Nutrition Support Enteral & Parenteral Nutrition

Nutrition Support

6400 Arlington Blvd, Falls Church, VA 220421-888-781-5388 www.nutritiondimension.com

Nutrition SupportEnteral & Parenteral Nutrition

7th edition • Revised August 2009

by Martha G. Acevedo, ms, rd

7950 Jones Branch Drive, 7th Floor, McLean, VA 221071-800-866-0919 • www.continuingeducation.com

Nutrition Support:Enteral & Parenteral Nutrition

7th Edition • Revised August 2009by Martha G. Acevedo, ms, rd

Martha G. Acevedo, ms, rd, is Operations Manager for Guest Services at Tri City Medi-cal Center in Oceanside, California. She participates in the nutritional care of patients in the Intensive Care Unit and oversees all nutrition and nutrition support activities at this 377 bed medical center, including training and education for a staff of seven dietitians and technicians. She has maintained her certification as a Certified Nutrition Support Dietitian since 1990, and was recognized by the Calif. Dietetic Assn. for Excellence in Clinical Dietetics in 1998.Education: MS (Biology & Nutrition), University of Bridgeport (magna cum laude); BS (Home Economics & Dietetics), University of Tennessee (magna cum laude).

© 1989-2009 Nutrition Dimension/Gannett Education, Inc.No part of this course may be reproduced, duplicated or copied in any way without the written per-mission of the copyright holder.

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

Graphic Design & Typesetting

EXPIRATION DATE: Students of all professions must submit this course for credit no later than August 30, 2014. Credit will not be awarded for this course after that date.

Course Code: RD114

This course approved for:RD/DTR................ 12.CPEUCDM............12.Clock.HoursDTR........................ 12.CPEU.

7950 Jones Branch Drive, 7th Floor, McLean, VA 221071-800-866-0919 (US & Canada) • 1-703-854-2531 (overseas) FAX:1-703-854-2531 • e-mail: [email protected]

Nutrition Support ii

How to Earn Continuing Education Credit

1. Read or watch the course material. Don’t forget to review the course objectives and take note of course tools available to you. The objectives provide specific learning goals and an overview of the course. Read the material in the order presented. If you need help with the material, please e-mail [email protected] with your specific question. We will forward your inquiry to the author, so allow adequate time for a reply.

2. CE credit will not be awarded for this course after August 30, 2014.

3. If you have an account on Nurse.com, TodayinPT.com, or TodayinOT.com, or NutritionDimension.com, please use that account username and password to sign in on ContinuingEduation.com. If you don’t already have one, please sign up for a user account. Click “sign up” or “login” in the upper right hand corner of any page on ContinuingEducation.com. If you have a CE Direct login ID and password (generally provided by your employer), please log in as you normally would at lms.nurse.com and search for this topic title.

4. Go to the “my courses” section of “my account.” Click on the title of the course you want to com-plete and then on “start course.”

5. Click “start test” to begin the exam. To earn contact hours, you must achieve a score of 75% on your multiple-choice exam for most courses. For webinar courses, you will need to achieve a score of 100%. You may retake the test as many times as necessary to pass. Clues are not provided on the exam. Certificates will be date/time stamped with the time and date of the day the user passes the test (Eastern Time, U.S.).

6. After successfully completing your exam click, “complete required survey.” In order to complete the test process and receive your certificate of completion, you must take a few moments to answer a brief survey about the course material.

7. After completing the survey, you will be taken to your transcript. Under Courses Completed, you can view, print, or e-mail your certificate.

8. Three months after you complete a course, you will receive an e-mail asking you to complete a follow-up survey. This is vital to our educational requirements so we can report our quality outcomes and effectiveness.

We report course completions to National Commission for Health Education Credentialing (NCHEC) quarterly and The Association of Nutrition & Foodservice (ANFP, formerly DMA) monthly. Other professions should follow their certifying organization’s reporting instructions. We keep a record of course completions for 7 years.

A Word About Copyrights: We encourage health professionals to use material from this course in their practice. Please follow these guidelines: (1) Credit the author, Nutrition Dimension/Gannett Education and any referenced source. (2) Course material may not be sold, published, or made part of any program for which a fee is charged, without written

permission from Nutrition Dimension/Gannett Education. (3) Inform Nutrition Dimension/Gannett Education by letter if you wish to make significant use of material from this

course (e.g. if you wish to duplicate Appendix pages for a training session or patient handout).

Nutrition Support

ContentsChapter Topic Page

1 Nutrition Assessment 3 Anthropometrics • Biochemical Review Energy Requirements • Protein Requirements Subjective Global Assessment

2 Enteral Nutrition 15 Normal Digestion • Enteral Nutrition Support Benefits of Enteral Feedings • Access • Formulas Methods of Feeding • Complications

3 Parenteral Nutrition 31 Criteria for Use • Access • Formula Preparation Energy Sources, Protein, Vitamins and Minerals Formulas • Monitoring and Complications

4 Gastrointestinal Disorders 45 GI Tract Problems • Malabsorption Short Bowel Syndrome • Pancreas

5 Stress and Sepsis 59 Stress Response • Nutrition Requirements • Energy Fat, Carbohydrate, Protein • Arginine and Glutamine Vitamins and Minerals • Nutritional Repletion

6 Obesity and Diabetes Mellitus 73 Determining Nutrient Needs • Nutritional Assessment Long-term Care • Diabetes

7 Respiratory Failure 79 Energy Requirements • Assessing Nutrient Needs Treatment Modalities • Formulas • ARDS Assessment and Monitoring

8 Renal Disease 89 Nutritional Assessment • Chronic Renal Failure Enteral Feedings • TPN • Acute Renal Failure • Protein

9 Liver Disease 101 Metabolism of Protein, Fat, Carbohydrates, Micronutrients Nutritional Assessment • Micronutrients Nutrition Support

10 Cancer Patients 109 Surgery, Radiation, Chemotherapy Nutrient Needs

11 AIDS and HIV-Positive Patients 117 Effects of AIDS on Immune System Nutrition Assessment • Nutrition Support

12 Transition to Home Care 125 Guidelines for Home Nutrition Support Complications of Long-term TPN

Appendices 131 Review Question Answers • Physical Changes of Malnutrition • Height & Weight Tables Creatinine • Height Index • Anthropometric Measurement Standards • Tricep Skinfold/ Arm Muscle Circumference • Non-nutritional Factors • Nutrient Absorption • TPN Monitoring Form Recommended • Dietary Allowances • Standard TPN Admixtures • Determining TPN Values • Metabolic Complications of TPN

Exam 147

iii

Nutrition Support

Learning ObjectivesAfter completing this course, the student will be able to:

1. Describe the pros and cons of using anthropometric measurements for the nutrition assess-ment of the critically ill patient.

2. Analyze the usefulness of serum albumin, prealbumin and transferrin in assessing the nutri-tional status of a critically ill patient.

3. Determine the caloric needs of patients with the following types of diseases: severe sepsis, obesity, liver disease, renal disease and pulmonary disease.

4. Determine the type, amount, route and method of enteral feedings for hospitalized patients with the diseases listed in objective #3.

5. List five causes of diarrhea in hospitalized patients.

6. Discuss four complications of enteral feedings and the cause of each complication.

7. Analyze enteral formulas and discuss the pros and cons of the type and amount of protein, carbohydrate and fat found in each one.

8. Determine if a hospitalized patient is a candidate for total parenteral nutrition (TPN).

9. Calculate the total calories, nonprotein calories, total protein, calorie to nitrogen ratio and amount of fat in TPN solutions.

10. Identify metabolic complications that occur with TPN, the cause of the complications and a plan of action if the complications occur in a patient.

11. Design a nutrition care plan for a patient who has had his jejunum and ileum removed, beginning post-op and continuing until the patient is discharged.

12. Discuss how liver, renal and pulmonary disease impact the following nutritional needs of hospitalized patients: calories, protein, fat, carbohydrate, electrolytes and vitamins and minerals.

13. Explain how AIDS and ARC impact the nutrition needs for calories, protein, fat, carbohy-drate, electrolytes and vitamins and minerals.

iv

1Nutrition Support

Introduction

Nutrition support is complex nutrition care provided to those patients who are,or have been, critically ill. It also applies to care provided to those patients with diseasestates that affect their nutritional status and/or ability to utilize particular nutrients. Ithas evolved from simple tube feedings into a highly complex system which meets thenutrition needs of patients who would not otherwise have survived medical crises.

Nutrition support patients can vary from an elderly patient with dementia whorequires enteral (gastric or duodenal tube) feedings, to a patient who has had significantgastrointestinal surgery and requires parenteral (intravenous) feedings, to a patient whohas acute renal failure and septic shock and cannot digest and utilize nutrients exceptthrough intravenous feedings.

Nutrition support is, therefore, a varied and highly specialized field, requiring anincreased level of knowledge by the nutrition care practitioner. This knowledge basecan only come with experience and the continual study of appropriate literature, as newideas and research are promulgated and new feeding formulas developed. No doubt thefield will continue to grow and change, making some practices now in use obsolete.

The American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) is an excel-lent resource for the person interested or involved in nutrition support. ASPEN pro-duces a bimonthly journal, Journal of Parenteral and Enteral Nutrition (JPEN), that pro-vides state-of-the-art information on research and trends in nutrition care, and hasdevised standards of care for various areas of nutrition support and standards of prac-tice for the different disciplines providing care. Also published by ASPEN is a bi-monthly publication Nutrition in Clinical Practice, a more hands-on resource which canbe invaluable in your practice and several excellent reference books.

ASPEN has a certification process for its members. Currently, nutrition supportcertification is attainable for qualified dietitians, nurses, physicians, and pharmacists;the designation is CNSC (Certified Nutrition Support Clinician).

2Nutrition Support

Dietitians in Nutrition Support, a practice group of the American Dietetic Associa-tion, is also an excellent resource for dietitians, dietetic technicians and students inter-ested in nutrition support. This practice group publishes an informative bimonthlynewsletter, Support Line, and conducts workshops across the country.

