN = (BUN1 x Vu2) - (BUN1 x Vu1) +BUN x KrU O c. Calculate PCR: PCR = (GUN + 1.2) (9.35)

Urea Kinetic Modeling

PCR = protein catabolic rate (g/24 hrs) GUN = urea nitrogen generation rate (mg/min) PCR (g/24hr) = [GUN(mg/min) + 1.2] x 9.35 KrU = residual urea clearance (ml/min) UUN = urinary urea nitrogen (mg/ml) BUN = serum urea nitrogen (mg/ml) Uv = volume of urine collection (ml)BUN = mean BUN = BUN 1 + BUN2 (mg/ml) 2

t = time of urine collection (min) Vu = estimated urea volume of body water (ml) O = time interval between blood samples (min) BUN1 = post-dialysis BUN (mg/ml) or first BUN measured BUN2 = pre-dialysis BUN (mg/ml) or second BUN measured Vu1 = urea volume of dry body weight gain (ml) Vu2 = Vu1 + interdialytic weight gain (ml)


Another method to determine protein requirements is with utilization of glomeru-lar filtration rate (GFR). Protein is restricted according to the level of glomerular filtra-tion per minute, with more protein being allowed with a higher GFR.

Glomerular filtration rate is determined by looking at the patient’s age, sex, and serum creatinine levels. Calculations to determine GFR are shown below

Caloric requirements can be determined through indirect calorimetry, by using a factor/kg, or by using a factor/BEE, as shown on the following page.

Glomerular Filtration Rate For women: GFR = [98 - 0.8(age - 20)] x 0.9 serum creatinine

For men: GFR = [98 - 0.8(age - 20)] serum creatinine

Protein Restriction

GFR Protein allowed 25 - 70 0.6 - 0.7 gm/kg/day <25 0.28 gm/kg/day <5 1.0 - 1.2 gm/kg/day (with dialysis)

Protein Requirements: Renal Disease

Pre-dialysis 0.6 - 0.8 gm/kg/day Acute renal failure with continuous renal replacement therapy 1.5 - 2.0 gm/kg/day Chronic failure w/hemodialysis 1.2 gm pro/kg/day Chronic failure w/peritoneal dialysis 1.2 to 1.5 gm pro/kg/day


Since water-soluble vitamins are lost in the dialysate, supplementation of these vita-mins becomes necessary. In performing a nutritional assessment on a dialyzed patient, we should be aware of the symptoms of deficiency of pyridoxine, ascorbic acid, and folic acid, since need for these vitamins appears to be greater in dialyzed patients (due to inadequate intake and increased losses).

The need for supplementation of fat-soluble vitamins is as yet undetermined, but supplementation of vitamin A should be avoided because of the danger of toxicity. Min-eral supplementation is not generally recommended because of the potential for toxicity with decreased renal clearance. However, we should be aware of the potential for zinc deficiency, especially in the patient with uremia on dialysis.

Reports that at least 60 percent of hemodialyzed patients are malnourished (Da-vis, 1991) should reinforce the knowledge that nutritional assessment and appropriate nutritional support is vital in this group of patients. Knowledge of the types of deficien-cies that can occur is important. We should also be able to evaluate protein status and requirements and should be able to predict caloric requirements so that the patient does not become further malnourished.

Case study: renal disease MM was an active 38-year-old woman with lupus. She was 5' and weighed 176 lb.

She was admitted to the ICU in respiratory failure and appeared to be in renal failure, which was thought to be acute. Her needs were assessed at 1700 to 2100 kcal/day and 60 to 90 gm protein/day.

An adjusted body weight of 55 kg was used and caloric needs were established utilizing a factor of 30 to 40 kcal/kg. Protein needs were established using a factor of 1.0 to 1.5 gm/kg. BUN was 69, creatinine was 5.2, phosphorus was 8.3, albumin was 3.1. Abnormal labs were explained as being related to the renal failure. The mild protein depletion was related to recent poor intake; it later progressively depleted further as a result of the stress of the renal and respiratory failure. Albumin levels dropped to a low of 2.3, but as MM improved, her albumin levels gradually rose to 2.7 and continued to improve.

Caloric Requirements Starvation/mild stress 1.0 to 1.3 x BEE Moderate stress 1.5 x BEE Sepsis 1.75 to 2.0 x BEE

Or the following calculations can be utilized: Weight maintenance 30 to 35 kcal/kg Weight loss 25 kcal/kg Weight gain 35 to 40 kcal/kg


Eventually, MM was able to tolerate enteral feedings of Nepro. MM progressively improved and eventually was able to initiate oral intake and her enteral feedings were discontinued. Her nutritional status continued to improve.

While she continued to require daily dialysis, it was hoped that her renal function would improve enough to allow for less frequent (or even cessation of) dialysis.

Case study #2: renal diseaseMP is a 67-year-old female admitted with congestive heart failure and end-stage

renal disease. She also has a history of chest pain, hyperlipidemia, hypertension, and hy-pothyroid. Her medications include Synthroid, Lopid, Lopressor, Procardia XL, Lanoxin, Vasotec, PhosLo, Nephrocaps, Colace, and Senokot. She is 5' and weighs 54.4 kg (111 per cent of IBW). BUN is 53, cr is 8.8, Na is 133, K is 5.5, Cl is 97, CO2 is 20, glucose is 105, alb is 3.8, phos is 8.5 with calcium of 8.9, and chol is 117 with TG of 313.

MP claims to follow a low sodium diet at home and that her weight varies with dialysis. Her primary complaint is of constipation. After further questioning, we deter-mine that she has had excessive fluid intake since her last dialysis three days earlier; this has contributed to her developing congestive heart failure.

MP appears fairly well nourished, with typical lab values for a dialysis patient. She may not be fully compliant with her diet or medications at home, however, as evidenced by fluid overload, elevated phosphorus, and continued elevation of her triglyceride lev-els. Ongoing diet instructions must continue.

review questions1. Why does the COPD patient often present in a malnourished state?2. What changes occur in lung function with malnutrition?3. Your patient is a 5’3" 90 lb female with emphysema. What are her nutrient require-

ments?4. List three reasons for the weight loss seen with cancer.5. What nutritional problems occur with small bowel resection?6. Your patient is a 6', 160 lb man with lung cancer. He has had a left lower lobe resection

and is currently undergoing chemotherapy. What are his nutrient needs and what nutritional problems should you look for?

7. What biochemical abnormalities occur with liver disease?8. Would anthropometrics be of use in assessment of liver failure patients?9. Your patient is a 5’10" 170 lb male who presents with cirrhosis related to alcoholic liver

disease. He is alert and oriented and is able to take some food orally. You’re asked to assess nutrient requirements.

10. What is the best laboratory assessment of protein status in the patient with renal disease?

11. What vitamins may need supplementation in renal failure?


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132:1347-1365, 1985.Windisch PA, Papatheofanis FJ, Matuszewski KA. Recombinant human growth hormone for AIDS-

associated wasting. Ann Pharmacother 32(4):437-445, 1998.


Chapter Eight:Nutritional Assessment

in Disease States,Part II

CardiaC disease While it was once thought that the heart was spared from malnutrition, it has now

become clear that the heart can be profoundly impacted by nutritional depletion. Nutri-ents impacting cardiac function include thiamin, potassium, calcium, phosphorus and magnesium.

With malnutrition, a decrease in cardiac size (volume) occurs; this is proportional to the decrease in body weight. This occurs not only in cardiac patients who become malnourished, but also is not uncommonly seen in patients with anorexia nervosa (Mills, 1985).

We’re also aware that thiamin deficiency, beri-beri, can cause cardiac problems. Beriberi presents as congestive heart failure and arrhythmias. While beriberi is not com-monly diagnosed in the United States, it can occur in alcoholic patients who are thiamin deficient. Chronic thiamin deficiency can lead to structural changes in the heart. I once had a patient, an immigrant from Vietnam, who was diagnosed as thiamin deficient. This deficiency was likely directly related to her diet, which consisted primarily of re-fined rice and fish.

Other nutritional deficiencies that can impact cardiac function are depletion of cal-cium, magnesium, potassium, and phosphorus (Mills, 1985). These ions play a role in the electrical stimulation of the heart, and thus can impact normal rhythms. The patient with significant cardiac compromise may well be at risk for malnutrition.

Cardiac cachexia has been defined as the syndrome of severe under- or malnutri-tion found in patients with chronic congestive heart failure (Mills, 1985; Poindexter, 1993). Congestive heart failure is a condition that happens when the heart is unable to pump adequate oxygenated blood out to all of the other organs and extremities. What


results is an increase in total body water because the heart is unable to effectively pump the fluid out.

Patients with congestive heart failure are often underweight and complain of early satiety and poor appetite. The weight loss may, in fact, be greater than what is appar-ent, because of the fluid retention (Poindexter, 1993; Talamini, 1987). Appetite and intake may be diminished not only because of the illness, but also because of the treatment for the illness. Low sodium diets may be unappealing to the patient who is not accustomed to this type of restriction.

Medications utilized to treat the illness can cause nausea and vomiting. Diarrhea may occur because of malabsorption associated with hypomotility (which can occur because of diminished blood flow to the gastrointestinal tract) as well as the medications that may be prescribed to treat the underlying illness.

Nutrient requirements increase because of an increased work of breathing (similar to that of a patient with COPD) and increased demands of the enlarged heart (Mills, 1985). A decreased intake of adequate nutrients accompanies these increased nutrient demands.

Not only does the patient decrease his intake because of nausea, etc., but he will also be at risk for decreased intake because of depression associated with the illness, a decreased ability to procure, prepare, or even eat meals, and an inability to digest ade-quate amounts of foods. This occurs because of the venous engorgement of the stomach, liver, and pancreas and can cause intolerance to normal amounts of food intake (Poind-exter, 1993; Talamini, 1987). Digestion may also be impeded by decreased oxygenation to the tissues of the gastrointestinal tract because of the inability of the heart to pump as efficiently.

A vicious cycle then begins, as the compromised heart leads to malnutrition and the malnutrition further compromises the heart. A normal response to congestive heart failure is enlargement of the ventricle. This enlargement or compensation does not oc-cur with malnutrition (Poindexter, 1993). The ventricular wall then becomes stiff and there is atrophy of the myocardial cells. Cardiac reserve becomes limited or absent.

In assessing the patient with congestive heart failure, we must take into consider-ation that weights may not be reflective of true weights, because of the fluid retention. Albumin and transferrin levels may be depleted because of inadequate intake, because of decreased production in the liver, and because of the dilutional effect of the excess fluid volume (Poindexter, 1993; Talamini, 1987).


Because of decreased perfusion to other organs, the kidney function is compro-mised. As a result, BUN and creatinine levels may be elevated. Diuresis of the excess fluid may be accompanied by a decrease in potassium levels because of the wasting of potassium that can occur with the use of some diuretics. Diuretics can also cause deple-tion of calcium, sodium, magnesium, thiamin, zinc, iron, and folate (Talamini, 1987).

Nutrient intake should be evaluated, as with other patients, with a dietary history, and, in the hospital, with calorie counts, to assure adequacy. Nutrient requirements are shown below (Poindexter, 1993).

Nutritional support of the cardiac patient with congestive heart failure should be carefully administered because of the danger of fluid overload.

Biochemical Changes: Congestive Heart Failure

Decreased levels: Albumin Transferrin Potassium Calcium Sodium Magnesium

Increased levels: BUN Creatinine

Deficiencies of: Thiamin Zinc Iron Folate

Nutrient Requirements: Congestive Heart Failure Caloric requirements: No stress: 1.2 to 1.3 x BEE Stress: 1.3 to 1.5 x BEE

Protein requirements: 1.2 to 1.5 gm/kg/day

Vitamin/Mineral requirements: Multivitamin every day Supplementation of magnesium, calcium, iron, and zinc as needed.


Case study #1: CardiaC diseaseMG is a 62-year-old female who is admitted to the critical care unit with conges-

tive heart failure and diabetes mellitus. She describes shortness of breath, recent poor appetite and intake, no recent weight loss, and a general malaise. Her laboratory values reveal an albumin level of 2.5; BUN is 32, cr is 1.5, potassium is 2.9, cholesterol is 300 and glucose is 205. She is 5' tall and weighs 134 lb; her typical weight is 160 lb. Her medications include Mevacor, Lasix, potassium supplements, an antihypertensive agent, an oral antihyperglycemic agent, and estrogen replacements. She is determined to be fluid overloaded and after gentle diuresis, her weight is 120 lb. Her albumin level rises to 2.7 and potassium corrects to normal with appropriate potassium replacement.

As her shortness of breath resolves after diuresis, her appetite slowly returns and her intake improves to meet her needs of approximately 1400 kcal/day and 60 gm pro-tein/day. She is counseled on a 1500 kcal diabetic 2 gm sodium diet and is instructed to limit her fluid intake to 1500 to 2000 cc/day. She is discharged on the same medications and is followed as an outpatient.