This course will provide practical guidelines and references for the nutrition carepractitioner, focusing on the clinical practitioner’s role. Methods of nutrition assess-ment, an overview of enteral and parenteral regimens, and guidelines for the nutritionsupport of patients with specific diseases and conditions are included. As in all areas ofnutrition, research has changed accepted clinical practice and calculations. This coursereflects the latest thinking in clinical practice, and will be updated periodically through-out its publication period as information emerges.

Throughout the course, I refer to specific brand-name feeding formulas. I wish toemphasize that these are included because they are in general use in hospitals every-where. No mention of a brand name should be construed as an endorsement, exceptwhere I have pointed out that one product meets specific criteria. There are no commer-cial objectives to any such mention, and neither I nor Nutrition Dimension, Inc., hasreceived any incentives or consideration for mentioning a specific brand name or com-pany. Rather, I have attempted to use my own experience and that of the sources citedin this course in the most practical way: by making specific points in terms the averagepractitioner can understand and use in his or her daily work.

Because of the complex nature of the topic and the fact that only an objective post-examination is available, I have included review questions at the end of each chapter,and provided answers and discussion as an appendix. I strongly advise that the studentattempt to complete these questions before reading the answers. They are not “extra.”Rather, they are an integral part of the course, and will serve to illuminate the textualmaterial and facilitate completion of the post-exam. The case studies I’ve designedsimulate typical problems and situations that occur in hospital care — many of them, infact, are drawn from actual cases. Since nothing is ever totally “by the book,” these willhelp the student see how a case can change, and how seemingly minor variations in labvalues can be important. Again, I urge the student to follow these discussions closely.

In the 20 years since the first edition of this course was published, numerousdietitians have responded with cogent observations and thoughtful advice for making itbetter. Throughout the period, these recommendations have enabled me to make minorcorrections and clarifications in the text, which the publisher was able to incorporate insubsequent printings. It is impossible to name all the dietitians who took the time towrite or call with advice, but their input and concern is greatly appreciated, as is that ofthe reviewers for certification, who also made many excellent suggestions.

3Nutrition Support

Chapter One:Nutrition Assessment

Nutrition assessment is a valuable tool in the early identification of malnutritionand/or undernutrition. Malnutrition and/or undernutrition has been estimated tooccur in at least one in five hospitalized patients. The incidence increases to almost 50percent in patients with a longer length of stay (Hill, 1992). Often a patient’s nutritionalstatus will deteriorate during a hospital stay. Reasons for this decline in nutritionalstatus may include anorexia with resultant decreased intake, surgery, infection, medica-tion interactions, chemotherapy and radiation therapy.

Malnutrition may increase the incidence of sepsis, cause poor wound healing andpoor respiratory effort, and decrease absorption of nutrients (Cerra, 1984). The patientwith malnutrition is at increased risk for infection because of compromised lymphocytefunction and growth. Antibodies, phagocytes and macrophages all have diminishedfunction and/or effectiveness (Kline, 1999). Morbidity associated with malnutrition hasbeen estimated at 25 percent, while mortality due to malnutrition alone occurs in about5 percent of cases. Protein stores are depleted by as much as 75 gm/day during theinitial stages of malnutrition (Cahill, 1988). Early nutrition therapy may decrease apatient’s propensity to develop malnutrition and delay or prevent the onset of thesecomplications.

The first step in providing appropriate nutrition therapy is nutrition assessment. Inperforming a nutrition assessment, the practitioner must review all aspects of thepatient’s history, appropriate current factors, and clinical and biochemical parameters.Initially, something as simple as a nutrition screening should be carried out (see charton the following page). The information obtained in the screening can be used as areference point for comparison later in the hospital course and can assist in identifyingthe patient at increased risk for nutrition problems during the hospital stay.

4Nutrition Support

After the initial screening has identified a patient as high risk, further evaluationshould include examination for any overt clinical signs of malnutrition. Obvious calo-rie/protein malnutrition may be manifested by muscle wasting, edema or ascites, andchanges in hair and skin condition. Symptoms of vitamin and mineral deficiencies mayinclude changes in the condition of the skin, eyes, mouth and gums. Neurologicalchanges such as ataxia, convulsions and encephalopathy may occur with malnutrition.A more complete listing of physical changes associated with malnutrition can be foundin Appendix #1. Another course in this series, Nutrition Assessment: Tools and Techniquesalso outlines the complexities of assessment in more detail.

Clearly, one of the most important components of assessment is height andweight. These give an indication of current nutritional status, as well as of chronicchanges in nutritional status. Height helps in determining ideal body weight (IBW).

This figure can be determined by using the Metropolitan Life Insurance Height/Weight Tables (Appendix #2) or the Hammwi method:

Males: 106 lb, plus 6 lb per inch over 5 feet +/– 10 percentFemales: 100 lb, plus 5 lb per inch over 5 feet +/– 10 percent

A comparison of actual weight to IBW should be made to determine the existence ofunderweight or obesity, as shown on the next page. Factors such as edema, ascites, andfluid overload should be taken into account in the assessment of weight for height data.

Nutritional Screening

Height and weight Chewing/swallowing problemsDiet history Diagnosis & chewingWeight change history Laboratory dataAppetite Bowel habits

Ideal Body Weight Comparison

> 200 percent = Morbidly obese> 150 percent = Obese> 120 percent = Overweight80 to 90 percent = Mild caloric depletion70 to 80 percent = Moderate caloric depletion< 69 percent = Severe caloric depletion

Hopkins B: Assessment of nutritional status. In Nutrition Support Dietetics. ed. by ShrontsEP, ASPEN, Silver Spring MD, pp 15-60, 1989.

5Nutrition Support

Another comparison — actual weight to usual weight — can be made to determinethe relevance of changes in body weight. This comparison may be more important thanother assessments in the clinical setting as an indicator of malnutrition. An uninten-tional and/ or unexplained weight loss or gain of more than 10 percent of body weightwithin 6 months or 7.5 percent within 3 months has been associated with increasedsurgical mortality, and should alert the clinical practitioner to the possibility of compli-cations affecting nutritional status.

Body mass index (BMI) compares weight to height and is sometimes utilized todetermine the incidence of obesity and/or malnutrition.

ANTHROPOMETRICS

The use of anthropometrics, including measurements of skinfolds, mid-arm cir-cumference, mid-arm muscle circumference, and arm muscle area, is of limited value incare of the critically ill patient. Since anthropometric measurements represent chronicchanges, they are of more use in the assessment of the long-term outpatient and thepopulation as a whole. Anthropometrics, other than height and weight, are not oftenutilized. They are more useful in tracking long-term patients to assess changes in nutri-tional status.

Nonetheless, the nutrition care practitioner should be familiar with the processes ofobtaining these measurements and of their utilization in assessing the patient. Measure-ments of skinfolds, including triceps skinfolds (TSF), involve the use of skinfold cali-pers. Interpretation of the results can be found in Appendix #3.

The technique is refined with practice, but different measurements may occur withdifferent practitioners or with the same practitioner at different times. The accuracy ofthis measurement should be considered variable at best.

Skinfold measurements provide a means of identifying subcutaneous fat stores.Interpretation of these measurements is done by comparing the actual patient value to apreestablished standard value, developed from data derived from the National Healthand Nutrition Examination Survey (NHANES II), as shown in Appendix #3.

BMI

BMI =

19-25 appropriate weight (19-34 yr)21-27 appropriate weight (>35 yr)>27.5 obesity

27.5-30 mild obesity30-40 moderate obesity

>40 severe or morbid obesity

17-18.5 mild malnutrition16-17 moderate malnutrition

<16 severe malnutrition

weight (kg)Height2 (m2) (height squared (meters squared))

6Nutrition Support

The values were obtained from subjects ranging from 1 to 74 years of age(Hopkins, 1989; Grant, 1985). A percentage of standard calculation is then used toidentify the level of caloric depletion, as shown below:

Percent of Standard = X 100

Measurements of mid-arm circumference (MAC) and mid-arm muscle circumference(MAMC), with determination of arm muscle area (AMA), are of some use in determiningthe status of somatic protein stores. The chart on the following page shows the formulasused to determine MAMC and AMA and the standards to which these values can becompared.

Another means by which nutritional status can be determined, especially in theelderly, is body mass index, or BMI. BMI is determined by dividing the patient’s weightby his height squared and then comparing to standards. BMI correlates well to body fat,but may be skewed in very ill patients who have reduced LBM. A desirable BMI is 24 to29, with evidence of nutritional depletion with a level less than 24 and possible obesitywith a level greater than 29 (Burns, 1992).

Another standard for measuring muscle mass is the creatinine height index (CHI).Creatine is found primarily in muscle tissue and is continually converted to creatinine,which is almost totally excreted in the urine. Thus, the level of creatinine in the urine isa good indicator of creatine levels in the body, and can be used to estimate lean bodymass (Waiser, 1987).

Urine collected during a 24-hour period is analyzed for creatinine content. Thislevel is then compared to pre-established standards, shown below. Appendix #2 listsexpected creatinine height index values.

patient valuestandard value

Arm Measurement Standards

(all measurements in centimeters)

MAMC = MAC – (3.14 x TSF)AMA = [MAC – (3.14 x TSF)]2

4 π

TSF MAC AMAStandards Standards Standards

Male 12.5 29.3 25.3Female 16.5 28.5 23.2

7Nutrition Support

Measurement of creatinine excretion has limitations, and is subject to certainvariables. Dietary intake of creatinine, creatine and protein can affect the level of creati-nine excreted and, therefore, the CHI.

Since creatinine excretion, as well as lean body mass, decreases with age, CHI maynot be an accurate reflection of muscle mass for the elderly population (Waiser, 1987).CHI is also of little or no use in patients with renal failure, since creatinine excretion islimited or absent in these patients. Also, expected values may change with body framesize. Because of these variables, CHI is not often used as a nutrition parameter. I do notuse it, because of the variables associated with body frame, age and renal function.

BIOCHEMICAL REVIEW

Laboratory and biochemical studies and values in nutrition assessment are of useprimarily in assessing visceral protein status, the status of hepatic protein synthesis andmicronutrient status (vitamins, minerals and electrolytes).