MG’s laboratory values are typical of the patient with CHF and she may become at risk for cardiac cachexia. Clearly, her renal function is slowly becoming compromised because of inadequate perfusion or the effects of diabetes mellitus. She is retaining fluid as is evidenced by the weight loss with diuresis; the albumin level corrects slightly with removal of fluid but remains depleted, likely related to her recent poor intake. This could be indicative of early malnutrition.

Case study #2: CardiaC diseaseRR is a 65-year-old male hospitalized with an acute myocardial infarction. His

medical history includes: unstable angina, hypertension, smoking, thirty pound weight loss over the last three months (22 percent of his usual weight), anemia, and an aor-tobifemoral graft. His admitting weight is 49.5 kg at a height of 5’4". His medications included Norvasc and Pepcid. Admitting lab values were fairly normal except for a CPK of 729, albumin of 3.4, hemoglobin of 9.7, and cholesterol of 121. He relates a history of a full gastrointestinal workup that was negative. Plans are made for a transfusion and a cardiac catheterization.

He is placed on a cardiac diet and requests a diet consult. He states that he always gets hungry when hospitalized and wants larger portions and an HS snack. He further states that he eats when he gets hungry at home, usually once per day. His needs are assessed to be 1300 to 1700 kcal/day and 50 to 75 gm protein/day. Preferences are noted and a snack at bedtime is provided. He is eating 100 per cent of his meals and snacks and gradual weight gain is noted. He is determined to be at moderate nutritional risk related to his anemia and recent unexplained weight loss.

My thoughts on his weight loss is that it may be related to an inadequate intake at home (remember that he “eats when hungry – once per day” and that his cholesterol is 121). The fact that he is ravenous in the hospital could be related to his inability to smoke


while hospitalized. We must consider, though, that his metabolic rate may be elevated and that he may be unable to eat much at one time because of underlying cardiac or pulmonary disease.

Gastrointestinal diseaseDiseases of the gastrointestinal tract can play a significant role in the development

of malnutrition. Just as significant is the role malnutrition can play in the alteration of normal gastrointestinal function. Assessment of this group of patients must include a review of the affected portion of the digestive tract and should consider treatments for the illness itself, to include surgery and medications. We’ve already discussed the impact of therapies for the treatment of cancer on the gastrointestinal tract and will not repeat that discussion here.

Evaluation of the patient with problems of the gastrointestinal tract should begin with a diet history and an evaluation of any chewing or swallowing problems. The pa-tient who has had a cerebral vascular accident or other neurological or muscular diseas-es may experience dysphagia (difficulty in swallowing). A speech pathologist can be of assistance in determining the degree of dysphagia, where the problem lies and with the treatment of the problem. A modified barium swallow or video esophagogram can also be used to determine the extent of the patient’s swallowing disorder. Other problems associated with the mouth that can contribute to malnutrition are shown in the chart below.

Factors Affecting Nutrition

EsophagusStricturesVaricesSurgical resection

StomachSurgical resection GastrectomyGastroparesisGastric outlet obstruction

MouthPoor dentitionStomatitisDysphagiaSwallowing disordersSurgical procedures: - Glossectomy - Surgical resection - Jaw wiring - Corrective surgery


The esophagus may contribute to nutritional depletion if the patient has difficulty swallowing because of strictures, resection due to cancer, or if esophageal varices related to liver disease are present. Problems associated with the stomach can have a significant impact on nutritional status. While the body usually adapts to resection of the stomach, or gastrectomy, nutritional problems can and do occur.

If a patient has had a portion or all of his stomach removed, look for deficiencies of B12, unless B12 injections are given. Intrinsic factor may be absent with any resection of the stomach and intrinsic factor is necessary for the absorption of vitamin B12. Gastrec-tomy can also cause dumping syndrome because of the loss of the pyloric sphincter between the stomach and duodenum. Dumping can cause malabsorption of carbohy-drates and fats, as well as some vitamins.

The presence of a gastric outlet obstruction can prevent adequate nutrient intake. This problem can occur with stenosis of the pylorus and changes in gastric empty-ing time related to surgery (Lang, 1989). With any problem of the stomach, significant weight loss is not uncommon (Stralovich, 1993). Iron deficiency anemia may occur with decreased amounts of gastric acids; this can occur with gastrectomy, with drug treatment to decrease gastric acid secretions, and in the elderly.

The area where most digestion occurs is in the small intestine, to include the duo-denum, jejunum, and ileum. Protein is metabolized to amino acids, fats to glycerol and fatty acids, and carbohydrates to mono- and disaccharides. Inflammatory bowel disease, including Crohn’s disease and ulcerative colitis, can have a substantial effect on nutri-tional status, especially during acute phases.

inflammatory and other bowel diseasesCrohn’s disease generally occurs in all portions of the intestines (both small and

large) and can be manifested by anorexia, diarrhea, vomiting, and weight loss. Compli-cations associated with Crohn’s disease that can impact nutritional status include fistu-las, bowel perforation, bowel obstruction, and abscesses.

Ulcerative colitis occurs in the colon and is manifested by diarrhea, anorexia, and weight loss; complications include toxic megacolon, fistula, and obstruction. Nutritional deficiencies or inability to maintain weight occurs in 65 to 78 percent of patients with Crohn's disease and in 18 to 72 percent of patients with ulcerative colitis (O'Keefe, 1996; Burke, et al., 1997).

Besides the obvious problem of decreased intake, the patient with inflammatory bowel disease may well have malabsorption of protein, fat, and carbohydrate, as well as the fat-soluble vitamins, and vitamins C, B12 and folate. These deficiencies occur because of inadequate intake, malabsorption, and through drug-nutrient interactions. Because of the associated diarrhea, deficiencies of zinc, magnesium and copper can occur as well. Iron deficiency and calcium deficiency may be present. Nutrient requirements are in-creased with the presence of fistula, infection, or with the inflammatory process.


Iron deficiency anemia is common in patients with ulcerative colitis (80 percent) and with Crohn’s disease (40 percent) (Fleming, 1990). Macrocytic anemia related to malabsorption of vitamin B12 occurs with Crohn’s disease (Kelly and Nehra, 2001).

Obviously, the presence of malabsorption will lead to nutritional depletion. Mal-absorption can be caused by a number of factors; whatever the cause, the results are problematic. Malabsorption can affect all of the macronutrients, including carbohydrate (although less common), fat (related to bacterial overgrowth, decreased resorption of bile salts, administration of medications, and pancreatic insufficiency), and protein (related to enzymatic deficiencies).

Short bowel syndrome is a condition that occurs when greater than 50 percent of the small bowel is resected. A myriad of problems can then occur, with changes in motility and malabsorption. Diarrhea is common and steatorrhea (passage of large amounts of fats in the feces) may occur. Resection of the jejunum causes the body to adapt by increasing the role of the ileum. The ileum can take on the absorptive role of the jejunum, but this adaptation takes time. Initially, jejunal resection can result in mal-absorption of lactose, fat, and protein; dumping type symptoms may be present.

Resection of the ileum, on the other hand, can cause significant problems. Severe malabsorption and steatorrhea may occur, depending on the amount of the ileum that has been resected. Significant bacterial overgrowth can occur with the removal of the ileocecal valve. This occurs because of the lack of a barrier between the ileum and the colon and the migration of bacteria from the colon to the ileum. Bacterial overgrowth can cause malabsorption of carbohydrate, protein, fat, and fat-soluble vitamins.

Nutritional assessment of the patient with gastrointestinal disease should include a thorough review of any problems associated with digestion. These problems might include diarrhea, steatorrhea, vomiting, anorexia, and weight loss. We should also look for symptoms of deficiencies of fat-soluble vitamins, vitamin B12, vitamin C, folate, iron, calcium, zinc, magnesium, and other trace elements.

Nutrition Problems with GI Diseases

Protein deficiency Carbohydrate deficiency Fat malabsorption/deficiency Weight loss Anorexia Diarrhea Vitamin C deficiency Fat soluble vitamin deficiency Vitamin B12 deficiency Folate deficiency Zinc deficiency Magnesium deficiency Copper deficiency Iron deficiency Calcium deficiency Magnesium deficiency


Obvious caloric depletion is usually easily assessable, but assessment of fat and muscle stores is very important. Laboratory assessment will often reflect depletion of protein stores, with diminished levels of albumin, transferrin, and other protein mark-ers. Anemia, whether related to B12 deficiency, folate deficiency, or iron deficiency, may be present as well.

Caloric requirements may be increased by as much as 150 to 200 percent, especially in the patient with significant malabsorption after major gastrointestinal surgery. Protein requirements are increased by an equal amount, up to 2 gm protein/kg/day.

The pancreas also plays an important role in normal digestion and absorption. Pancre-atitis can be evidenced by severe abdominal pain, nausea, vomiting, and abdominal disten-tion. Serum amylase and lipase levels will be elevated; glucose and triglyceride levels may also be elevated. Calcium levels are often low. Since pancreatitis may be associated with alcoholism, we should be aware of the problems associated with this, including a deficiency of thiamin. Malabsorption may occur.

Caloric requirements are estimated to be greater in acute versus chronic pancreatitis, and are shown in the table below.

Case study: Gastrointestinal diseaseDE, a 66-year-old female, was admitted to the hospital with retroperitoneal leio-

myosarcoma and had a nephrectomy. Post-surgery, she developed pancreatitis and later developed a pancreatic fistula. Adding to the complications, she was ventilator-depen-dent.

Because of her pancreatitis and the fistula, she was placed on TPN shortly after her admission to the ICU. At that time she was 5’2" and was reported to weigh 125 lb, although this was inaccurate as her weight was later established to be 180 lb. Her abnor-mal laboratory values included an albumin of 2.0, a phosphorus of 2.6, and a glucose of 247. Her amylase was 867.

These labs could be explained in the following ways. The albumin was likely de-pleted because of recent poor intake and, more importantly, because of the recent sur-gery and the stress associated with the surgery and pancreatitis. The phosphorus could

Nutrient Requirements: Gastrointestinal Disease

Malabsorption 1.5 - 2.0 x BEE 1.5 - 2.0 gm pro/kgPancreatitis, acute 1.3 - 1.5 x BEE 1.5 - 2.0 gm pro/kg chronic 1.0 - 1.3 x BEE 1.0 - 1.3 gm pro/kg

Supplementation of appropriate vitamins and minerals is indicated


be low because of the refeeding syndrome. The glucose was likely elevated because of the pancreatitis. The amylase, of course, was a symptom of the pancreatitis.

After initiation of TPN and administration of IV albumin, DE’s albumin levels rose progressively to 3.1 after approximately three weeks on TPN. Her pancreatitis appeared to be improving and oral intake was initiated. Her albumin levels remained stable, while amylase levels dropped. She had difficulty tolerating even clear liquids, so oral intake was held and TPN was increased.

Three months after initiation of TPN, her albumin level had climbed to 3.9, but her glucose levels remained high, at 239. Amylase levels had dropped to 159, but triglyc-eride levels had risen to 362, an indication that she was no longer tolerating the fat in the TPN. With a decrease in the administration of lipid from daily to two times a week, triglyceride levels dropped to 189. DE appeared to be progressively improving and was tolerating limited amounts of clear liquids.

Two weeks later, however, she experienced a septic episode. Her albumin level dropped to 2.7, amylase levels climbed to 237 and she developed metabolic alkalosis. The alkalosis was attributed to the loop diuretics that she had been receiving and the Lasix was discontinued. Her BUN and creatinine levels rose to 55 and 2.8, respectively. Sodium was 148, potassium was 3.2, chloride was 98, and CO2 level was 39.

After her recovery from the septic episode, low rate elemental feedings, 10 cc/hour, were implemented and the TPN continued. Albumin levels rose to 3.2 and BUN and creatinine levels dropped slightly to 52 and 2.2. The alkalosis had stabilized, enteral feedings were tolerated and progressively increased.

However, the enteral feedings eventually were not well tolerated and were dis-continued. BUN and creatinine levels rose to 65 and 2.7 and albumin levels rose to 4.0. Because of the problems associated with DE’s respiratory status, the decision was made to change her TPN to a 40 percent fat, 40 percent carbohydrate mixture with 20 percent protein. Protein intake was reduced as well. She tolerated this change well, was even-tually weaned from the ventilator, and her nutrition status remained stable until her discharge to a rehabilitation hospital.

DE was a complicated patient whose pancreatitis extended her hospital stay. How-ever, her nutritional status improved throughout her stay and she was adequately nour-ished, as evidenced by her improved laboratory data and the fact that her weight did not change appreciably.

metaboliC stress and sepsisNutritional assessment of the patient who is stressed, either metabolically or emo-

tionally, or septic, is much the same as the nutritional assessment of any patient. How-ever, you should be aware of the changes that occur metabolically with stress and sepsis as the nutritional assessment is completed. Nearly all of the normal metabolic pathways may be altered with stress, causing aberrations in biochemical values and potential depletion of caloric and protein stores.


During the stress response, illustrated below, stimulation of the autonomic nervous system causes increased production of catecholamines (epinephrine and norepineph-rine), decreased release of insulin and increased release of glucagon, as shown on the following page.

The increase in catecholamines is thought to be responsible for the increased meta-bolic demands during the stress response (Shronts and Lacy, 1993). Why does this reac-tion occur? The body under stress has an increased oxygen demand; these changes allow for increased provision of oxygen and nutrients to tissues requiring them.

What follows this initial response are changes in the way nutrients are metabolized. The liver increases synthesis of glucose (by as much as 200 percent), but the glucose is underutilized because of insulin resistance, causing decreased uptake of glucose into the cells (Shronts and Lacy, 1993; Nelson and Long, 1989). This results in hyperglycemia.

Glucose synthesis increases through increased glucagon production by the pan-creas, mobilization of fatty acids from adipose tissues, and oxidation of branched-chain amino acids for gluconeogenesis. Protein depletion, as evidenced by depleted muscle mass, occurs with the use of protein for as much as 25 percent of the energy require-ments.

ACTH

The Stress Response

HYPOTHALAMUS

BRAIN (Receives stress signal)

EpinephrineNorephinephrine

Adrenal Medulla

PITUITARY GLAND

GlucocorticoidsAldosterone

Mineralocorticoids

Adrenal CortexInsulin

Glucagon

• Growth hormone• Prolactin• Vasopressin

CRF (corticotropin-releasing factor)

Neural

Sympathetic AutonomicNervous System

Pancreas TSH

Thyroid Gland

Thyroxine


Protein synthesis is decreased, with less available for immune tissues, and protein metabolism is altered, with increased production of acute phase proteins, and break-down of proteins for gluconeogenesis and ureagenesis. Muscle protein is catabolized to make amino acids available for energy and for acute phase proteins (Shronts and Lacy, 1993). Fat breakdown is increased and hepatic synthesis of fatty acids and triglycerides is increased (Hasselgren and Fischer, 1987). This change can cause an elevation of tri-glyceride levels. Ketones are decreased.

Effects of Stress Hormones on Metabolism

GlucocorticoidsIncrease: protein breakdown fat breakdown glucose mobilization

Decreases: Insulin action

AldosteroneConserves: sodium, potassium

Growth hormoneIncreases: protein breakdown fat breakdown

CatecholaminesIncrease: protein synthesis fat breakdown glucose synthesis

InsulinDecreases: protein synthesis fat synthesis GlucagonIncreases: protein synthesis glucose synthesis

GLUCOSE

Cholesterol

Fat

Carbohydrate

Protein

Increased glycogen breakdownDecreased gluconeogenesis

Decreased protein synthesisDecreased protein for immune organs and cells

Increased fat breakdownIncreased fatty liver / cirrhosisIncreased arterial plaque

Decreased steroid hormone production

Increased blood sugarIncreased glycosuriaDecreased tissue sensitivity to insulin

InsulinBlood Sugar

STRESS

STRESS

HORMONES

Alterations in Metabolism During Stress


assessmentAs stated earlier, nutritional assessment for this group of patients is much the same

as for other patients. Complete histories, including medical, dietary, and psychosocial, should be obtained. A review of pertinent medications should also be completed. An-thropometric measurements (i.e. skinfold and arm circumference measurements) are of little value. Weight should be determined and compared to preadmission weight. Changes can occur because of fluid shifts and changes in body composition.

Serum protein parameters are impacted by the stress response and can also be affected by hemodilution or hemoconcentration. Because of the shift to increased pro-duction of acute phase proteins, serum albumin levels may be depleted. Other protein parameters, such as transferrin, prealbumin, and retinol-binding protein may decline as well. Nitrogen balance studies may be helpful to determine the degree of catabolism and the protein requirements.

Cell-mediated immunity is compromised with the malnourished and stressed patient. The stress response itself may precipitate the anergy, thus the anergy may not be reflective of nutritional status.

Assessment of caloric requirements is best done through indirect calorimetry if a metabolic cart is available. However, the stressed patient may not be a good candidate for measurement through indirect calorimetry. Remember that those patients receiving a high degree of ventilatory support and patients who have air losses through chest tubes or through the tracheal cuffs are not candidates for indirect calorimetry.

While we once thought that stressed patients had much higher metabolic needs than nonstressed patients, we now know that overfeeding can be harmful to these per-sons. Caloric requirements are outlined in the table on the next page (Shronts and Lacy, 1993). Protein requirements are, obviously, increased during stress and sepsis. In fact, the desirable nonprotein-calorie to nitrogen ratio is estimated to be approximately 100:1.

LIVER(Protein synthesis)

Glucose

Tissue repair Albumin

AMINO ACIDPOOL

Gut

(enzymes, secretory IgA)

Skin(collagen)

Muscles Urea(Stress level indica-

tor)

Protein Metabolism During Stress

Acute PhaseProteins

FibrinogenComplementRetinol-binding proteinPrealbumin


Further protein requirement recommendations are shown in the table below (Shronts and Lacy, 1993).

Of course, compromise of renal or liver function should be considered when as-sessing protein requirements. It is important to note, however, that while a patient is stressed or septic, serum proteins will probably not normalize until the body shifts away from production of acute phase proteins. A rise in serum proteins may indicate that the patient is recovering. Also remember that bedrest can cause a decrease in albumin levels. Levels may not correct themselves until the patient is up and moving.

Glutamine appears to be an essential amino acid during stress and sepsis and is the preferred fuel for the gastrointestinal cells. Glutamine appears to protect the gut lining and cells from atrophy and breakdown. This breakdown of the gut lining that can occur with sepsis, malnutrition, and disuse of the gastrointestinal tract can lead to transloca-tion of bacteria from the gut to the blood. This, in turn, can lead to systemic sepsis and worsening of the patient’s condition. Glutamine is normally provided through oral or enteral intake, but is often lacking when a patient is fed via a parenteral formula.

Arginine may be an essential amino acid during stress and hypermetabolism. Arginine appears to enhance the immune response through improving the response of macrophages and lymphocytes (Shronts and Lacy, 1993; Daly, et al., 1988). Arginine also appears to stimulate the secretion of growth hormone, prolactin, and insulin (Kirk and Barbul, 1990; Alexander, 1991, 1995).

Glucose levels are frequently elevated with stress and sepsis because of the in-creased production of glucose by the liver, as well as increased insulin resistance. Fats may be well tolerated but should be limited to only 30 percent of total calories. We should monitor the tolerance of fat through review of serum triglyceride levels.

Stress and sepsis can impact the status of many nutrients. Loss of body cell mass causes losses of potassium, magnesium, phosphorus, zinc, and sulfur. Anabolism increases the needs for zinc, vitamin C, phosphorus, potassium, and magnesium. We should moni-tor these patients throughout their stay for changes associated with deficiencies of various

Caloric & Protein Requirements with Stress

Caloric Requirements25 - 30 kcal/kg/d 1.3 - 1.5 x BEE Protein Requirements1.5 - 2.0 gm/kg/d (80 - 100 nonprotein calories/gm nitrogen) (adequate glutamine and arginine)


vitamins and minerals. This monitoring can be accomplished through physical examina-tion and through assessment of laboratory data. TPN patients with stress and sepsis are most at risk for metabolic complications. Appendix #14 summarizes the metabolic assess-ment and monitoring that is necessary in these patients.

Case study: sepsis and stressJC is a 91-year-old male who is admitted to the ICU with diagnosis of “strangulated

hernia.” An exploratory laparotomy reveals abdominal sepsis, necrotic colon, and peri-tonitis. A hemicolectomy, cholecystectomy, and biopsy of a pancreatic mass is performed during surgery. A gastrostomy is placed during surgery as well.

Post-surgery, his albumin level falls to 1.3 and he becomes hemodynamically unstable. He develops respiratory failure. Appropriate measures are taken and the next day, TPN is initiated since he has become hemodynamically stable and his acidosis is improved. Antibiotics are started as well.

His laboratory values are near normal except for an albumin level of 2.2, amylase of 293, cholesterol level of 32, and triglyceride level of 47. On admission, his weight was 45 kg and he was 5’7" tall. His needs were assessed at 1500 to 1800 kcal/day and 50 to 70 gm protein/day. His TPN provided 1555 non-protein-calories, 1785 total calories, and 57 gm protein. Two days later he became unresponsive and dopamine was added for blood pressure support.

His respiratory failure progressed into adult respiratory distress syndrome. Labora-tory values remained stable but his prognosis was poor. Two days later, his abdominal sepsis worsened and he was diagnosed with multi-system organ failure.

His laboratory values of note were a BUN of 48, potassium of 5.8, phosphorus of 3.9, glucose of 158, albumin of 3.0 (he was given IV albumin), total bilirubin of 2.5, magnesium of 1.7, cholesterol of <50, and triglyceride level of 78. Three days later, after the patient showed no improvement, the decision was made to provide comfort care only.

JC was obviously malnourished upon admission with a weight at about 77 percent of IBW and severe depletion of serum albumin levels (this could also be related in part to the surgery and sepsis). Other symptoms of malnutrition are the markedly low levels of serum cholesterol and triglycerides.

His condition continued to worsen throughout his hospital stay and lab values continued to show worsening sepsis, with elevations of his WBC. A decrease in protein utilization was seen by the continued low albumin, in spite of support with IV albu-min, and rising BUN and bilirubin. Serum glucose levels rose as the patient was unable to effectively utilize glucose, and triglycerides rose as well, indicating poor utilization of fat.

The problems caused by stress and sepsis are compounded by the patient’s ad-vanced age. In the following section, we’ll discuss assessment of elderly patients in more detail.


Case study #2: stress and sepsisCF is a 77-year-old male admitted with an abdominal aortic aneurysm. His accom-

panying medical history includes: chronic obstructive pulmonary disease, arterioscle-rotic cardiovascular disease, peripheral vascular disease, hypertension, and atrial flut-ter. His surgical history includes a ruptured abdominal aortic aneurysm repair, cardiac catheterization, and embolectomy. He also has a history of developing adult respiratory distress syndrome during a previous hospitalization. He is admitted to the ICU after sur-gical repair of his AAA and is intubated. Pulses on his right foot appear diminished; an arteriogram is done and he returns to surgery for a right embolectomy and fasciotomy. His admitting weight is 79.9 kg at 5’11".

Upon discussion with his daughter and wife, we learn that he had a 30 lb weight loss during his hospitalization the previous month and his usual weight was 186 lb. (Note his current weight is approximately 176 lb.) Admitting labs include a hemoglobin of 10.0, albumin of 2.2, cholesterol of 92 with triglycerides of 88 and a glucose of 119. TPN is initiated and provides 1920 cc, 1943 kcal, and 96 gm protein, along with electro-lytes, multivitamins, and trace elements.

Two days later, labs remained stable, with the exception of BUN of 50 and creati-nine of 2.6, with a white blood count of 21.3. He remains intubated but weaning trials have begun. Transfusions and intravenous albumin are given. X-rays reveal the presence of ileus and no bowel sounds are present.

This patient is determined to be at serious nutritional risk as evidenced by a 30 lb weight loss over one month (it’s possible that his weight of 79.9 kg is artificially high because of fluid overload with the fluids given during surgery); albumin of 2.2 (this could be artificially low because of the fluid and third spacing and should improve with the administration of IV albumin); a low cholesterol; recent poor intake; and significant medical and surgical history.

His needs are determined to be 2000 to 2400 kcal/day and 80 to 96 gm protein (ad-justed to 1 to 1.2 gm/kg with the possibility of renal failure [as indicated by the elevated BUN and creatinine]).

Case study #3: stress and sepsisDG is a 73-year-old male admitted with differential diagnosis of acute appendicitis.

He is taken to surgery for an appendectomy and is found to have an infarcted bowel; a resultant cecotomy and incidental appendectomy is performed. DG’s course progresses routinely until post-op day #2, when he develops a fever. He continues to spike temper-atures to 103° F, becomes diaphoretic, and is disoriented.

He is transferred to the ICU and diagnosed with septic shock. His comorbidities include a history of a coronary artery bypass graft (CABG) 15 years prior, cardiomyopa-thy with an ejection fraction of 27 percent, left bundle branch block, and congestive heart failure.