A simple method to determine if intake is adequate during illness is throughnitrogen balance studies. Since approximately 80 to 90 percent of all urinary nitrogen iscomprised of urinary urea nitrogen (UUN), nitrogen balance is determined by themeasurement of UUN in a 24-hour urine collection. Increasing UUN by 20 percent willaccount for the non-urea urinary nitrogen losses. This value is then utilized in theformula below.

Nitrogen balance = — [(UUN x 1.2) + (2 to 4)]

A nitrogen balance of less than minus 2 suggests catabolism; a balance of morethan plus 4 indicates anabolism. Nitrogen balance studies tend to overestimate thenitrogen actually lost and are dependent on the accuracy of urine collection and therecording of protein intake. For the patient on total parenteral nutrition (TPN), theamount of nitrogen per gram of protein will vary with the amino acid formula utilized.(I generally use the figure 6.06.)

Creatinine Height Index (CHI)

% Cr Excretion = X 100

AveragesFemales: 18 mg Cr/kg IBW (range 16-22 mg)Males: 23 Crkg IBW (range 20-26 mg)

Interpretation: >80% = mild depletion60 – 80% = moderate depletion<60% = severe depletion”

actual 24 hour Cr excretionexpected 24 hour Cr excretion

24 hour protein intake (gm)6.25

8Nutrition Support

Nitrogen balance studies are difficult to complete in patients with hepatic or renalfailure and may be inaccurate in those patients with protein-losing enteropathies,malabsorption, abscesses, and fistulas. It was determined that a twelve hour urinecollection for UUN can give a satisfactory estimate of a 24-hour UUN if the figure isdoubled (Candio, et al., 1991). This process works most effectively with those patientson parenteral nutrition support; 24-hour urine collections are necessary for the patienton enteral or oral feedings.

Urea kinetic modeling and urinary nitrogen appearance (UNA) can be used in thepatient with acute or chronic renal failure. While urea kinetic modeling is more accuratethan UNA, it requires the use of complicated equations and frequent blood draws.Measurements of weight and BUN are taken over 1 to 3 days and during interdialyticintervals (Hopkins, 1993; Tayek, 1988). The following formula is then utilized to deter-mine urinary nitrogen appearance (UNA):

(BUNf - BUNi) x 0.6BW + (BWf - BWi) x BUNfwhere i = initial, f = final, BUN = blood urea nitrogen (gm/liter), and BW = body weight (kg)

Tests to determine a patient’s level of immunocompetence may be an effectiveindicator of nutritional status. A malnourished patient is at increased risk for opportu-nistic infections. Total lymphocyte count (TLC) is recognized as a measure of immunefunction and has also been used in determining nutritional status, as shown on thefollowing page, using the white blood count and the percentage of lymphocytes fromthe blood count differential.

However, TLC is depressed by factors other than nutritional status. These factorsinclude infection, steroid or immunosuppressive therapy, cancer and its conjunctivetherapies, surgery, and certain inherited and acquired immune deficiency states(Hopkins, 1989; Lang, 1989; Glassman, 1986).

Immune response can also be tested with delayed hypersensitivity skin testing. Atleast three antigens to which the patient has likely been exposed (Candida, purifiedprotein derivative [PPD], Trichophyton, and mumps) are injected subcutaneously. Re-sponse to the injections is monitored. A healthy immune system responds by producinga localized reaction around the injection site within one to two days.

Total Lymphocyte Count

TLC = white blood count X

1500 to 1800 = mild depletion900 to 1500 = moderate depletion

< 900 severe depletion

Cerra FB: Pocket Manual of Surgical Nutrition. CV Mosby Col., St. Louis, 1984.

% lymphocytes100

9Nutrition Support

A positive response, swelling around the injection site, indicates adequate immu-nocompetence and nutritional status. If the area of swelling is less than 5 mm in diam-eter, the patient has altered or poor immunocompetence and may also be malnourished.Non-nutritional factors can affect immunocompetence, so delayed hypersensitivity skintesting is not commonly utilized. Total lymphocyte count and delayed hypersensitivitytesting are rarely utilized at present for nutrition assessment.

Hepatic protein production can be studied by utilizing biochemistry values, suchas albumin, transferrin, thyroxine-binding prealbumin, and retinol-binding protein.Serum albumin comprises 50 percent of all serum protein but has a half-life of about 20days, making 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 of the chemical orsubstance. In assessing a patient, and especially in addressing the adequacy ofrenourishing a patient, always keep the half-life in mind. ) Decreased albumin levels areassociated with poor outcome, increased length of stay, increased incidence of complica-tions, and death (Shronts, Fish, Hammond, 1998).

Appendix #4 shows non-nutritional factors affecting serum albumin levels, and thechart at the top of the next page outlines the level of protein depletion associated withvarious albumin, transferrin, and prealbumin levels.

Transferrin’s shorter half-life (8 to 10 days) makes it a somewhat more exact mea-sure of nutrition status and is more useful in liver disease than albumin. Serum transfer-rin levels are affected by many of the same factors as those that have an effect on albu-min levels, as shown in Appendix #4. Transferrin can be estimated by measuring totaliron-binding capacity (TIBC) levels in patients who are not obviously malnourished.The formula used should be standardized for each individual institution, based onactual measurement of transferrin and TIBC levels, which are then used to create anequation so that transferrin can be determined from TIBC. Examples of some practitio-ners’ formulas are:

Calculating Transferrin Levels

Blackburn: Transferrin (mg/dl) = 0.8 TIBC (mg/dl) – 43Heymsfield: Transferrin (mg/dl) = 0.9 TIBC (mg/dl) – 4.5

Grant: Transferrin (mg/dl) = 0.87 TIBC (mg/dl) + 10

Protein Depletion

Albumin Transferrin PrealbuminMild: 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 gm/dl 5 to 10 mg/dlSevere: 2.1 gm/dl < 100 mg/dl <5 mg/dl

10Nutrition Support

Thyroxine-binding prealbumin (or transthyretin) has a half-life of 2 to 3 days,making it a more appropriate measure of the adequacy of nutrition intervention. Itslevels are also affected by the same factors as albumin and transferrin. Retinol-bindingprotein’s half-life of only 12 hours makes it highly sensitive to acute changes. Its levelsare also affected by non-nutritional factors such as liver disease, renal disease, surgery,vitamin A deficiency, and chronic illness.

However, all of these (albumin, transferrin, prealbumin, and retinol-binding protein)are more a measurement of the body’s response to an acute illness or injury, especially inthose patients in a critical care setting. While levels may be considered, measurement ofthese markers does not aid in assessment of nutrition status in the critically ill patient(McClave, et al., 2009; Martindale and Maerz, 2006; Raguso, et al., 2003).

Assessment of vitamin and mineral status may be difficult since measurement ofserum levels does not reflect actual body stores of all micronutrients. Assessment of intakecan be determined from diet history and clinical examination to detect specific deficiencysymptoms. The recommended daily allowances (RDA) and dietary reference intakes (RDI)for vitamins and minerals are listed in Appendix #7 (RDA, 1989; DRI, 1997; DRI, 1998).

ENERGY REQUIREMENTS

Several methods of assessing nutrition requirements are available to the practitio-ner. If metabolic carts are available, indirect calorimetry can be used to determinerequirements through the measurements of oxygen consumption, carbon dioxideproduction, and minute ventilation. The Weir equation, calculating resting energyexpenditure (REE) is used to determine needs (Compher, 1993):

REE = 1.44 x [(3.9 x VO2) + (1.1 x VCO2)]For repletion: 1.5 x REEFor maintenance: 1.3 x REE

Adjustment of REE is done to account for activity since REE is measured at asteady state. Requirements for basal energy expenditure (BEE) can also be estimatedusing the Harris-Benedict equation, a formula developed in 1919 on 239 healthy adults:

Males: 66.5 + (13.75 X wt. (kg) + (5 X ht. (cm) – (6.76 X age)Females: 655 + (9.56 X wt. (kg) + (1.85 X ht. (cm) – (4.68 X age)

Once the BEE is determined, stress factors are applied to correct for various stressstates. Another method for calculating energy needs, utilizing caloric needs per kilo-gram of body weight, is utilizing a factor of 25 to 30 kcal/kg and/or less in the obesepatient — where permissive underfeeding is recommended (see chapter onobesity)(McClave, et al., 2009). You’ll note that caloric requirements are lower than whatwe once thought.

Carol Ireton-Jones has adapted the Harris-Benedict equation to account for thepresence of trauma, burns, and/or intubation (Ireton-Jones, 1989; Hopkins, 1993),shown on the following page.

11Nutrition Support

PROTEIN REQUIREMENTS

Protein requirements, determined from nitrogen balance studies described earlier,can also be calculated from ideal body weight and by utilizing predetermined caloricneeds and specified calorie/nitrogen ratios. The RDA for protein is 0.8 gm/kg of bodyweight. This factor changes with various disease states and will be discussed in laterchapters. Calorie/nitrogen ratio is based on the patient’s clinical condition. A level of150 to 1 is generally accepted as reasonable, but this recommendation changes withstress, renal disease, liver disease, etc.

Another method of calculating protein needs is based on the patient’s weight anddisease condition. As the severity of the disease increases, so does the need for protein.In trauma patients, the protein needs increase to 1.5 to 2.0 gm protein/kg. In patientswith impaired kidneys or liver function, protein needs may need to be lower. In thefollowing chapters the protein needs of various disease states will be discussed.

Nutrition assessment is only the first step in providing nutrition care and supportto our patients. With experience, the ability to make accurate assessments will improve.The practitioner should continue to remain aware of changes in the patient’s medicalstatus as well as of changes in the methods of nutrition assessment.

SUBJECTIVE GLOBAL ASSESSMENT

Once you have completed a review of the patient’s medical and dietary history andassessed nutrition status by examining the patient’s physical condition, you can adaptthis data for use in completing a subjective global assessment (SGA).