Diagnostic tests reveal leakage at the anastomosis and DG returns to surgery for a bowel resection with resultant ileostomy. Post surgery, he continues with support from mechanical ventilation, pressors (to support blood pressure), and antibiotic therapy. He is sedated with Diprivan (propofol), a short half-life sedative that is lipid-based. His admitting weight of 175 lb has increased to 195 lb post-operatively. His albumin is 1.3, BUN 52, cr 2.2, hemoglobin 9.2, bilirubin 9.6, and glucose is 158.

DG’s needs are determined to be 1800 to 2100 kcal/day and 80 to 120 gm protein/day. TPN is initiated with a total nutrient admixture providing 1700 kcal and 84 gm pro-tein. The propofol provides an additional 350 kcal/day. Triglyceride levels are checked the following day; levels return at 713 and the lipid is removed from the TPN. Triglyc-eride levels remain greater than 400, even after the propofol is discontinued. The family reports no known history of hyperlipidemia.

This patient is determined to be at serious nutritional risk as evidenced by severe hypoalbuminemia, two surgical procedures within five days, significant sepsis, poor tolerance to full nutrition support related to sepsis and a “shock liver”, and the inability to readily utilize the GI tract due to “leaky” anastomosis, sepsis, and a resultant abscess.

nutritional assessment of elderly patientsOur population is aging; the incidence of older Americans (greater than age 65)

who have chronic diseases and conditions is estimated to be at 85 percent (Burns, 1992). As aging occurs, many physiological changes occur as well. Lean body mass decreases by as much as 1 to 2 percent per year, affecting all organs (Baden, Karkeck, and Chernoff, 1993). Skeletal and visceral protein stores diminish, along with an increase in adipose tissue. These changes are affected by both physiological changes and changes in lifestyle (Szauter, 1993).

Sarcopenia is present, characterized by a decline in skeletal muscle mass, and may be caused by alterations in cytokine regulation and changes in growth hormone, andro-gen, and estrogen production, changes in intake and protein metabolism, and lifestyle alterations, resulting in muscle atrophy (Evans, Campbell, 1993; Kehayias, Heymsfield, 1997; Lexell, Dutta, 1997).

Physical Changes with Aging

Decreased lean body mass Decreased cardiac functionDecreased skeletal protein stores Decreased kidney functionDecreased visceral protein stores Decreased GI motilityIncreased adipose tissue Decreased absorption: Decreased total body water B12 , fat, iron,calcium, zincDry mouth Change in taste sensationDecreased immune efficiency


Starting at age 30, adipose tissue increases by 0.5 to 1.5 percent per year. A decline in total body water occurs and there is a generalized decrease in bone density (Burns, 1992; Baden, Karkeck, and Chernoff, 1993).

The function of organs becomes altered in aging. Cardiac function becomes less efficient, with decreased oxygen transport. Renal function also diminishes, resulting in decreased glomerular filtration rates and increased serum creatinines. The functional ability of the gastrointestinal tract is changed, with decreased motility and malabsorp-tion, especially of fat.

Decreased absorption of vitamin B12 is common because of the decrease in the amount of gastric acid secreted (and, thus, intrinsic factor). There is decreased absorp-tion of iron, calcium, and zinc as well.

Diverticular disease and constipation is common. It’s estimated that as many as 50 percent of people over 65 have lost their teeth (Burns, 1992). This is accompanied by xerostomia (dry mouth) and altered taste sensation (Szauter, 1993). The elderly are more susceptible to infection because of the less efficient immune function, as evi-denced by decreased levels of response to antigens (Baden, Karkeck, and Chernoff, 1993).

Aside from these physiological changes, the elderly are subject to changes in their nutritional status because of the inability to purchase or prepare foods, either because of financial limitations or physical limitations. Because the elderly often have to purchase medications on a limited income, there may be no money left to purchase good quality food, subjecting them to the possibility of under- or malnutrition. The elderly may be more subject to depression, especially after the death of a spouse or significant other. Ap-proximately 15 to 40 percent of elderly people are alcoholics. We’ve reviewed the prob-lems associated with alcohol abuse; these are the same or are exacerbated in the elderly (Collinsworth, 1991).

The elderly often take numerous medications, both prescription and over-the-coun-ter. This problem can be significant because of the drug-nutrient interactions that can occur. As stated earlier, the purchase of medications can overrule the purchase of food. Medications can alter nutrient intake; cause anorexia, decreased digestion and absorp-tion; and change metabolic rates.

In assessing nutritional status of the elderly, the first steps should be the attain-ment of an accurate height and weight. As with other patients, assessment of any weight change should be made. Height of the elderly tends to decrease because of bone disease, vertebral collapse, and other changes. Other anthropometric measurements are of little use in the elderly because there are no good standards established for this population (Szauter, 1993). Anthropometrics are also difficult to obtain in the elderly because of changes in body composition and skin turgor.

Perhaps a better indicator of weight and height status is a measurement of body mass index (Burns, 1992; Baden, Karkeck, Chernoff, 1993; Szauter, 1993). BMI correlates well with body fat and can be easily calculated by dividing body weight (kg) by the


square of the height (meters), as shown on the next page. (The woman in the example shown below may be nutritionally depleted.)

The BMI may appear to be skewed according to factors we use to evaluate other patients, but remember that the elderly have higher levels of body fat.

Laboratory parameters may or may not be helpful in this population. Serum albu-min appears to be the most reliable measure of protein status, but is normally low in the elderly and can be impacted by fluid status (Baden, Karkeck, and Chernoff, 1993; Sza-uter, 1993). Since transferrin level is associated with iron status, it is not as good a mea-sure because of the higher incidence of iron deficiency anemia in the elderly.

Prealbumin and retinol-binding protein appear to be just as sensitive markers in the elderly as in the younger population. Serum cholesterol levels are an important evalu-ating tool: low levels (less than 160 mg/100 dl) may signify inadequate intake. Other laboratory parameters appear to be well maintained and are of the same validity as they are in the younger population. Cell-mediated immunity testing reflects increased anergy with aging.

In assessing our elderly patients, we should take the time to get a complete dietary history, eliciting help from caregivers and family members and determining whether the patient uses such programs as Meals on Wheels and Senior Citizen’s Centers. We should inquire and check on dentition and oral problems and look for symptoms of vitamin deficiencies in the mouth. We should examine the patient’s ability to purchase, prepare, and eat meals. We should examine the medical history for cerebral vascular accident, chronic illness, etc.

Calculation of Body Mass Index BMI = weight (kg) ÷ height (m)2

Desirable BMI: 24 - 29 Possible nutrient depletion: <24 Possible obesity: >27

Example 70-year-old woman who is 5'3" and weighs 125 lb

125 lb = 56.75 kg 63 inches = 160 cm = 1.6 m

BMI = 56.75 1.6 m2

BMI = 22.17

= 56.75 2.56

= 22.17


The Nutrition Screening Initiative has outlined the best indicators of poor nutrition status, as noted in the following table.

What are the nutritional requirements of the elderly? Basal energy requirements appear to diminish with age because of changes in activity levels and increased fat stores with decreased lean body mass. Use of the Harris-Benedict equation may be valid because it accounts for age (Baden, Karkeck, and Chernoff, 1993). Appropriate factors for stress may be applied.

Protein requirements appear to be the same as for the younger population. For maintenance and without the presence of renal or liver disease, recommendations have been made for protein intake of 1.0 to 1.1 gm/kg. Fat intake should be limited to ap-proximately 30 percent of total calories, but may be liberalized if intake is poor and the patient is losing weight.

Requirements for vitamins B6, B12, and folate may increase in the elderly. This oc-curs because of the decreased production of gastric acids and resultant decreased ab-sorption of folate and B12. In addition, many drug-nutrient interactions decrease avail-ability of folate and B6. Fat-soluble vitamin nutriture should be monitored. Sulfa drugs and anticoagulation drugs can alter absorption and effectiveness of vitamin K. Vitamin D levels may diminish because of lack of exposure to sunlight and decreased intake of

*Activities of Daily Living: Bathing, Transferring, Dressing, Continence, Personal hygiene, Feeding

**Instrumental Activities of Daily Living: Shopping, Food preparation, Transportation, Use telephone,

Housekeeping, Laundry, Managing finances, Managing medications

Indicators of Poor Nutritional Status Significant weight loss over time loss of 5 percent in 1 month loss of 7.5 percent in 3 months loss of 10 percent in 6 months Significantly above IBW (>20 %) Significantly below IBW (<20 %) Significant decrease in albumin (<3.5 gm/dl) Significant change in function loss of 2 ADL* or one nutrition-related IADL** Inappropriate food intake Other nutrition-related disorder: e.g. osteoporosis, folate deficiency


foods containing vitamin D, among other reasons. Increased needs for fat-soluble vita-mins may exist because of decreased absorption and metabolism.

Little research on the nutritional needs of the elderly has been completed. With the aging population in the United States, it is clear that we need better tools and standards for assessment of the nutritional status of the elderly.

Case study: elderly patientEB was a 93-year-old woman admitted to the hospital with pneumonia and for a

cholecystectomy. She had a history of “heart problems,” hypothyroidism, arthritis, car-diomegaly, and a poor appetite for three days. She was 5’2" and weighed 120 lb.

A history of dementia was reported by the husband. Her admitting laboratory data included an albumin of 3.1, iron level of 6, hemoglobin of 11.7, hematocrit of 35.3, and an MCV of 75. Her medications at home included Cardizem, indomethacin, Voltaren, thyroid, nitroglycerin, and prednisone. While hospitalized, IM B12 injections were given and iron supplementation was initiated since it had become evident that she was B12 and iron deficient.

After cholecystectomy, her laboratory data included: albumin of 2.5, Hgb of 11.9, Hct of 36.6, MCV of 74, and MCH of 24.1. Her sodium level dropped to 131, likely because of overhydration during surgery. This could also partially explain the drop in serum albumin levels. She remained confused and oral intake was poor.

Her needs were estimated to be 1400 to 1600 kcal/day and 55 to 65 gm protein/day, based on a weight of 55 kg with a factor of 25 to 30 kcal/kg/day and 1.0 to 1.2 gm protein/kg/day. (Note: In elderly patients it is important not to overfeed protein, since renal function may be somewhat compromised. It is better to be conservative so as not to tax the kidneys.)

EB’s intake slowly improved but remained inadequate related to her confusion. Lab values remained stable and she was discharged for further recuperation to a skilled nursing facility.

review questions1. The CHF patient may become malnourished and suffer from cardiac cachexia. What

causes this weight loss and depletion of nutritional stores?2. What nutritional problems can occur with a gastrectomy?3. Your patient has had an ileal resection with removal of the ileocecal valve. What nutri-

tional problems might you anticipate?4. Your patient is admitted with an increased amylase and lipase. Glucose is 286 and TG

level is 600. What are the protein/calorie requirements for this 5’4", 125 lb, 60-year-old female?

5. What amino acids appear to become essential in the stressed state?


6. A 20-year-old male, 6' tall and weighing 150 lb, is admitted to ICU after a motor ve-hicle accident with a broken femur, fractured pelvis and internal injuries. What are his nutrient requirements?

7. What changes occur physiologically with aging?8. Your patient is a 78-year-old male who is 5’9" and weighs 150 lb. Calculate BMI and

assess nutritional status.

referenCesAlexander JW. Arginine and lipids. Unpublished lecture at ASPEN 15th Clinical Congress, 1991.Alexander JW. Arginine. Unpublished lecture at Advances in Clinical Practice: Disease-Specific Nutri-

tion Support, San Diego, 1995.Baden A, Karkeck JM and Chernoff R. Geriatrics. In: Nutrition Support Dietetics, 2nd ed. Gottschlich

MM, Matarese LE, and Shronts EP, Eds. Silver Spring MD: ASPEN, 1993.Burke A, Lichtenstein GR, Rombeau JL. Nutrition and ulcerative colitis. Baillieres Pract Res Clin Gas-

troenterol 11: 153-74, 1997.Burns JT. Nutritional assessment: adjusting for age. Support Line XIV No. 4, 1992.Collinsworth R. Elder Care. AORN Journal 54(3):622-631, 1991.Daly JM, Reynolds J, et al. Immune and metabolic effects of arginine in the surgical patient. Ann Surg

2084:512-523, 1988.Evans Wj, Campbell WW. Sarcopenia and age-related changes in body composition and functional

capacity. J Nutr 123(2 Suppl):465, 1993.Fleming CR. Enteral and parenteral nutrition. In: Therapy of Inflammatory Bowel Disease: New Medi-

cal and Surgical Approaches. Peppercorn MA (ed). New York: Marcel Dekker; 1990.Gray DS and Kaminski MV. Stress. In: Hyperalimentation: A Guide for Clinicians. Kaminski MV, ed.

New York: Marcel Dekker, Inc., 1985.Hasselgren P and Fischer JE. Nutritional support in sepsis. In: Nutritional Support in Critical Care.