As described by Detsky, et al., specifically, five criteria obtained in the history and

Energy Expenditures for Hospitalized Patients

For ventilator-dependent patients:EEE = 1784 – 11 (age) + 5 (wt) + 244 (S) + 239 (T) + 804 (B)

Estimated Energy Expenditure (EEE) = kcal/d; wt is in kg;S =sex (male = 1, female = 0);

T = trauma (1 if present; 0 if absent);B= burn (present=1;absent=0)

For spontaneously breathing patients:EEE = 629 – 11 (A) + 25 (W) – 609 (O)O = obesity (1 if present; 0 if absent)

For patients with Swan-Ganz catheters:REE = CO (cardiac output) x Hgb (SaO2 – SvO2) x 95.18

SaO2 = % saturation of arterial blood; SvO2 = % saturation of venous blood

12Nutrition Support

physical are utilized in the SGA. These include weight change history, dietary intakechange, gastrointestinal symptoms, the patient’s ability to function and the diseaseprocess and its relation to nutritional needs. Physical assessment of loss of subcutane-ous fat, muscle wasting, ankle edema, sacral edema and ascites is also considered in therating of the patient based on SGA.

Weight loss over the previous 6 months of less than 5 percent is considered minor,5 to 10 percent weight loss is considered potentially significant and a weight loss ofgreater than 10 percent is definitely significant.

Changes in dietary intake are described as normal or abnormal; the length anddegree of abnormal intake are also considered. Any gastrointestinal symptom (nausea,vomiting, diarrhea and anorexia) lasting longer than two weeks is also noted. Func-tional ability is the patient’s energy level (i.e. bedridden, housebound, working). Themetabolic demand placed on the body by the illness is characterized as no stress, lowstress, moderate stress and high stress (Detsky, et al., 1987).

Criteria for History and Physical

*Weight change history: <5% weight loss over 6 mo. = minor depletion5-10% weight loss over 6 mo. = potentially significant depletion>10% weight loss over 6 mo. = significant depletion

*Change in dietary intake: Normal vs. AbnormalLength of change ____________ Degree of change ______

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

Functional ability of patient: bedridden house bound 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: 0 = normal

1+ = mild depletion2+ = moderate depletion3+ = severe depletion

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

*primary importance

13Nutrition Support

Physical assessment is characterized as: 0 = normal; 1+ = mild; 2+ = moderate; and3+ = severe, as used to assess degree of loss of subcutaneous fat, muscle wasting, ankleand 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 Cis “severe malnutrition” (Detsky, et al., 1987).

The most emphasis is placed on weight changes, poor dietary intake, loss of subcu-taneous tissue and muscle wasting. In fact, weight loss and the pattern of weight lossappears to be the most important component of SGA. Disadvantages to using the SGAtechniques 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 beginning to use SGA, Jeejeebhoy suggests that we begin by performing assess-ments together as a group so as to attain a consensus and more consistency from practi-tioner to practitioner.

I feel that many of us use subjective global assessment without even knowing thatis what we are doing. This type of assessment comes more easily with experience andexposure to a variety of patients, diseases and illnesses. For a more detailed discussionon SGA, refer to Detsky, et al., 1987.

REVIEW QUESTIONS

Note: These review questions are an important part of the course. Please take thetime to complete them in writing, and compare your answers with those given at theend of the coursebook. Completing the review questions in each chapter will also helpyou with the post-examination.

1. Why are anthropometrics of limited use in the nutrition assessment of the critically illpatient?

2. What are the best parameters for use in assessing protein status in critically ill pa-tients?

3. What factors other than nutrition status affect parameters of protein status?4. What are the caloric and protein requirements of a 30-year-old female, 5’8" tall, 130 lb,

hospitalized with multiple trauma after an automobile accident?5. What are the caloric and protein requirements of a 75-year-old male, 5’7" tall, 205 lb,

in the ICU with respiratory failure after a coronary artery bypass graft?

REFERENCES

Burns JT: Nutritional assessment: adjusting for age. Support Line XIV No. 4, 1992.Cahill G: Starvation: some biological aspects. In Nutrition and Metabolism in Patient Care. Kinney J,

Jeejeebhoy K, Hill G, et al., Eds. WB Saunders, Philadelphia, 1988.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. CV Mosby Co., St. Louis, 1984.Compher C: Calorimetry, body composition, nitrogen balance, labs. Unpublished address at A.S.P.E.N.

17th Clinical congress, San Diego, 1993.

14Nutrition Support

Detsky AS, Baker JP, O’Rourke K, et al.: Predicting nutritional associated complications for patientsundergoing gastrointestinal surgery. JPEN 11:440-446, 1987.

Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D and fluoride. National Acad-emy Press, Washington DC, 1997.

Dietary reference intakes for thiamine, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid,biotin and choline. National Academy Press, Washington DC, 1998.

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. (self published), Seattle, 1985.Hill GL: Body composition research: implications for the practice of clinical nutrition. JPEN 16:3;197-218,

May-June 1992.Hopkins B: Assessment of nutritional status. In Nutrition Support Dietetics. Shronts EP, Ed. A.S.P.E.N.,

Silver Spring, MD, 1989.Hopkins B: Assessment of nutritional status. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM,

Matarese LE, and Shronts EP, Eds. A.S.P.E.N., Silver Springs, MD, 1993.Ireton-Jones CS: Indirect calorimetry. In: Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A,

Eds. A.S.P.E.N. Publ, Rockville, MD, 1989.Kline DA: Nutrition & Immunity, Part I Immune Components & Nutrients. Eureka, CA: Nutrition Dimension, 1999.Lang CE and Cashman MD: Nutritional status. In: Dietitian’s Handbook of Enteral and Parenteral Nutrition.

Skipper A, ed. Rockville, MD: A.S.P.E.N. Publ. Co., 1989.Martindale RG and Maerz LL: Management of perioperative nutrition support. Curr Opin Crit Care 12:

290-294, 2006.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition

support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) andAmerican Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) JPEN 33(3): 277-316, 2009.

Raguso CA, Dupertuis YM, Pichard C: The role of visceral proteins in the nutritional assessment ofintensive care unit patients. Curr Opin Clin Nutr Metab Care 6: 211-216, 2003.

Recommended Dietary Allowances. 10th ed. National Academy Press, Washington, DC, 1989.Shronts EP and Lacy JA: Metabolic support. In Nutrition Support Dietetics, 2nd ed. Gottschlich MM,

Matarese LE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.Shronts EP, Fish JA, Hammond KP. Nutrition assessment. In Merritt FJ, Souba WW, KeethCK, et al. (eds).

The A.S.P.E.N. Nutrition Support Practice Manual. Silver Spring, MD: American Society for Parenteraland Enteral Nutrition, 1998.

Tayek JA: Albumin synthesis and nutritional assessment. Nutr Clin Prac 3:6:219-221, 1988.Waiser M: Creatinine excretion as a measure of protein nutrition in adults of varying age. JPEN 11:5:73S-

77S, 1987.

15Nutrition Support

Chapter Two:Enteral Nutrition

“If the gut works, use it!” This rule of thumb for clinical dietitians has beenreinforced by research showing the importance of maintaining healthy gut mucosa inthe critically ill patient. Enteral nutrition should be used “..if the GI tract is functional(sufficient in length and in absorptive capacity)..” and if the patient is unable “..to takenutrients through the oral route either totally or in part.” (JPEN, 2009).

NORMAL DIGESTION

The gastrointestinal tract acts to break down, metabolize and transport foods sonutrients can be utilized by the body. Chewing initiates the breakdown of foodstuffs inthe mouth. Salivary amylase, present in saliva, digests starch into polysaccharides,oligosaccharides and maltose.

Food then passes through the esophagus to the stomach, where it mixes withhydrochloric acid and pepsin. Except for the presence of intrinsic factor (necessary forthe absorption of vitamin B12), the stomach is not as vital to the digestive process as thelower portions of the digestive tract. Digestion of protein begins in the stomach; diges-tion of carbohydrate and fat takes place in the duodenum.

The food (now called chyme) passes through the pyloric sphincter into the duode-num, which is approximately 25 cm long. The release of chyme into the duodenumcauses the release of enzymes by the pancreas and the gastrointestinal tract, as well asthe release of hormones into the bloodstream.

16Nutrition Support

Digestion of starch occurs primarily here, by means of pancreatic amylase. Intesti-nal brush border enzymes further hydrolyze the oligosaccharides so that they can laterbe absorbed across the microvilli in the small intestine.

Normally, 90 to 95 percent of digestion occurs in the jejunum and ileum. Thecombined length of these two organs is about 260 cm. Protein digestion, which began inthe duodenum, continues here with the help of trypsin, chymotrypsin, and elastase. Thefree amino acids, dipeptides, and tripeptides are released and then absorbed across theintestinal mucosa via carrier-mediated mechanisms, also known as “pumps.”

Bile, made by the liver and released by the gall bladder, is important in the diges-tion of fat by acting as an emulsifier, allowing lipases to break down triglycerides tomonoglycerides, lysolecithin and free fatty acids. Micelles — complexes of approxi-mately 20 fatty acids, monoglycerides, lysolecithin and bile — are absorbed via thebrush border into the lymph system before entering the bloodstream. The fatty acidsend up in the liver where they are further metabolized.

Cells comprising the brush border villi are replaced every 3 to 5 days; their replace-ment is affected by nutritional status and the availability of various vitamins and miner-als. Nutrient deficiencies affecting the regeneration of the villi can compromise diges-tion and absorption.

Absorption of vitamin A and thiamine, iron, and calcium occurs in the duodenum.The jejunum and ileum are responsible for the absorption of vitamin C, thiamine,riboflavin, folic acid, niacin, B6, pantothenic acid, biotin, B12, copper, zinc, iodine, andvarious other minerals and electrolytes. Normal digestion can be altered by surgery,sepsis, trauma, malnutrition and illness. Physiologically, the body may be better served

Fat Digestion & Absorption

Long Chain Triglycerides (LCT)• Digested in intestine into monoglycerides and fatty acids• Formed into micelles to be absorbed into the body• Absorbed into the lymph system before the bloodstream• Fats metabolized in the liver before the rest of the body

Medium Chain Triglycerides (MCT)• Are not broken down in the intestines• Are absorbed directly into the bloodstream• Can be utilized by the cells before reaching the liver• Preferable in patients with fat malabsorption

17Nutrition Support

by the continued use of the digestive tract, as much as tolerable, during these times. Agood knowledge of normal digestion and absorption can assist in adapting nutritionsupport for the care of the sick patient. Appendix #5 lists gastrointestinal tract (GI)absorption sites.

Simple bowel rest can cause a significant decrease in the activity of the transportsystems for amino acids and glucose (Martindale, 1996). Motility of the bowel can beprofoundly affected by medications such as anesthetics. Other drugs that can impact themotility of the GI tract include anticholinergic agents, tricyclics, glucocorticoids, etc.(Martindale, 1996).

ENTERAL NUTRITION SUPPORT

Enteral nutrition is technically defined as any nutrition given via the GI tract.Generally, however, enteral nutrition has come to mean any nutritional intake providedthrough artificial means, i.e. a tube, inserted into some portion of the GI tract. A.S.P.E.N.has established guidelines for the use of enteral nutrition in patients (A.S.P.E.N., 2002,2009).

The primary criteria for enteral nutrition is the inability to ingest adequate nutri-ents by mouth and a gastrointestinal tract that can be used safely and effectively. Thechart on the next page lists when enteral nutrition support should be used routinely.

A.S.P.E.N. and the Society for Critical Care Medicine recommend that enteralfeedings should be initiated in critically ill patients who are “..unable to maintainvolitional intake.” (McClave, et al., 2009)

Enteral feedings should be initiated early, especially in those patients who arecritically ill. Artinian, et al., (2006) found that initiation of enteral feeding within 48hours of admission in critically ill patients resulted in a 20 percent decrease in ICUmortality and a 25 percent decrease in hospital mortality, with the greatest influenceseen in the sickest patients.

Enteral nutrition may be of use in the patient with major trauma and major sur-gery, with head injuries, in acute pancreatitis, in conjunction with radiation and chemo-therapy, and in liver and renal failure. Feeding through the GI tract may be of limiteduse during intensive chemotherapy and in the immediate postoperative or post-stressperiod, even in a well-nourished patient who will likely resume oral intake within 5 to 7days.

Enteral feedings are contraindicated for the patient with bowel obstruction, intrac-table vomiting, severe diarrhea, some forms of GI bleeding, persistent aspiration, andproblems with access that cannot be overcome, as shown on the following page(A.S.P.E.N., 2002; Kudsk, 1996).

18Nutrition Support

Acute enteritis and removal of more than 90 percent of the small bowel may becontraindications for the use of enteral nutrition support. The chart on the followingpage shows when enteral support should not be used. Contrary to what many think,postoperative ileus does not always preclude the use or tolerance of enteral feedings.Small bowel motility returns within 4 to 6 hours of surgery while gastric motility isresumed within 12 to 24 hours of surgery. Ileus in the colon can last as long as five daysbut enteral feedings can still be accomplished (Mueller, 1996).

• Inadequate oral intake for previous 5-7 days(patients w/protein/calorie malnutrition)

• Oral intake < 50% of needs for previous 7 to 10 days(previously well-nourished patients)

• Severe dysphagia

• Major full-thickness burns

• Small bowel resection with concurrent TPN(to provide faster recovery of small bowel)

• Low output enterocutaneous fistulas(unnatural openings from the GI tract to the skin)

Enteral Nutrition Criteria

Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients.JPEN 26(suppl):1Sa-138SA, 2002.

Enteral Nutrition Contraindications

• Complete obstruction of small or large bowel• Ileus• Severe diarrhea or vomiting without reponse to medication• High output external fistulas of the GI tract• Acute GI hemorrhage• Severe acute pancreatitis• Hypovolemic or septic shock (with mean arterial pressure <60 mm HG)• Extremely poor prognosis• Patient’s or guardian’s wish to forgo enteral support

Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN26(suppl):2002; Guidelines for the provision and assessment of nutrition support therapy in the

adult critically ill patient, JPEN 33:3, 2009.

19Nutrition Support

BENEFITS OF ENTERAL FEEDINGS

Feeding through the gastrointestinal tract is more physiologically sound thanfeeding with total parenteral nutrition. Enterally supplied nutrients first pass throughthe liver on their way to becoming completely metabolized. The liver helps to metabo-lize nutrients so that they can be used most effectively by other organs and cells. TPN-provided nutrients are exposed to other organs as well as the liver after being intro-duced to the bloodstream.

The presence of nutrients and growth factors inside the gastrointestinal tract isnecessary to effectively preserve gut villi and gut integrity. The villi is preservedthrough a maintenance of blood flow to the mucosa (Kudsk, 1996). The gastrointestinalvilli have been shown to atrophy with TPN alone (Souba, 1984). In stressed states,glutamine is required in increased amounts. Glutamine is a gut fuel; stimulation of villivia feeding increases the availability of glutamine for the gut.

When enteral nutrition is not utilized, immune response lessens (decreased IgAsecretion) , with a resultant increase in bacterial growth and possible gut bacterialtranslocation (Alexander, 1998; Hernandez, et al., 1999; Lara, Jacobs, 1998; Border, 1988).Bacterial translocation may occur with gut villi atrophy and bacterial overgrowth.

Gut atrophy can increase the permeability of the gut, resulting in the bacterialtranslocation and increased risk for systemic infection, as well as an increased risk formulti-organ dysfunction syndrome (Jabbar, et al., 2003; Kudsk, 2002). Glutamine, avail-able in enteral feedings and supplemented in elemental feedings, appears to be prefer-entially utilized by the small intestine for fuel in the starved or stressed state (Souba,1984; Bell, et al., 1989). The presence of an energy source for the gut is important inpreventing gut atrophy. Benefits of enteral feedings include:

• Improved immune response;• Decreased villous atrophy;• Prevention of bacterial translocation;• Improved nutrient availability to liver;• Improved nutrient metabolism by liver; and• Less expensive.

ACCESS

Attaining access to the gastrointestinal tract for enteral feedings is not as difficultas one might think. Nasogastric tubes can be utilized in patients with an intact gagreflex. However, these tubes may increase the risk of aspiration. Ideally, nasoenterictubes should be passed into the duodenum or jejunum, as the critically ill patient maybenefit because of delayed gastric emptying and increased risk for aspiration withnasogastric tubes.

Placement of tubes into the duodenum requires more skill and may require fluo-roscopy or endoscopy. Number 8 or #10 French tubes are usually well tolerated by mostpatients and can be used for most types of feedings. Smaller tubes are utilized for

20Nutrition Support

nasojejunal (NGJ) feedings. However, larger-bore tubes (#12 to #14 French) may benecessary when more viscous feedings are utilized (Krey, 1989).

Enterostomies are necessary when longer-term enteral nutrition support is indi-cated. A gastrostomy tube can be placed into the stomach either percutaneously viaendoscopy (PEG) or surgically. Gastrostomy tubes are usually #16 to #26 French in size(Duh, 1996). Gastrostomies are most often used in patients who have intact sphinctersand are able to absorb and metabolize most nutrients, but who are unable to takeenough nutrients orally to maintain or improve their nutritional status.

Once a gastrostomy is placed, feedings can usually be initiated within two hours(JPEN, 2009). Some studies have shown that 93 percent of the prescribed feeding isgiven to patients with a gastrostomy while only 55 percent of prescribed feeding isprovided to the patient with a nasogastric tube (Cummins, et al., 1995; Park, et al., 1992).

In those patients where gastric feedings are contraindicated (i.e. post significantgastrectomy, severe gastroparesis, or atrophic gastritis), a needle catheter or larger-borejejunostomy may be utilized (Kirkland, 1989). Jejunostomy feedings can be initiatedwithin 12 to 24 hours after placement through a tube that ranges from #8 to #14 French(Duh, 1996).

Jejunostomy feedings are associated with a decreased risk for aspiration; twosphincters (esophageal and duodenal) and the ligament of Treitz separate the esophagusfrom the feeding site. Since aspiration occurs anywhere up to 89 percent of patientsreceiving enteral feedings, jejunostomy feedings may be beneficial in that the aspirationrisk falls to 0.67 to 1.37 percent (Kearns, 1996). However, the incidence of Clostridiumdifficile (C. diff) associated diarrhea is significantly higher in patients with post pyloricfeedings (JPEN, 2009).

FORMULAS

Enteral formulas can generally be classified into four categories: intact nutrients,predigested or elemental, disease-specific, and modular, with subcategories, shown inthe chart on the following page.

Intact nutrient formulas can be used with an intact and fully functional GI tract.They are generally well tolerated in those patients who are anorectic, cachectic andcatabolic. They can also be used in patients who experience dysphagia or other swal-lowing disorders, or who are otherwise unable to ingest oral nutrition.

Standard intact nutrient formulas are usually lactose-free and generally are iso-tonic. Usually inexpensive, they are composed of approximately 55 percent caloriesfrom carbohydrate, 10 to 15 percent from protein and 30 percent from fat. Some of theintact formulas are more nutrient-dense than the conventional feedings (1.2 kcal/mL asopposed to 1.0 kcal/mL) and contain canola oil rather than more saturated fats.

21Nutrition Support

Calorically-dense intact nutrient formulas can be used in those patients requiringfluid restriction, cyclic feedings or bolus feedings. These feedings contain 1.5 to 2.0kcal/mL and are usually higher in nitrogen as well. Tolerance to these formulas is not asgood, since the increased fat used to make them calorically dense is cleared more slowlyfrom the stomach.

Fiber-enriched intact nutrient formulas are usually isotonic and can be used inthose patients with either diarrhea or constipation. Patients with impaired gastricemptying should not be given a fiber rich formula (Charney, 2001). Many facilitiesutilize fiber enriched formulas as their “house” formula. Fiber content of enteral formu-las ranges from 5 to 14 gm/l.