Lang CE, Ed. Rockville MD: Aspen Publ, Inc., 1987.Kehayias J, Heymsfield S, Eds. Symposium: Sarcopenia: Diagnosis and mechanisms. J Nutr 127:989S,

1997Kelly DG, Nehra V. Gastrointestinal disease. In: The Science and Practice of Nutrition Support: A Case

Based Core Curriculum. Gottschlich MM, Fuhrman MP, Hammond KA,, Holcombe BJ, Seidner DL, eds. Dubuque IA: Kendall/Hunt Publishing Company, 2001.

Kirk SJ and Barbul A. Role of arginine in trauma, sepsis, and immunity. JPEN 14:226S-229S, 1990.Lang CE. Nutrition support in gastrointestinal disease. In: Nutrition Support Dietetics. Shronts EP, Ed.

Silver Spring MD: ASPEN, 1989.Lexell JL, Dutta C, Eds. Sarcopenia and physical performance in old age: Proceedings of a workshop.

Muscle Nerve 5:S1, 1997.Mills CB. Nutritional support in cardiac disease in: Hyperalimentation: A Guide for Clinicians. Kamin-

ski MV, Ed. New York: Marcel Dekker, Inc., 1985.Nelson KM and Long CL: Physiological basis for nutrition in sepsis. Nutr in Clin Prac 4(1):6-15, 1989.O'Keefe SJ. Nutrition and gastrointestinal disease. Scand J Gastroenterology Suppl 220: 52-59, 1996.Poindexter SM. Cardiac failure. In: Nutrition Support Dietetics, 2nd ed. Gottschlich, MM, Matarese LE

and Shronts EP, eds. Silver Spring MD: ASPEN, 1993.Shronts EP and Lacy JA. Metabolic support. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM,

Matarese LE and Shronts EP, Eds. Silver Spring MD: ASPEN, 1993.


Stralovich A. Gastrointestinal and pancreatic disease. In: Nutrition Support Dietetics, 2nd ed. Gott-schlich MM, Matarese LE and Shronts EP, Eds. Silver Spring MD: ASPEN, 1993.

Szauter KEM. Geriatric Nutrition. Unpublished discussion at ASPEN 17th Clinical Congress, San Diego, 1993.

Talamini MA. The cardiac patient. In: Nutritional Support in Critical Care. Lang CE, ed. Rockville MD: Aspen Publ., Inc., 1987.

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Chapter two 1. Dietary history components might include a 24-hour food record, a 24-hour intake recall, food

frequency questionnaires, food diaries, and calorie counts. These should include eating pat-terns and an estimation of intake as well as types of foods eaten.

2. Ideal body weight can be determined by referring to height-weight tables such as the Metro-politan Life Insurance Company tables. You can also use the Hammwi method. For example, a man who is 6 feet tall should weigh 178 lb, + or - 10 percent, depending on body frame size. (106 lb + 12 X 6 = 178 lb).

3. Triggers for further investigation into nutritional status would include anything that increases metabolic demand, needs, or nutrient losses. Examples are: a history of surgeries or illnesses in the recent past, chronic disease, use of certain medications and unexplained weight loss.

4. Aspects of the socioeconomic status important to the nutritional assessment include income, ability to shop or cook, living alone or with a caregiver, disabilities, smoking and substance abuse.

Chapter three

1. Symptoms of protein-energy malnutrition include dry, easily pluckable, sparse or thinning hair, change in hair color, fat and muscle wasting, beading of ribs and edema.

2. Symptoms of thiamin deficiency include edema, cardiomegaly and anorexia.3. Advantages of anthropometrics include: inexpensive, safe, easy to do, and can be used at the

bedside. Disadvantages include: discrepancies in measurements from practitioner to practi-tioner, inaccurate calibration of calipers, changes in tissue composition in critical illness and difficulty in positioning the patient correctly.

4. The best comparison of weight values is the comparison of actual weight to usual weight.5. Components of SGA include: weight change, dietary intake, gastrointestinal symptoms, func-

tional ability, disease state, subcutaneous fat, muscle wasting, ankle or sacral edema, and ascites.

6. Parameters used in PNI: albumin, triceps skinfold, transferrin, and delayed hypersensitivity.7. To complete an instant nutrition assessment, use albumin and total lymphocyte count.

Chapter Four

1. Sodium levels might be low because of a) hemodilution from overhydration, especially after resuscitation; b) severe diarrhea or high fistula output where sodium is lost; and c) the patient might have SIADH with an abnormal stimulation of ADH because of stress.

2. Sodium might become elevated with the administration of a hypertonic enteral formula with-out adequate fluid.

3. Losses of potassium can occur via gastrointestinal route (vomiting, diarrhea, nasogastric suc-tion), urinary route (diuretics, mineralocorticoids, medications), chronic renal disease, sweat, refeeding syndrome, and intracellular shifts of potassium.

Review Question Answers

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4. Nutrients that are depleted during refeeding are potassium, magnesium, and phosphorus. Potassium shifts into the new cells that are being synthesized and the administration of dex-trose and subsequent release of insulin cause a shift of potassium intracellularly. Phosphorus decreases because the administration of dextrose and subsequent insulin release stimulates a shift of phosphorus into the cells. Phosphorus often becomes depleted during starvation, as well. Magnesium plays a vital part in anabolism and must shift intracellularly during the formation of new cells.

5. An anion gap metabolic acidosis will show a decreased level of bicarbonate, normal or low chloride, a decrease in pH, and an elevated potassium. This can occur with diabetic ketoaci-dosis, lactic acidosis, dehydration, and ingestion of ethanol, methanol, ethylene glycol, or salicylates.

6. The body compensates for a respiratory acidosis with a metabolic alkalosis as the kidneys retain more bicarbonate to bring pCO2 levels down and pH up to near normal.

7. This is probably not a true hypocalcemia. Although adjusted calcium levels may not always be accurate, we can see that with hypoalbuminemia, the proportion of bound calcium is lower. To be more accurate in assessing the calcium level, we should obtain an ionized calcium. However, an adjusted calcium reveals a level of about 8.8.

Chapter Five

1. I would not use CHI because of a) the difficulty in obtaining a 24-hour urine; b) CHI decreases with age and no real parameters are available for the elderly; c) there are no parameters for large or small frames – only for medium frames; and d) CHI does not consider dietary intake of protein and creatinine.

2. N in = 20 gm protein + 52 gm protein = 72 gm protein = 72 gm protein/6.25gm N = 11.5 gm N in N out = (UUN of 9 X 1.2) + 4 = 14.8 gm N out N balance = 11.5 gm N in - 14.8 gm N out = -3.3 3. For the most part, albumin is not a good marker of nutritional status. It may be a good marker

long-term, but in acute care too many other factors besides nutritional status can influence albumin levels.

4. Prealbumin’s half-life of two to three days makes it a better nutritional marker than transferrin (half-life of eight to 10 days) and albumin (half-life of 21 days).

5. Anergy is a lack of immune response and is important to determine in assessing nutritional and immune status.

6. Cholestasis can occur with use of TPN exclusively without using the gastrointestinal tract. It can also occur with overfeeding calories, especially carbohydrate calories.


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Chapter Six

1. To determine the needs of a 63-year-old female, 5'3" tall, weighing 170 lb, with the Harris- Benedict equation, use IBW of 52 kg:

Adjusted body weight: BEE = 655 + 497 + 296 -295 = 1153 kcal Stress factor = 1.3 to 1.5 X BEE (1153) Total energy needs = 1500 to 1729 kcal/day Ireton-Jones Equation = 1925 – 630 + 260 = 1555 kcal/day Cal/kg factor = 25 - 30 kcal/kg = 1300 to 1560 kcal/kg Protein requirements = 1.5 to 2.0 gm pro/kg/day = 78 to 104 gm pro/day

2. Vitamin and mineral deficiencies associated with malabsorption include: A, D, E, K, folate, B 12, zinc, copper, and iron.

3. Vitamin and mineral deficiencies associated with alcoholism include: vitamin C, thiamin, pyridoxine, folate, and zinc.

4. Vitamin B12 deficiency is associated with a gastrectomy because of the lack of intrinsic factor.

Chapter Seven

1. The COPD patient may be malnourished because of a) increased work of breathing with fatigue and inability to eat, prepare meals, or shop with resultant weight loss; b) ulcer dis-ease and abdominal discomfort because of medications; and c) hypermetabolic state.

2. Changes that occur in lung function with malnutrition may include: decreased respiratory rate, decreased tidal volume, decreased muscle mass, decreased inspiratory pressure, decreased vital capacity, decreased expiratory strength, decreased minute ventilation, and decreased surfactant production.

3. Caloric requirements: 1400 to 1800 kcal/day, with increased calories from fat Protein requirements: 60 to 80 gm protein/day Adequate vitamins, minerals, especially phosphorus4. Reasons for the weight loss with cancer: increased needs because of the increased activity

of the Cori cycle; anorexia with early satiety because of neurotransmitters, serotonins, and free fatty acids; change in taste and smell; chemotherapy and related complications; radia-tion therapy and related complications; surgery and related complications.

5. Problems that may occur with small bowel resection include: diarrhea, decreased transit time, malabsorption, B12 deficiency, fat soluble vitamin deficiency, calcium deficiency, magnesium deficiency, and electrolyte abnormalities.

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6. Caloric requirements: 2200 to 2500 kcal/day; Protein requirements: 108 gm protein/day. May experience nausea, vomiting, diarrhea, stomatitis, decreased intake, anorexia. Monitor vita-min and mineral nutriture.

7. Biochemical abnormalities that may occur with liver disease include: increase or decrease in glucose; decreased albumin, fibrinogen, prothrombin, and urea levels; increased ammonia levels; increased aromatic amino acids; and decreased branched-chain amino acids.

8. Anthropometrics would probably be of little use because of fluid shifts and the fact that an-thropometrics are of little use acutely. Could possibly be used in long-term care.

9. Caloric needs: 1900 to 2700 kcal/day; Protein needs: 115 gm protein/day. Supplement with thiamin, multivitamins.

10. Transferrin is the best protein parameter in renal disease because of its decreased sensitivity to fluid shifts and shorter half-life.

11. In renal failure, should supplement all B vitamins (especially B6), Vitamin C and folate.

Chapter eight

1. Weight loss and depletion of stores occurs because of early satiety, anorexia, dietary restric-tions, drug-nutrient interactions, nausea, decreased GI motility, diarrhea, increased work of breathing, venous engorgement of the stomach, liver, and pancreas, and decreased delivery of oxygen to the GI tract.

2. Nutritional problems that occur with gastrectomy include: malabsorption, B12 deficiency, folate deficiency, calcium deficiency, fat-soluble vitamin deficiencies, dumping syndrome, weight loss.

3. Problems that can occur after ileal and ileocecal valve resection include: steatorrhea, malab-sorption, water-soluble and fat-soluble vitamin deficiencies, bacterial overgrowth, weight loss, depletion of fat stores, zinc deficiency.

4. Calorie needs: 1600 to 1825 kcal/day (BEE = 1217); Protein needs: 85 to 115 gm protein/day.5. Glutamine and arginine appear to be essential in stress.6. Calorie needs (kcal/kg method) = 1700 to 2050 kcal/day; BEE method = (BEE = 1782 kcal) =

2300 to 2700 kcal/day; Protein needs = 102 to 136 gm protein/day. Monitor for depletion of potassium, magnesium, phosphorus, zinc, and vitamin C.7. Aging causes decreased lean body mass; decreased skeletal and visceral protein stores; in-

creased adipose tissue; decreased total body water; dry mouth; change in taste; decreased cardiac and kidney function; decreased GI motility; decreased absorption of B12, fat, iron, calcium, and zinc; and decreased immune function.

8. Weight = 68 kg; Height = 177.8 cm or 1.78 m BMI = 21.5 — the patient may be nutritionally depleted.

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Requires assistance in bathing more than one part of body, or not bathed.

Requires assistance in gathering clothes, get-ting dressed. Remains undressed.

Does not go to toilet room for elimination.

Doesn’t get out of bed.

Supervision required for control, requires catheter, or is incontinent.

Requires assistance in feeding, or is partly or completely fed via tubes or intravenous access.

aCtivity independent aSSiStanCe dependent

Activities of Daily Living Checklist

Adapted from: S. Katz,JAMA (1963); (Gallo, 1988)

Requires assistance in bathing only one part of body (back, legs, etc.).

Requires assistance only for tying shoes.

Requires assistance in go-ing to toilet room, cleaning self, rearranging clothing or using night bedpan/commode.

Moves in an out of bed or chair with assistance or support.

Has occasional accidents.

Requires assistance for cut-ting meat, buttering bread, opening containers, etc.

bathing

dreSSing

toileting

tranSFer

Conti-nenCe

Feeding

Is able to get into and out of tub unassisted, if tub is usual method of bathing.

Gathers own clothes and gets completely dressed without assistance.

Goes to toilet room, cleans self, rearranges clothes (may use cane, walker or wheel-chair). Uses night bedpan or commode, empties it in morning.

Moves into and out of bed and chair without assistance (may use cane or walker).

Controls urination and bowel movements com-pletely.

Feeds self. Able to handle utensils, open containers, etc.

Appendix #1

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Looks up numbers, dials, receives calls.

Drives own car, or travels alone on bus or taxi.

Completes all shopping with available transporta-tion.

Plans and cooks full meals.

Does heavy housework (i.e. scrubs floors, washes windows).

Takes medications at right time in proper dosage.

Handles daily buying needs, manages accounts, writes checks, pays bills on time.

aCtivity independent aSSiStanCe dependent

Adapted from: Duke University (1978); (Gallo, 1988)

Instrumental Activities of Daily Living Checklist

Answers phone, dials op-erator in emergency, but must have help getting numbers, dialing.

Travels, but not alone.

Shops, but not alone.

Prepares light foods, warms up prepared meals, but cannot prepare full meals.

Does light housework only. Requires help with heavy tasks.

Requires reminders about taking medications, or as-sistance preparing meds.

Manages daily buying needs, but requires help in balancing checkbook, paying bills on time.

Cannot use telephone.

Cannot travel.

Unable to shop.

Cannot prepare any meals.

Cannot do any housework.

Cannot take medications by self.

Unable to manage money at all.

tele-phone

traveling

Shopping

preparing

mealS

houSe-work

mediCa-tion

money

Appendix #2

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Drug-Nutrient Interactions

Appetite SuppressantsAnorexiantsCNS StimulantsChemotherapeuticsColchicineBulking agents

Appetite StimulantsTricyclic antidepressantsGlucocorticoidsThyroid hormonesInsulin

Altered Taste PerceptionCaptoprilPenicillamineClofibrateChemotherapy

Altered Nutrient AbsorptionAluminum hydroxideChemotherapeutics

Colchicine

Mineral oil

Cholestyramine

Clofibrate

PenicillamineSulfasalazine

Altered Nutrient ExcretionLaxatives

Furosemide

ThiazidesAspirin

Altered Nutrient MetabolismPhenobarbitalIsoniazidEstrogens

Use for short timeMonitor weight loss, nutritional statusMonitor closelyMonitor closely, use for short timeDon't take before meal

Counsel patientCounsel patientCounsel patientCounsel patient

Counsel patientCounsel patientCounsel patientCounsel patient

Change to other antacids if possibleSupplement high calorie and protein drinks, vitamins & minerals

Supplement diet, limit alcohol, monitor for lactose intolerance

Take on an empty stomach

Supplement 1 hour before or 4-6 hours after Decrease fat/cholesterol intake

Supplement vitamin B6 if necessarySupplement may be necessary

Counsel patient about bowel habits

Increase dietary potassium, supplement

Increase dietary potassium, supplement

Supplement if long-term use

May need to supplement folic acid, vitamin DSupplement B6Watch total calorie intake, fat intake. Supple-ment with multivitamins and minerals.

Appendix #3

drug interaCtion reCommendationS

Central nervous systemCentral nervous systemNausea, vomiting, GI damageGI damageSensation of fullness

May only last 2-3 monthsTaste lost or alteredDecreased acuity, unpleasant aftertasteVaries, based on the drug

Binds phosphorus in GI tractGI mucosal damage, nephrotoxic

GI mucosal damage, decreased transit time, decreased absorption of: B12, carotene, fat, electrolytesDecreased absorption: fat-soluble vitamins, carotene

Binds, decreases absorption of fat, iron, carotene, vitamins: A,D,K, folic acidDecreased absorption: B12, medium chain triglycerides, iron, sugarsComplexation vitamin B6Decreased absorption: folate, iron

Increased: sodium, calcium, potassium

Increased: potassium, sodium Decreased: calciumIncreased: vitamin C, potassiumMay cause deficiency of: vitamins D, K, folic acid; may cause decreased bone density

Competitive inhibitor vitamin B6Increase degradation: folic acid, vitamins C, B2, B6Increased: triglycerides, HDL cholesterol, coagulation proteinsDecreased: LDL cholesterol

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Drug-related Nutritional ProblemsANTACIDS1. Aluminum hydroxide: interferes with absorption of phosphate, causing osteomalacia; may cause constipation 2. Magnesium hydroxide may cause diarrhea 3. Calcium carbonate: may raise sodium levels; interferes with absorption of thiamin and iron LAXATIVES1. Irritants: Increase motility of intestinal tract a. Are usually coated and should not be taken with alkaline fluids such as milk b. May cause dependency and potassium deficiency 2. Saline laxatives: retain water in the intestines and induce peristalsis; can cause electrolyte imbalance 3. Lubricants: reduce bowel transit time; mineral oil can decrease absorption of fat soluble vitamins 4. Stool softeners and bulk formers: person must drink a lot of fluids or they will not work PENICILLAMINE1. Interferes with the absorption of certain nutrients when taken with food 2. Take 2 hours before or 3 hours after a meal 3. Patient loses ability to taste salty and sweet food ANTIBIOTICS1. Do not take with acid juices 2. Increases potassium excretion 3. Causes unpleasant taste in mouth 4. Tetracycline: Milk and dairy products interfere with drug absorption; should not be taken with iron supplements (separate by at least 2 hours); decreases synthesis of vitamin K5. Neomycin: Has side effects of nausea, vomiting and diarrhea ANTICOAGULANTS1. Vitamin K will interfere with anticoagulant function 2. Vitamin E should be avoided as it will increase the tendency to bleed ANTI-INFLAMMATORY AGENTS; CORTICOSTEROIDS1. Avoid alcohol2. Tends to increase appetite, weight and fluid retention ANTI-LIPIDEMIC AGENTS1. Cholestyramine: Traps bile acids and passes through the feces, lowering cholesterol 20 - 35 percent 2. Clofibrate: Influences the production of cholesterol by interfering with the protein that carries cholesterol around the body; leaves unpleasant aftertaste 3. Lovastatin: Reduces cholesterol 30 - 40 percent by blocking the enzyme that the liver needs to manufacture cholesterol ANTI-PARKINSON’S DRUGS1. L-dopa causes bitter taste in mouth and can cause constipation and gas 2. Vitamin B6 interferes with action of L-dopa 3. High protein diets may interfere with the absorption into the brain CARDIOVASCULAR MEDICATIONS1. High fiber diet delays absorption of digitalis DIURETICS1. Usually result in potassium losses2. Potassium levels should be monitored and use of potassium-rich foods should be encouraged GRAPEFRUIT JUICE1. Can cause increased serum levels of many drugs, including Alprazolam, Cyclosporine, Dihydropyridine, Calcium Channel Blockers, Triazolam, Midazolam, Carbamazepine, Lovastatin, and Buspirone.

Appendix #4

R: this statement about Grapefruit juice is new

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Drugs Impacting Nutrient Metabolism

nutrient drugS impaCting metaboliSm

Ascorbic Acid (Vitamin C) Adrenal Corticosteroids, Barbiturates, Levodopa, Salicylates, Sulfonamides, Tetracycline

Folic Acid Adrenal Corticosteroids, Alcohol, Anticonvulsants, Barbiturates, Isoniazid, Salicylates, Sulfonamides, Tetracycline, Triamterene

Pyridoxine Adrenal Corticosteroids, Anticonvulsants, Diuretics, Hydralazine, Isoniazid, Levodopa, Sulfonamides

Vitamin A Adrenal Corticosteroids, Colchicine, Cholestyramine, Clofibrate, Petrolatum Liquid

Vitamin B12 Alcohol, Anticonvulsants, Barbiturates, Cholestyramine, Clofibrate, Colchicine, Para-aminosalicylic Acid, Phenobarbital, Potassium, Sulfonamides, Triamterene

Vitamin D Adrenal Corticosteroids, Anticonvulsants, Barbiturates, Cholestyramine, Petrolatum Liquid

Vitamin K Anticoagulants, Anticonvulsants, Cholestyramine, Petrolatum Liquid, Salicylates, Tetracycline

Calcium Aluminum Hydroxide, Anticonvulsants, Cholestyramine, Digitalis, Glycosides, Mercurial Diuretics, Tetracycline, Thiazide Diuretics, Triamterene

Iron Alcohol, Antacids (Carafate), Cholestyramine

Potassium Adrenal Corticosteroids, Colchicine, Penicillin, Diuretics except Spironolactone and Triamterene

Zinc Alcohol, Tetracycline, Thiazide Diuretics

Adapted from Schlenker, 1984

Appendix #5

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626364656667686970717273747576

128-134130-136132-138134-140136-142138-145140-148142-151144-154146-157149-160152-164155-168158-172162-176

131-141133-143135-145137-148139-151142-154145-157148-160151-163154-166157-170160-174164-178167-182171-187

138-150140-153142-156144-160146-164149-168152-172155-176158-180161-184164-188168-192172-197176-202181-207

109-121111-123113-126115-129118-132121-135124-138127-141130-144133-147136-150139-153142-156145-159148-162

118-131120-134122-137125-140128-143131-147134-151137-155140-159143-163146-167149-170152-173155-176158-179

Ht. Small medium large Ht. Small medium large (incHeS) Frame Frame Frame (incHeS) Frame Frame Frame

Metropolitan Life Height-Weight Tables men (age 25-59) women (age 25-59)

585960616263646566676869707172

102-111103-113104-115106-118108-121111-124114-127117-130120-133123-136126-139129-142132-145135-148138-151

Men are wearing 5 lbs. of clothing, and shoes with 1-inch heels Women are wearing 3 lbs. of clothing and 2-inch heelsSource: Metropolitan Life Insurance Company (ALL WEIGHTS IN POUNDS)

Age-Height-Weight Ranges age: 35 45 55 65

58596061626364656667686970717273747576

92-11995-12398-127101-131105-136108-140112-145115-149119-154122-159126-163130-168134-173137-178141-183145-188149-194153-199157-205

107-135111-139114-143118-148122-153126-158130-163134-168138-174143-179147-184151-190156-195160-201165-207169-213174-219179-225184-231

115-142119-147123-152127-157131-163135-168140-173144-179148-184153-190158-196162-201167-207172-213177-219182-225187-232192-238197-244

99-127103-131106-135110-140113-144117-149121-154125-159129-164133-169137-174141-179145-184149-190153-195157-200162-206166-212171-218

Weight for height ranges for men and women without clothing and shoes, as determined by Ger-ontology Research Center studies.Source: Andres 1985

heigh

t

i

n

i

n

C

h

e

S

Appendix #6

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Name: Date:

LOCATIONTIME AMOUNT FEELINGSFOOD/BEVERAGE/PREPARATION

DIRECTIONS: Write down everything you ate and drank yesterday. Include when and where you ate it, how much you ate, and how you felt while eating. Be sure to include all hidden items, such as margarine, oil, salad dressing, condiments, sugar in your coffee, etc. Try to be as accurate in your measurements as possible.

Food Diary

Appendix #7

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Food Frequency Form

Appendix #8

Please check the column that shows how often you eat the following foods.Check only one column for each food.