Predigested or elemental feedings require minimal digestion and can be utilized inthe patient with a partially or minimally functional gastrointestinal tract. Elemental andpeptide feedings can be used in patients with decreased absorptive capacity, such asthose with Crohn’s disease, gastrointestinal fistulas and malabsorption. They may alsobe utilized in patients with pancreatitis.

Elemental feedings contain only 1 to 4 percent calories from fat (vegetable oil),while peptide formulas contain as much as 30 percent calories from fat (from vegetableoils and MCT oils).

Peptide formulas have an osmolality of about 450 mOsm/kg, while elementalfeedings are even more hypertonic (500 to 800 mOsm/kg). The hypertonicity is causedby the presence of amino acids, di- and tripeptides, and simple carbohydrates.

Hypotonic or hypertonic feedings may delay gastric emptying and can causediarrhea. Because the gut needs to maintain isotonicity in relation to the bloodstream, ahypertonic solution will be made more isotonic by the gut taking up fluid, therebyincreasing the potential for diarrhea.

Peptide formulas may improve anabolism and nitrogen balance better than el-emental formulas. Some peptide formulas may also stimulate protein absorption andreduce diarrhea in hypoalbuminemic patients (Brinson and Koltz, 1988; Skipper, 1989).Peptide formulas will be discussed further in a later chapter.

Enteral Formulas

• Intact nutrient formulas – standard or calorically dense, includingfiber containing formulas

• Predigested or elemental formulas – peptide formulas

• Disease-specific formulas

• Modular formulas

• Immune-modulating formulas

22Nutrition Support

Disease-specific formulas have been developed for liver disease, renal failure,pulmonary disease, stress and sepsis, diabetes and AIDS. All are lactose-free and maybe hypertonic. Disease-specific formulas are generally more expensive and usuallyrequire some digestion and absorption. Most formulas contain adequate vitamin/mineral supplementation once calorie/protein requirements are met. These formulaswill be discussed at greater length in later discussions of specific diseases.

Modular formulas are utilized in those patients where the above formulas are notsatisfactory because of specific nutrient needs of a patient. Modules are available for theaddition of carbohydrate, fat, protein, vitamins and minerals. Generally, commerciallyprepared formulas meet patients’ needs. Modular formulas are more difficult to use andmonitor and require a highly trained staff to insure that they are mixed properly, there-fore are more likely to be used in a teaching hospital.

Immune-modulating formulas are supplemented with arginine, glutamine, nucleicacid, omega-3 fatty acids, and antioxidants. A.S.P.E.N. and SCCM guidelines suggestthat these formulas should be utilized for patients with the following conditions: majorelective surgery, trauma, burns, head and neck cancer, and in critically ill patients onmechanical ventilation. These formulas should only be utilized with caution in patientswith severe sepsis (McClave, et al., 2009).

The literature suggests that arginine deficiency occurs in these conditions. Theaddition of RNA and eicosapentaenoic acid (EPA) and docosohexaenoic acid (DHA)enhance the immune response. The omega-3 fatty acids also appear to aid in decreasingthe incidence of cardiac arrhythmias, the incidence of acute respiratory distress syn-drome (ARDS), and the likelihood of sepsis (Calo, et al., 2005; Gadek, et al., 1999; Singer,et al., 2006; Pontes-Aruda, et al., 2006).

Utilization of the immune-modulating formulas is also associated with reducedduration of mechanical ventilation, morbidity related to infection, and reduced lengthof stay (McClave, et al., 2009). However, in patients with severe sepsis, the supplementa-tion with arginine may have an adverse effect (Dent, et al., 2003; Berletolini, et al., 2003).

The utilization of an enteral formula supplemented with omega-3 fatty acids(EPA), borage oil, and antioxidants in patients with ARDS and Acute Lung Injury (ALI)has been suggested to decrease ICU length of stay, number of ventilator days, incidenceof organ failure and incidence of mortality (Gadek, et al., 1999; Singer, et al., 2006; Pon-tes-Aruda, et al., 2006).

METHODS OF FEEDING

Once the type of feeding has been determined and access to the GI tract has beenattained, the method of feeding should be decided upon. A patient can be fed withbolus feedings, intermittent feedings, or continuous feedings.

In a critically ill patient, or a patient just beginning enteral feedings, continuousfeedings are generally utilized. Continuous feedings require the use of a feeding pumpor gravity drip and usually run over a 12- to 24-hour period. Continuous feedings are

23Nutrition Support

always recommended for feedings that run into the small intestine (although gravity andbolus feedings can be administered into the small intestine) and may also be used forfeeding into the stomach. Continuous feedings may allow for attainment of calorie andprotein needs more quickly, in fact, within 24 to 48 hours (JPEN, 2009), and may reducethe risk for aspiration associated with high residuals and gastroesophageal reflux.

Continuous feedings of isotonic formula are usually implemented with full-strength feedings at a rate of 10 to 40 mL/hour. Full strength isotonic feedings areutilized because hypo- and hypertonic feedings are associated with delayed gastricemptying. The feeding rate is then increased gradually by 10 to 20 mL/hr every 8 to 12hours until adequate to meet the patient’s nutrition needs, within 96 hours for thecritically ill patient.

Intermittent feedings usually do not require the use of a feeding pump, but use agravity-drip system. Feedings are given in a volume of 250 to 400 mL over 30 minutesor more, every three to six hours. The feedings are spaced throughout the day and givento patient tolerance, but based on nutrition needs. Patients may be fed in this manner asoften as six to eight times per day. Intermittent feedings are used only for feedings intothe stomach and are only recommended for the patient who is stable and not criticallyill. Residual in the stomach should be checked before each feeding.

Bolus feedings are generally not recommended in the critically ill patient becauseof the increased risk for aspiration and other complications, such as vomiting anddiarrhea. Bolus feedings are similar to intermittent feedings, in that a large volume isadministered. However, bolus feedings are given over a very short period of time (aslittle as 10 minutes), via syringe or feeding bag.

COMPLICATIONS

DIARRHEA

A patient receiving enteral nutrition via a tube should be monitored closely at first.Gastric residuals, as well as the presence of bowel sounds, abdominal distention, nauseaand/or vomiting should be checked as needed.

Diarrhea may necessitate a change in the method of feeding, the type of feeding orthe strength of feeding. Gastric residuals of up to 250 to 500 mL (McClave, et al., 2009and 2005; Montejo, et al., 2009; Pinilla, et al., 2001; Taylor, et al., 1999) should be accepted;however, always pay attention to the patients’ physical symptoms (i.e. abdominaldistention, nausea, and vomiting) and adjust or hold the feeding accordingly. If thegastric residual is greater than 250 mL after a second check, consideration should begiven to usage of a gastric motility agent. Increases in abdominal girth of greater than 8to 10 cm necessitate temporary holding of the enteral feeding (Ideno, 1993). Feedingsshould be held with gastric residuals of greater than 500 mL (JPEN, 2009).

Diarrhea is invariably blamed on the tube feeding. However, diarrhea may also becaused by medications, including sorbitol-based medications, antibiotics and certain

24Nutrition Support

antacids. Sorbitol is often found as a component of liquid-based medications and maybe in foods, such as pear nectar. Doses of sorbitol at levels greater than 10 gm can causean osmotic diarrhea (Johnston, et al., 1994). Medications containing magnesium (likeantacids), potassium, or phosphorus should also be ruled out as the cause of any diar-rhea (Hamaoui and Kodsi, 1997).

Because of the third spacing (accumulation of fluid interstitially or intercellularly)and changes in osmotic pressures that occur with hypoalbuminemia, diarrhea mayoccur. Other causes of diarrhea include malabsorption with short bowel syndrome,Crohn’s disease, ulcerative colitis, AIDS, pellagra and antibiotic-associated enterocolitis.The patient with poorly controlled diabetes mellitus may also be at a higher risk fordiarrhea (Eisenberg, 1993).

Diarrhea may occur from contamination, a problem which should decrease withthe use of closed systems (a method for enteral feedings in which the formula is pro-vided in a sealed container or bottle which is spiked and hung for feeding withoutbeing opened). The advantages of closed feeding systems include reduced risk ofcontamination and/or spoilage and increased hang time by the bed. Closed feedingbags and sets are safe for 24 to 48 hours (Vanek, 2000; Wagner, 1994).

• C. diff colitis and antibiotic associated colitis. Clostridium difficile is an anaerobicspore-forming rod that is increasingly found in both infants and adults, especially inadults who have been hospitalized or in a nursing facility and/or have been givenantibiotics. Antibiotic therapy alters the gastrointestinal flora; C. diff colonizes in thebowel and releases toxins; these toxins result in diarrhea and colitis (Yimam, 2007). Theonset of diarrhea occurs within days or months of antibiotic therapy. The antibiotics andantimicrobials that are most often associated with C. diff diarrhea are ampicillin,amoxicillin, cephalosporins, and clindamycin (Yimam, 2007). Most cases resolve withtreatment — i.e. Metronidazole (Flaggyl®) or oral Vancomycin. Relapse or recurrenceoccurs in 8 to 50 percent of cases; risks for recurrence include age, an ICU stay, newdelivery of antibiotics, hypoalbuminemia, and an extended hospital stay (Aslam, 2006;Bartlett, 2006). C. diff infections, however, can worsen and evolve into pseudomembra-nous colitis, with symptoms of profuse diarrhea, leukocytosis, and marked abdominaltenderness and distension.

The occurrence of C. diff colitis and antibiotic-associated colitis does not precludecontinued enteral feedings. In fact, the presence of enteral feeding may aid in decreas-ing C. diff toxin production in the colon and decrease the amount/frequency of diarrhea.The use of probiotics may be helpful in reducing the risk of developing antibioticassociated diarrhea (Jenkins, et al., 2005) and may be useful for both the prevention andtreatment of C. diff colitis (Dendukuri, et al., 2005). However, one should exercise cau-tion with the introduction of probiotics (live bacterial cultures) in a critically ill orimmunocompromised patient. In patients with recurrent C. diff infections, some studiessuggest that the use of the probiotics S. boulardii (Florastar®) and L. rhamnosus GG(Culturelle®) may be of benefit (McFarland, 2006). Also, fiber-containing enteral formu-las may reduce diarrhea in some patients.

25Nutrition Support

Isotonic formulas should be utilized as often as possible. Diarrhea can also becontrolled with banana flakes and soluble fiber as well as with medications such asparegoric, Lomotil®, Lactobacillus acidophilus (lactinex), or antidiarrheals only after C.difficile has been ruled out. Changes in the formula to an elemental or peptide formulamay be necessary, especially in the patient with malabsorption or intestinal atrophy.However, some studies suggest that there is no difference in the incidence of diarrheawhen intact formulas are used in contrast to small peptide formulas (Heimburger, et al.,1997). The patient with uncontrolled and excessive diarrhea (greater than 3 L/day) thatworsens with enteral feedings and improves when feedings are held may benefit frombowel rest and TPN (Delegge, 2006).

ASPIRATION PNEUMONIA

Aspiration pneumonia is also a risk for the enterally fed patient, especially if thetube is placed into the stomach or upper portion of the duodenum. For this reason,tubes should be placed distal to the ligament of Treitz, if possible. Aspiration is reportedat an incidence of 0.8 to 95 percent in enterally fed patients; however, the rate of aspira-tion pneumonia that is clinically significant is only 1 to 4 percent (Cataldi-Betcher, et al.,1983; Winterbauer RH, et al., 1986; Metheny and Clouse, 1997; Metheny, 1993).

Patients with a previous history of aspiration (at a level of 48 times more likely),head injury and decreased level of consciousness, sedation, depressed or absent coughor gag reflex, mechanical ventilation, and/or delayed gastric emptying are at increasedrisk for aspiration (Hamaoui and Kodsi, 1997; JPEN, 2009). Tests to determine whetheraspiration has occurred include utilizing glucose oxidase reagent strips to test forglucose (from the feeding) in aspirations (Metheny and Clouse, 1997).

In its 2009 guidelines for enteral feeding, A.S.P.E.N. recommends that the head ofthe patient’s bed be elevated 30 to 45 degrees to decrease the risk of aspiration.

Blue dye should not be added to enteral formulas. Several authors have noted anincreased incidence of toxicity from the addition of blue dye to formulas. This toxicityresulted in systemic sepsis and death in some cases. Blue dye appears to be absorbed insome cases, especially in the critically ill. The composition of blue dye is similar to thatof ADP; the blue dye replaces the ADP in cellular respiration, thus stopping it, resultingin cellular death (Chima, 2001; Doig, et al., 1998; Maloney, et al., 2001; Maloney, et al.,2002; Seidner, 2002; Zillich, et al., 2000).

The focus should be on prevention rather than detection of aspiration. Keep thehead of the bed elevated at a 30 to 45-degree angle; monitor gastric residuals; strive forpostpyloric placement of feedings; and utilize intermittent or continuous feedings(Drakulovic, et al., 1999; Grant and Martin, 2000; Ibanez, et al., 1992; Metheny, et al., 1990;Metheny, et al., 1999; Torres, et al., 1992).Biochemical parameters, such as serum glucose,blood urea nitrogen (BUN), electrolytes and phosphorus, should be monitored forassessment of tolerance. These levels should also be closely monitored for evidence ofdehydration in the patient with diarrhea as well as those with infection and sepsis.

26Nutrition Support

Glucose levels may increase with refeeding, but may also be associated with stress,steroid administration and diabetes mellitus. The management of glucose shouldinclude the maintenance of serum levels between 110 to 150 mg/dl (McClave, et al.,2009), and may require the use of insulin or oral hypoglycemic agents.

Increased BUN may indicate excessive protein intake, but is also associated withgastrointestinal bleeding, prerenal states, renal failure and dehydration.

Electrolytes should be monitored to assure adequate fluid and potassium intake.Phosphorus is affected by refeeding, anabolism, and renal disease. Phosphorus shouldbe supplemented in patients with serum levels less than 2 mg/dl (Skipper, 1989). Sometube-fed patients become hyperphosphatemic with nutrition support and may requirethe use of phosphate binders or a change to a low-phosphate feeding.

REFEEDING SYNDROME

Refeeding syndrome is another potential complication for the enterally fed patient,especially if he was quite malnourished or starved for a number of days. Starvation notonly depletes the body of fat and muscle stores, but also depletes water and minerals.Once refeeding starts and the Krebs cycle and the glucose-insulin system is stimulated,there is an increased uptake of glucose, phosphorus, magnesium, water, and othernutrients into the cells.

This occurrence, along with the depletion of phosphorus that occurs during starva-tion, can result in a severe depletion of phosphorus in the extracellular space. Refeedingsyndrome is defined as “the metabolic and physiologic consequences of depletion,repletion, compartmental shifts, and interrelationships of phosphorus, potassium,magnesium, glucose metabolism, vitamin deficiency, and fluid resuscitation” (Solomonand Kirby, 1990). Low phosphorus levels can cause serious complications, includingcardiac arrhythmias, congestive heart failure, paralysis, confusion, rhabdomyolysis,anemia, thrombocytopenia, decreased platelet function, and acute ventilatory failure(Solomon, 1990). With refeeding syndrome, you may also see a decrease in serumpotassium and magnesium, as these nutrients move intracellularly during anabolism.Start slowly with feeding to reduce risk.

Research and development of new enteral products is constant. Several productsutilize short-chain peptides for more efficient absorption. (Peptide transport across theintestinal wall does not require the use of the sodium pump.) Use is often restricted tohypoalbuminemic and critically ill patients.

Short-chain fatty acids (SCFA) — acetate, propionate, and butyrate — form in thegastrointestinal tract as a by-product of the digestion and fermentation of enterallyprovided fiber. SCFA are further metabolized to ketones and glutamine.

SCFA are the primary fuel preferred by the mucosa of the colon (Palacio, 1990); upto 540 kcal/day from SCFA can be absorbed. The colon obtains 60 to 70 percent of itsenergy requirements from SCFA (Cummings and MacFarlane, 1997). These fatty acidsare also important in preventing gut atrophy, both in the colon and in the small intestine

27Nutrition Support

(although to a lesser extent). Fiber (or SCFA, if a patient is unable to tolerate dietaryfiber) increases blood flow to the colon, stimulates enzyme secretion by the pancreas,and promotes mucosal cell growth in the intestine (Rombeau and Kriple, 1990). Theseeffects may help to decrease the incidence of bacterial translocation. Gut atrophy ap-pears to decrease when SCFA are added to TPN solutions (Rombeau and Kriple, 1990).Patients who cannot tolerate fiber-containing formulas may benefit from the addition ofSCFA to both enteral formulas and TPN.

Enteral nutrition support appears to be the best means of support for nearly allpatients, including the critically ill. Used correctly in conjunction with oral feedingsand/or total parenteral nutrition, enteral nutrition should enable the nutritional reple-tion necessary for wound healing and recovery from acute or chronic illnesses. Theefficacy of the use of immune enhancing formulas is not entirely clear; therefore, I cannot endorse their utilization until further studies are completed (Klein S, et al., 1997;Jolliet P, Pichard C, et al., 1999).

REVIEW QUESTIONS

1. Which access site for a tube feeding is preferred after a gastrectomy?2. What type of formula would you recommend for a CVA patient with dysphagia?

Where would the tube be placed?3. What feeding regimen would you recommend for a cancer patient who receives all of

his nutrition needs at night while sleeping?4. What type of feeding would you recommend for a patient with diarrhea and a serum

albumin level of 2.8 gm/dl. What other factors would you consider?5. What method of enteral feeding is recommended for critically ill patients?6. What would you do if your tube-fed patient had high gastric residuals?7. What type of feeding would you recommend for long-term care?

REFERENCES

Alexander JW: Bacterial translocation during enteral and parenteral nutrition. Proc Nutr Soc 57:389-393, 1998.Artinian V, et al. Effects of early enteral feeding on the outcome of critically ill ventilated medical patients.

Chest 129: 960-963, 2006.A.S.P.E.N. Guidelines for the use of parenteral and enteral nutrition in adults and pediatric patients. JPEN

26S-1SA-138SA, 2002.Bell SJ, Pasulka SP and Blackburn GL: Enteral formulas. In: Dietitian’s Handbook of Enteral and Parenteral

Nutrition. Skipper A, Ed. A.S.P.E.N. Publ., Rockville, MD, 1989.Bertolini G, Iapichino G, Radrizzani D, et al. Early enteral immunonutrition in patients with severe sepsis:

results of an interim analysis of a randomized multicentre clinical trial. Intensive Care Med 29: 834-840, 2003.

Border JR: Gut-origin septic states. The Gastrointestinal Response to Injury, Starvation, and Enteral Nutrition.Ross Laboratories, Columbus, OH, 1988.

Brinson RR and Koltz BE: Diarrhea associated with severe hypoalbuminemia: a comparison of a peptide-based chemically defined diet and a standard enteral alimentation. Crit Care Med 16:130, 1988.

28Nutrition Support

Brinson RR and Pitts WM: Enteral nutrition in the critically ill patient: role of hypoalbuminemia. Crit CareMed 17:367-370, 1989.

Cataldi-Betcher EL, Seltzer MH, Slocum BA, et al.: Complications occurring during enteral nutritionsupport: A prospective study. JPEN. 1983;7:546-552.

Charney P: Eneteral nutrition: indications, options, and formulations. In: Gottschlich MM, Fuhrman MP,Hammond KA, et al. (eds) The Science and practice of Nutrition Support A Core-Based Core Curriculum.Dubuque, IA: Kendall/Hunt Publ Co., 2001.

Chima C: The safety of blue dye as a method of detection of pulmonary aspiration in hospitalizedpatients. Future Directions in Clinical Nutrition Management XX (2):1, 2001.

Calo L, Bianconi L, Colivicchi F, et al. N-3 fatty acids for the prevention of atrial fibrillation after coronaryartery bypass surgery: a randomized, controlled trial. J Am Coll Cardiol 45: 1723-28, 2005.