Name___________________________Date____________________________ 2-4 2-4 Hardly Times Once Times Once Ever or a Day Daily a Week Weekly Never Beef, pork, ham, hamburger Luncheon meats, hot dogs Chicken, turkey, poultry Fish, seafood Eggs Dried peas or beans (legumes) Peanut butter Nuts Cereals (dry or cooked) Grains Breads, rolls, biscuits Tortillas Crackers Rice Pasta, noodles, spaghetti, macaroni Milk Cheese Yogurt, pudding, custard Fruits Fruit juices Vegetables Water Added Fat Coffee, tea, cocoa Sodas, fruit flavored drinks Alcohol: beer, wine, whiskey Candy, sweets Cakes, pies, cookies, donuts, sweet rolls Potato chips, pretzels, corn/tortilla chips Ice cream

WEEKLY TOTALS:Meat ___________________Poultry _________________Fish ____________________Legumes ________________Eggs ___________________Breads & cereal ___________Rice & pasta ______________

Fruits & juices* ___________Vegetables* ______________Dairy products ____________Water ___________________Sodas ___________________Alcohol __________________

Cakes, pies _______________Chips ___________________Ice cream ________________Candy ___________________Fats ____________________Other ___________________

*Ask types to determine if they are high in vitamin A or C

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18

19

25

35

45

55

65

%male Female

90

237

236

246

257

260

266

264

95

245

249

264

272

274

280

279

Arm Muscle Circumference (mm)

75

13

15

16

16

16

14

15

90

20

20

20

20

20

19

19

95

24

22

24

23

23

22

22

5

4

4

5

5

6

5

4

25

6

7

8

8

8

8

8

75

22

24

27

29

30

31

29

90

26

30

34

35

36

36

34

95

30

34

37

38

40

38

36

10

12

11

12

14

16

16

14

25

15

14

16

18

20

20

18

10

5

5

6

6

6

6

6

50

18

18

21

23

25

25

24

% 5

10

10

10

12

12

12

12

50

9

10

12

12

12

11

11

18

19

25

35

45

55

65

male Female

AG

E

Triceps Skinfold Percentiles (mm)

Anthropometric Measurement Standards

5

226

238

243

247

239

236

223

10o

237

245

250

255

249

245

235

25

252

257

264

269

265

260

251

50

264

273

279

286

281

278

268

75

283

289

298

302

300

295

284

90

298

309

314

318

315

310

298

95

324

321

326

327

326

320

306

5

174

179

183

186

187

187

185

10

179

185

188

192

193

196

195

25

191

195

199

205

206

209

208

50

202

207

212

218

220

225

225

75

215

221

228

236

238

244

244

AG

E

Appendix #9

Source: Frisancho, AR. AJCN, 1981, 34:2540-2545

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Appendix #10

45

59

58

63

63

63

46

44

46

50

50

50

11

15

15

15

15

15

11

15

15

15

15

15

600

900

900

900

900

900

600

700

700

700

700

700

15

155

15

15

15

20

5

15

15

15

15

15

20

60

75

120

120

120

120

60

75

90

90

90

90

45

75

90

90

90

90

45

65

75

75

75

75

0.9

1.2

1.2

1.2

1.2

1.2

0.9

1.0

1.1

1.1

1.1

1.1

0.9

1.3

1.3

1.3

1.3

1.3

0.9

1.0

1.1

1.1

1.1

1.1

12

16

16

16

16

16

12

14

14

14

14

14

1.0

1.3

1.3

1.3

1.7

1.7

1.0

1.2

1.3

1.3

1.5

1.5

300

400

400

400

400

400

300

400

400

400

400

400

1.8

2.4

2.4

2.4

2.4

2.4

1.8

2.4

2.4

2.4

2.4

2.4

MALES

FEMALES

Vitamins Minerals

Dietary Reference Intakes:Recommended Dietary Allowances & Adequate Intakes¶

¶ Note: Bold print indicates the value is based on the Recommended Dietary Allowance (RDA), while regular print indicates the value is based on the Adequate Intake (AI).

* 1 ug vitamin D = 40 IU vitamin D

Source: Institute of Medicine, Food and Nutrition Board, National Academy of Science — National Research Council, 1997, 1998, 2000, 2001, 2005, 2011.

9-13

14-18

19-30

31-51

51-70

70+

9-13

14-18

19-30

31-50

51-70

70+

Vita

min

B 6 (m

g)

Niac

in (m

g)

Vita

min

B 12 (µ

g)

Fola

te (µ

g)

Thia

min

(mg)

Vita

min

C (m

g)

Ribo

flavi

n (m

g)

Vita

min

E (m

g)

Vita

min

D (µ

g)*

Vita

min

K (µ

g)

Prot

ein

(gm

)

Age

Vita

min

A (µ

g)

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1,300

1,300

1,000

1,000

1,000

1,200

1,300

1,300

1,000

1,000

1,200

1,200

1,250

1,250

700

700

700

700

1,250

1,250

700

700

700

700

240

410

400

420

420

420

240

360

310

320

320

320

8

11

8

8

8

8

8

15

18

18

8

8

8

11

11

11

11

11

8

9

8

8

8

8

120

150

150

150

150

150

120

150

150

150

150

150

40

55

55

55

55

55

40

55

55

55

55

55

20

25

30

30

30

30

20

25

30

30

30

30

700

890

900

900

900

900

700

890

900

900

900

900

1.9

2.2

2.3

2.3

2.3

2.3

1.6

1.6

1.8

1.8

1.8

1.8

2

3

4

4

4

4

2

3

3

3

3

3

4

5

5

5

5

5

4

5

5

5

5

5

375

550

550

550

550

550

375

400

425

425

425

425

25

35

35

35

35

35

21

24

25

20

20

20

Vitamins Minerals

* Choline is a dietary component.

Copp

er (µ

g)

Man

gane

se (m

g)Fl

uorid

e (m

g)

Chol

ine

(mg)

*

Chro

miu

m (µ

g)

Pant

othe

nic A

cid

(µg)

Biot

in (µ

g)

Phos

phor

us (m

g)

Calc

ium

(mg)

Iron

(mg)

Mag

nesi

um (µ

g)

Iodi

ne (µ

g)

Zinc

(mg)

Sele

nium

(µg)

Mol

ybde

num

(µg)

34

43

45

45

45

45

34

43

45

45

45

45

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Appendix #10, cont.DRI Values for Energya and Total Fiber

a For healthy moderately active Americans and Canadiansb PAL = physical activity level, EER = estimated energy requirement, TEE = total energy expenditure. The intake that meets the average energy expenditure of

individuals at the reference height, weight, and age.c AI = Adequate intake. Based on 14 gm/1,000 kcal of required energy.d ND = not determined. The observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nu-

tritional status, such as growth rate, normal circulating nutrient values, or other functional indicators of health. The AI is used if sufficient scientific evidence is not available to derive an Estimated Average Requirement (EAR). For healthy infants receiving human milk, the AI is the mean intake. The AI is not equivalent to an RDA.

c Subtract 10 kca;l/day for males and 7kcal/day for females for each year above 19 years

Energy – Active PALbEER (kcal/d) Fiber – AI (gm/d)c

Life Stage Group Male Female Male Female 0-6 months 570 520 (3 mo) NDd ND 7-12 months 743 676 (9 mo) ND ND 1-2 years 1,046 992 (24 mo) 19 19 3-8 years 1,742 1,642 (6 yr) 25 25 9-13 years 2,279 2,071 (11 yr) 31 26 14-18 years 3,152 2,368 (16 yr) 38 36 19-50 years 3,067e 2,403e (19 yr) 38 25 >50 years 3,067e 2,403e (19 yr) 30 21Pregnancy 14-18 years 1st trimester 2,368 (16 yr) 28 2nd trimester 2,708 (16 yr) 28 3rd trimester 2,820 (16 yr) 28 19-50yr 1st trimester 2,403e (19 yr) 28 2nd trimester 2,743e (19 yr) 28 3rd trimester 2,855e (19 yr) 28Lactation 14-18 years 1st 6 months 2,698 (16 yr) 29 2nd 6 months 2,768 (16 yr) 29 19-50 years 1st 6 months 2,733e (19 yr) 29 2nd 6 months 2,803e (19 yr) 29

DRI Values for Protein AI or RDA for Reference Individual (gm/day) EAR (gm/kg/d)a RDA (gm/kg/d)b AILife Stage Group Male Female Male Female Male Female (gm/kg/d)c

0-6 months 9.1 (AI) 9.1 (AI) 1.52 7-12 months 13.5 13.5 1.1 1.1 1.5 1.5 1-3 years 13 13 0.88 0.88 1.10 1.10 4-8 years 19 19 0.76 0.76 0.95 0.95 9-13 years 34 34 0.76 0.76 0.95 0.95 14-18 years 52 46 0.73 0.71 0.85 0.85 > 18 years 56 46 0.66 0.66 0.80 0.80a EAR = Estimated Average Requirement. The intake that needs the estimated nutrient needs of half of the individuals in a groupb RDA = Recommended Dietary Allowance. The intake that meets the nutrient need of almost all (97-98%) of individuals in a group.c AI = Adequate intake. The observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nu-


d EAR and RDA for pregnancy are only for the second half of pregnancy. For the first half of pregnancy the protein requirements are the ame as those of the nonpregnant woman.

e In addition to the EAR and RDA of the nonlactating adolescent or woman.

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Appendix #10, cont.DRI Values for Total Fat,

n-6 Polyunsaturated Fatty Acids (Linoleic Acid) & n-3 Polyunsaturated Fatty Acids (α-Linolenic Acid)

Total Fat n-6 PFAs n-3 PFAs AI (gm/d)a AI (gm/d)a AI (gm/d)a

Life Stage Group Male Female Male Female Male Female 0-6 months 31 31 4.4 4.4 0.5 0.5 7-12 months 30 30 4.6 4.6 0.5 0.5 1-3 years NDb ND 7 7 0.7 0.7 4-8 years ND ND 10 10 0.9 0.9 9-13 years ND ND 12 10 1.2 1.0 14-18 years ND ND 16 11 1.6 1.1 19-30 years ND ND 17 12 1.6 1.1 31-50 years ND ND 17 12 1.6 1.1 51-70 years ND ND 14 11 1.6 1.1 >70 years ND ND 14 11 1.6 1.1Pregnancy 14-18 years ND ND 13 1.4 19-50 years ND ND 13 1.4Lactation 14-18 years ND ND 13 1.3 19-50 years ND ND 13 1.3a AI = Adequate intake. The observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nu-


b ND = not determined. The observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nu-tritional status, such as growth rate, normal circulating nutrient values, or other functional indicators of health. The AI is used if sufficient scientific evidence is not available to derive an Estimated Average Requirement (EAR). For healthy infants receiving human milk, the AI is the mean intake. The AI is not equivalent to an RDA.

DRI Values for Carbohydrate

a EAR = Estimated Average Requirement. The intake that meets the estimated nutrient needs of half of the individuals in a group.b RDA = Recommended Dietary Allowance. The intake that meets the nutrient need of almost all (97-98 percent) of individuals group.c AI = Adequate Intake. The observed average or experimentally determined intake by a defined population or subgroup that appears to sustain a defined nu-

tritional status, such as growth rate, normal circulating nutrient values, or other functional indicators of health. The AI is used if sufficient scientific evidence is not available to derive an EAR. For healthy infants receiving human milk, the AI is the mean intake. The AI is not equivalent to an RDA.

EAR (gm/d)a RDA (gm/d)b

Life Stage Group Male Female Male Female AI (gm/d)c 0-6 months 60 7-12 months 95 1-3 years 100 100 130 130 4-8 years 100 100 130 130 9-13 years 100 100 130 130 14-18 years 100 100 130 130 >18 years 100 100 130 130Pregnancy 14-18 years 135 175 >19 years 135 175Lactation 14-18 years 160 210 >19 years 135 175

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Vitamin & Mineral Deficiencies

Vitamin Deficiency Symptom Causes

A decreased adaptation malabsorption, to dark; male sterility, increased excretion alterations in cellular growth

D rickets fat malabsorption, osteomalacia increased excretion hypocalcemia

E hemolytic anemia fat malabsorption premature infants low-birth-weight infants

K increased clotting times fat malabsorption, liver disease, drug therapy

C anemia increased metabolism, bleeding, gingivitis stress, alcoholism, weakness decreased intake

Thiamin decreased appetite alcoholism, neurological symptoms decreased intake cardiac changes

Riboflavin stomatitis decreased intake, dermatitis malabsorption; cheilosis increased needs: stress, surgery, burns Niacin scarlet tongue, decreased intake, stomatitis, dermatitis, increased requirements diarrhea, dementia, death Pyridoxine hypochromic, renal disease, liver disease, microcytic anemia; pregnancy, alcoholism, weight loss, depression, confusion advanced age

Biotin anorexia long-term TPN without adequate vomiting supplementation; nausea long-term antibiotics dermatitis, alopecia

Appendix #11

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Vitamin/Mineral Deficiency Symptom Causes

Folate megaloblastic, decreased intake, macrocytic anemia; malabsorption, stomatitis, increased needs, glossitis, alcoholism, gastrointestinal disorders drug therapy B12 megaloblastic, malabsorption macrocytic anemia; after gastrectomy decreased appetite, vegetarianism weight loss, neurological changes

Zinc decreased wound healing, alcoholism altered taste & smell, TPN without supplementation hair loss, malabsorption dermatitis, diarrhea decreased immune function decreased intake

Copper microcytic anemia, Wilson’s disease decreased wound healing, nephrosis altered immune function, malabsorption decreased glucose tolerance burns

Selenium muscle tenderness increased needs cardiomyopathy decreased intake growth retardation increased losses

Iron hypochromic, decreased intake microcytic anemia increased needs cheilosis malabsorption glossitis increased losses koilonychia

Vitamin & Mineral Deficiencies, Continued

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Tongue magenta Riboflavin glossitis Niacin, Folate, Iron, B6, B12

Skin xerosis Vitamin A, essential fatty acids follicular Vitamin A, essential fatty acids hyperkeratosis petechiae, Vitamin C, Vitamin K ecchymoses

Nails koilonychia Iron

Muscle wasting Protein-calorie malnutrition

Beading of ribs Vitamin D, Calcium

Ideal Creatinine Height Weight Excretion Creatinine (inches) (lbs.) (mg/24 hrs) Height Index

Condition Deficiency Condition Deficiency

Hair easily pluckable, Protein-calorie dyspigmented malnutrition

Eyes Bitot’s spots Vitamin A xerophthalmia Vitamin A night blindness Vitamin A angular palpebritis Riboflavin, Niacin

Gums bleeding, spongy Vitamin C

Lips angular stomatitis Riboflavin, B6, Iron cheilosis Riboflavin, B6, Niacin

Creatinine Height Index

Ideal Creatinine Height Weight Excretion Creatinine (inches) (lbs.) (mg/24 hrs) Height Index

8.178.288.368.408.518.628.768.868.989.119.249.389.499.619.80

128813251359138614261467151815551596164216911739178518311891

124127130133137141145149153158162167171176181

585960616263646566676869707172

101104107110113116119123128132136139143147151

83085187590092594997710061044107611091141117412061240

626364656667686970717273747576

5.635.685.745.815.875.936.016.096.236.326.426.516.606.696.78

womenmen

Appendix #12

Physical Changes with Malnutrition

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Protein Status Indicators

Energy Status Indicators

Immune Function

TPN

Renal Disease

Liver Disease

Cancer

Cardiac Disease

Pulmonary Disease

Diabetes Mellitus

Stress and Sepsis

Anemia

Disease/ConditionClinical Data andLaboratory Tests

Albumin, transferrin, prealbumin, retinol-binding protein, nitrogen balance

Weight, % ideal body weight, deviance from usual weight, recent weight loss

Total lymphocyte count, delayed hypersensitivity

Albumin, total protein, sodium, chloride, potassium, phosphorus, magnesium, glucose, CO2, BUN, cre-atinine, triglycerides, hemoglobin, hematocrit, blood gases, liver function tests

BUN, creatinine, creatinine clearance, potassium, calcium, phosphorus, sodium, glucose, glomerular filtration rate, albumin, hemoglobin, hematocrit, dry weight

Liver function tests (alkaline phosphatase, GGT, SGOT, SGPT, total bilirubin), albumin, transferrin, prealbumin, ammonia, glucose, cholesterol, triglycerides, protime

WBC, total lymphocyte count, energy indicators, protein indicators, calcium, amylase, hemoglobin, hematocrit, glucose

Cholesterol, triglycerides, lipid profile (HDL, LDL, VLDL) protein indicators, dry weight, potassium, magnesium

Blood gases, protein indicators, energy indicators, glu-cose, hemoglobin, hematocrit

Glucose, glycosylated hemoglobin, potassium, BUN, cre-atinine, triglycerides, protein and weight indicators

WBC, total lymphocyte count, hemoglobin, hematocrit, glucose, triglycerides, BUN, creatinine, protein indica-tors, liver function tests, acid-base balance

Hemoglobin, hematocrit, total iron-binding capacity, mean corpuscular volume (MCV), mean corpuscular hemo-globin (MCH), transferrin, ferritin

Comments

Use all available tests; (N bal-ance invalid with renal failure

Use these for all patients

Not valid under certain condi-tions (see chapter 5)

See liver disease section for list of liver function tests

Useful for chronic renal failure. Dialysis patients need additional monitoring

Use all available tests

Other labs may be useful, based on the type of cancer and location of the tumor

With diabetic ketoacidosis use chloride, HCO3, pH to determine acid-base balance

If refeeding syndrome pos-sible, monitor potassium, phosphorus, magnesium

These tests differentiate between causes of nutritional anemia

Appendix #13

Laboratory Tests for Various Diseases & Conditions

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Correct electrolytes in formula, slow down the rate of feeding and monitor labs daily until stable

Monitor glucose 6x/day, adjust insulin dose, increase lipid calories, decrease CHO calories if possible

Immediate glucose infusion; monitor glucose; taper off TPN gradually

Limit lipid emulsions to every other day, if tolerated, and meet caloric needs with increased carbohydrateDecrease potassium in formula

Increase potassium in TPN; determine if there are unrecognized losses

Increase PO4 in TPN. Monitor other minerals

Decrease PO4 in TPN. Individualize. Often no PO4 is given

Decrease Mg in TPN

Increase Mg in TPN

Limit carbohydrate in TPN. Reduce or discontinue TPN if severe

Reduce total calories or substitute fat calories for some CHO calories

Reduce amino acids and nitrogen in TPN

Increase Na in TPN and/or reduce fluids; determine if there are increased losses

Appendix #14

Metabolic Assessment & Monitoring of TPN Condition

Refeeding Syndrome

Hyperglycemia

Hypoglycemia

Hyperlipidemia

Hyperkalemia Hypokalemia

Hypophosphatemia

Hyperphosphatemia

Hypermagnesemia

Hypomagnesemia

Elevated LFTs

Increased CO2

Prerenal azotemiaIncreased BUN

Hyponatremia

Probable Causes Treatment

Overfeeding patients who haven't eaten in over 2 days or are severely malnourished. Rapid drop in serum PO4, Mg, K

Glucose intolerance, insulin-resistance, sepsis, diabetes, glucocorticoid drugs

Too much insulin, too abrupt discontinua-tion of TPN

Severe sepsis, stress, familial condition

Renal insufficiency, metabolic acidosis

Protein anabolism; insufficient K+ in TPN especially during initial refeeding; diarrhea, vomiting, fistulas; side effects of drugs; losses from gut or kidneys

Inadequate PO4 in TPN, especially dur-ing initial refeeding, alkalosis, metabolic acidosis, antacids, hypomagnesemia and hypokalemia, uncontrolled diabetes

Renal insufficiency or renal failure

Chemotherapy, aminoglycosides

Inadequate Mg in TPN: renal insufficiency, increased losses, impaired absorption in GI tract, severe diarrhea

Overfeeding or cholestasis from pancreatitis

Overfeeding with carbohydrate calories; lung disease

Excess amino acids; renal insufficiency, dehydration

Overhydration from TPN and IV fluids; increased losses from urine or gut; inad-equate sodium in TPN

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1. Sodium levels in the serum can fall because of:a. nasogastric suctioningb. syndrome of inappropriate anti-diuretic hormonec. diabetes insipidusd. a & be. all of the above

2. Low serum levels of _______ can be associated with ileus of the small bowel.a. sodiumb. potassiumc. magnesiumd. phosphorus

3. Albumin:a. maintains oncotic pressure.b. transports minerals, enzymes and hormones.c. transports drugs.d. transports amino acids and fatty acids.e. all of the above.

4. A 6' 158 lb male, 70 years old, comes to your floor after surgery to repair a fractured hip. What are his daily caloric needs, based on the Harris-Benedict equation?

a. 1700 caloriesb. 2000 caloriesc. 1500 caloriesd. 2900 caloriese. 3300 calories

5. Which vitamin(s) can be toxic in excessive amounts? a. vitamin Ab. vitamin D c. vitamin Ed. all of the abovee. vitamins A and D

6. Acute disease or injury related malnutrition is characterized by: a. an inflammatory processb. decreased muscle massc. potential for limited effectiveness of nutrition supportd. a, b & ce. none of the above

7. When obtaining a diet history, which socioeconomic factors should trigger further investigation? a. patient lives alone b. patient is a smoker c. patient has low income d. all of the above 8. Koilonychia is associated with deficiency of ________. a. vitamin B12 b. iron c. zinc d. folate e. sodium

Examination

Treatment

NAS11

Answer each question by checking the correct answer online or filling the circle corresponding to the correct answer on the answer sheet. There is one best answer for each question. If you want a record of your answers, photocopy the answer sheet or record your choices on another piece of paper. Do not detach the examination from the book. This exam has 40 questions.

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Examination cont‘d9. The COPD patient may benefit from which mix of nutrients? a. 50 percent fat, 50 percent carbohydrate b. 60 percent fat, 40 percent carbohydrate c. 30 percent fat, 70 percent carbohydrate d. 20 percent fat, 80 percent carbohydrate

10. _________ is the best indicator of nutrition status in the patient with renal failure. a. albumin b. transferrin c. prealbumin d. retinol-binding protein

11. The best evaluation of height/weight status in the elderly uses:a. comparison to IBWb. Body Mass Indexc. height/weight tablesd. adjusted IBWe. all the above

12. Metabolic acidosis is characterized by: a. low chloride and an elevated bicarbonate levelb. increased bicarbonate and near-normal chloridec. low pH and high pCO2

d. high pH and low pCO2

13. Lab values are: albumin, 2.3; potassium, 3.5; sodium 140; calcium, 7.7; cholesterol, 205. What is the adjusted calcium level?

a. 8.0 b. 7.7 c. 9.0 d. 11.2 e. 12.5

14. Cholestasis can occur with:a. underfeeding of carbohydrate calories b. overfeeding of carbohydrate caloriesc. TPNd. disuse of the GI tract e. b, c & d 15. A 5' tall, 180 lb, 60-year-old female is admitted for cholecystectomy. What weight would you use

to assess her needs? a. 180 lb b. 128 lb c. 110 lb d. 114 lb e. 155 lb

16. Which nutrient deficiencies are reflected by a similar anemia? a. iron and folate b. folate and B12

c. B12 and iron d. copper and zinc

17. Evaluation of the adequacy of a person’s diet can be accomplished with...a. food frequency questionnaires b. physical examc. serum albumin d. all of the above

NAS11

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Examination cont‘d

18. What vitamin is essential for the formation of collagen?a. vitamin D b. vitamin C c. vitamin B12 d. vitamin E

19. The best comparison of weight values is: a. actual weight to IBW b. actual weight to usual weightc. IBW to usual weight d. weight changes over timee. there is no good comparison

20. Methotrexate may cause deficiency of: a. folate b. folate & calcium c. calcium d. vitamin A e. iron

21. Resection of the _______ is the most problematic in terms of nutrient absorption. a. stomach b. duodenum c. ileum d. colon

22. Refeeding syndrome is characterized by: a. hypophosphatemia b. hypokalemia c. hypomagnesemia d. a, b & c

23. Aging is associated with changes in body composition, most characteristic of which is sarcopenia, which is:

a. a decline in skeletal muscle mass b. a decline in fat mass c. weight loss d. a type of anemia

24. Visceral protein stores are a ____________predictor of nutritional status in acute and chronic disease.a. excellent b. poor c. good d. fair

25. A 5’8" tall, 160 lb male, 40 years old, is admitted after an auto accident with multiple trauma. What are his protein needs?

a. 109 - 146 gm/day b. 73 - 109 gm/day c. 75 - 100 gm/dayd. 65 - 90 gm/day e. 130 - 160 gm/day

26. The incidence of malnutrition in hospitalized patients has been estimated at :a. 50 % b. 80 % c. 40 % d. 70 % e. 20%

27. What is the IBW for a 6' man who is 58 years old (based on Hammwi method)? a. 200 lb b. 161 to 195 lb c. 175 to 190 lb d. 150 lb e. can’t tell from data given

28. A magenta tongue is associated with deficiency of: a. thiamin b. riboflavin c. niacin d. pyridoxine e. zinc

29. What lab data is used to complete an “instant nutrition assessment”? a. albumin and potassium b. transferrin and total lymphocyte count c. albumin and total lymphocyte count d. prealbumin and potassium

NAS11

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30. The cirrhotic patient, a 5’8", 60 kg, 50-year-old with encephalopathy, has daily protein needs of a. 30 to 45 gm b. 48 to 60 gm c. 90 gm d. 65 to 75 gm e. 25 gm

31. ________ becomes an essential amino acid during stress and sepsis. a. alanine b. glutamine c. glycine d. leucine e. tyrosine

32. Metabolic alkalosis is compensated for in the body with: a. metabolic acidosis b. respiratory acidosis c. respiratory alkalosis d. a & b e. b & c

33. Which protein parameter is most affected by iron deficiency? a. albumin b. transferrin c. prealbumin d. retinol-binding protein

34. Your patient’s RQ is 1.2. What is your assessment? a. the patient is being fed appropriately b. the patient may be overfed c. the patient may be underfed d. the patient is receiving too many calories from protein

35. Which vitamin is often deficient in alcoholics? a. vitamin A b. thiamin c. niacin d. all of the above

36. Malnutrition occurs in hospitalized patients as a result of: a. poor diet history b. obesity c. drug-nutrient interactions d. inadequate nutrient intake, the inflammatory response and increased stress e. b & c

37. Niacin deficiency is characterized by: a. diarrhea b. dermatitis c. dementia d. all of the above

38. Anthropometrics measurements are excellent for assessment of nutritional status in the elderly. a. true b. false

39. Cancer patients may be: a. hypometabolic b. hypermetabolic c. normometabolic d. any of the above

40. The malnourished patient with congestive heart failure has an enlargement of the heart. a. true b. false

Examination cont‘d NAS11

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