Cummings J and MacFarlane G: Role of intestinal bacteria in nutrient metabolism. JPEN 21(6):3-11, 1997.Cummins A, Chu G, Faust L, et al.: Malabsorption and villous atrophy in patients receiving enteral

feeding. JPEN 19:3:193-198, June, 1995.DeLegge M. Enteral nutrition and gastrointestinal intolerance. When should we be concerned? Clinical

Nutrition Highlights 2(2): 2-7, 2006.Dendukuri N, Costa V, McGregor M, Brophy JM. Probiotic therapy for the prevention and treatment of

Clostridium dificile-associated diarrhea: a systemic review. CMAJ 173: 167-170, 2005.Dent DL, Heyland DK, Levy H, et al. Immunonutrition may increase mortality in critically ill patients with

pneumonia: results of a randomized trial. Crit Care Med 30: A17, 2003.Doig CJ, Sutherland LR, Sandham JD, et al.: Increased intestinal premeability is associated with the

development of multiple organ dysfunction syndrome in critically ill ICU patients. Am J Respir CritCare Med 158:444-451, 1998.

Drakulovic MB, et al.: Supine body position as a risk factor for nosocomial pneumonia in mechanicallyventilated patients: a randomised trial. Lancet 354:1851-58, 1999.

Duh QY: Decision tree for route of enteral nutrition support: placement techniques. Current Issues in EnteralNutrition Support, Report of the First Ross Enteral Device Conference, Columbus, OH, 9-14, 1996.

Eisenberg PG: Causes of diarrhea in tube-fed patients: a comprehensive approach to diagnosis andmanagement. Nutr Clin Prac 8:119-123, June, 1993.

Fowlie S and Eastwood MA: Oral nutrition and gastroenterology. Curr Opin in Gastroenterology 3:297-304,1987.

Gadek JE, DeMichele SJ, Karlstad MD, et al. Effect of enteral feeding with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Crit Care Med27: 1409-1420, 1999.

Grant M, Martin S: Delivery of enteral nutrition. AACN Clinical Issues 11(4): 507, 2000.Hamaoui E and Kodsi R: Complications of enteral feeding and their prevention. In: Clinical Nutrition. Enteral

and Tube Feeding, 3rd ed. Rombeau J and Rolandelli R. Eds. W.B. Saunders, Philadelphia, 1997.Heimburger D, Geels W, Bilbrey J, et al.: Effects of small-peptide and whole-protein enteral feedings on

serum proteins and diarrhea in critically ill patients: A randomized trial. JPEN 21:162-167, 1997.Hernandez G, Valasco N, Wainstein C, et al.: Gut mucosal atrophy after a short enteral fasting period in

critically ill patients. Crit Care 14:73-77, 1999.Ibanez J, et al.: Gastroesophageal reflux in intubated patients receiving enteral nutrition: effect of supine

and semirecumbent positions. JPEN 16:5:419-22, 1992.Ideno KT: Enteral nutrition. IN:Gottschlich MM, Matarese LM. Shronts EP (eds). Nutrition Support Dietetics

Core Curriculum, 2nd ed. Silver Spring, MD: Amercan Society for Parenteral and Enteral Nutrition; 98-99, 1993.

29Nutrition Support

Jabbar A, Chang WK, Dryden GW, McClave SA: Gut immunology and the differential response to feedingand starvation. Nutr Clin Pract 18: 461-482, 2003.

Jenkins B, Holsten S, Bengmark S, Martindale R. Probiotics: a practical review of their role in specificclinical scenarios. Nutr Clin Pract 20: 262-270, 2005.

Johnston K, Govel L, Andritz M: Gastrointestinal effects of sorbitol as an additive in liquid medications.Am J Med. 97:185-191, 1994.

Jolliet P, Pichard C, Biolo G, et al.: Enteral nutrition in intensive care patients. A practical approach. ClinNutr 18910;47-56, 1999.

Kearns PJ: Gastric vs. Small-bowel feeding. Current Issues in Enteral Nutrition Support, Report of theFirst Ross Enteral Device Conference, Columbus, OH, p 25-29, 1996.

Kirkland ML: Enteral and parenteral access. Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper,A, Ed. A.S.P.E.N. Publ., Rockville, MD, 1989.

Klein S, Kinney J, Jeejeebhoy K, et al.: Nutrition support in clinical practice: Review of published data andrecommendations for future research directions. JPEN 21:133-156, 1997.

Krey S, Porcelli K, Lockett G, et al.: Enteral nutrition. Nutrition Support Dietetics. Shronts E, Ed. A.S.P.E.N.,Silver Spring, MD, 1989.

Kudsk KA: Enteral vs. Parenteral nutrition: advantages and disadvantages. Jour Crit Care Nutr 3:2:3-9,1996.

Kudsk KA: Current aspects of mucosal immunology and its influence by nutrition. Am J Surg 183: 390--398, 2002.

Lara TM, Jacobs DO: Effect of critical illness and nutritional support on mucosal mass and function. ClinNutr 17:99-105, 1998.

Maloney JP, et al.: Systemic absorption of food dye in patients with sepsis. NEJM 343(14):1047.Maloney JP, Ryan TA, Brasel KJ, et al. Food dye use in enteral feedings: a review and a call for a morato-

rium. Nutr Clin Prac 17:169-181, June, 2002.Martindale RG: Postoperative critical care nutrition: feed the gut early. Jour Crit Care Nutr 3:2:9-18, 1996.McClave SA, Lukan JK, Steefater JA, et al.: Poor validity of residual volumes as a marker for risk of

aspiration in critically ill patients. Crit Care Med 33: 324-330, 2005.McClave SA, Martindale RRG, Vanek VW, McCarthy M, et al.: Guidelines for the provision and assessment

of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM)and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) JPEN 33 (3): 277-316, 2009.

McFarland. AmJGastro 101: 812, 2006.Metheny N, Aud M, Wunderlich R: A survey of methods used to detect pulmonary aspiration of enteral

formula in intubated tube fed patients. American Journal of Critical Care 8(3):160, 1999.Metheny N, Smith L, Wehrle M, et al.: pH, color, and feeding tubes. RN p.25, January 1998.Metheny NA, Clouse RE: Bedside methods for detecting aspiration in tube-fed patients. Chest 111:724-731,

1997.Metheny NM: Minimizing respiratory complications of nasoenteric tube feedings: State of the science.

Heart Llung.22:213-223, 1993.Metheny N, Reed L, Wiersema L, et al.: Effectiveness of pH measurements in prediction of feeding tube

placement: An update. Nursing Research 42(6):324, 1993.Metheny M, McSweeney M, Wehrle M, et al.: Effectiveness of the ascultatory method in predicting feeding

tube location. Nursing Research 39(5):262, 1990.Montejo JC, Minambres E, Bordeje L, et al.: Gastric residual volume during enteral nutrition in ICU

patients: the REGANE study. Intensive Care Med 2009, in press.Moore FA, Moore EE, Kudsk KA, et al.: Clinical benefits of immune-enhancing diet for early postinjury

enteral feeding. JPEN 36:607-615, 1994.

30Nutrition Support

Mueller CM: Enteral nutrition management: gastroparesis, ileus, pseudo-obstruction, diarrhea. CurrentIssues in Enteral Nutrition Support, Report of the First Ross Enteral Device Conference, Columbus,OH, 55-58, 1996.

Palacio JC and Rombeau JL: Dietary fiber: a brief review and potential application to enteral nutrition.Nutr Clin Prac 5:99-106, 1990.

Park RHR, Allison MC, Lang J, et al.: Randomised comparison of percutaneous endoscopic gastrostomy andnasogastric feeding in patients with persisting neurological dysphagia. Br Med J 304:1406 -1409, 1992.

Pinilla JC, Samphire J, Arnold C, et al.: Comparison of gastrointestinal tolerance to two enteral feedingprotocols in critically ill patients a prospective, randomized controlled trial. JPEN 25: 81-86, 2001.

Pontes-Aruda A, Aragao AM, Albuquerque JD: Effects of enteral feeding with eicosapentaenoic acid,gamma-linolenic acid and antooxidants in mechanically ventilated patients with severe sepsis andseptic shock. Crit Care Med 34: 2325-2333, 2006.

Rombeau JL and Kripke SA: Metabolic and intestinal effects of short-chain fatty acids. JPEN 14:5S: 181S-185S, 1990.

Seidner Dl: Preventing enteral tube feeding-associated aspiration: something no one should get blue inthe face over. Nutr Clin Prac 17:140-141, June, 2002.

Singer P, Theilla M, Fisher H, et al.: Benefit of an enteral diet enriched with eicosapentaenoic acid andgamma-linolenic acid in ventilated patients with acute lung injury. Crit Care Med 34: 1033-1038, 2006.

Skipper A: Monitoring and complications of enteral feeding. Dietitian’s Handbook of Enteral and ParenteralNutrition. Skipper A, Ed. A.S.P.E.N. Publ., Rockville, MD, 1989.

Solomon SM and Kirby DF: The refeeding syndrome: a review. JPEN 14:1:90-97, 1990.Souba WW, Smith RJ, and Wilmore DW: Glutamine metabolism by the intestinal tract. JPEN 9:5:608-617, 1984.Taylor SJ, Fettes SB, Jewkes C, Nelson RJ. Prospective, randomized, controlled trial to determine the effect

of early enhanced enteral nutrition on clinical outcome in mechanically ventilzted patients sufferinghead injury. Crit Care Med 27: 2525-2531, 1999.

Torres A, et al.: Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: theeffect of body position. Annals of Int Med 116:540-43, 1992.

Vanek V: closed versus open enteral delivery systems: a quality improvement study. Nutr Clin Pract 15:234-243, 2000.

Wagner DR, Elmore MF, Knoll DM. Evaluation of “closed” versus “open” systems for the delivery ofpeptide-based enteral diets. JPEN 18: 453-457, 1994.

Winterbauer RH, During RB, Barron E, et al.: Aspirated nasogastric feeding solution detected by glucosestrips. Ann Intern Med 95:67-68, 1986.

Yimam F: Tossing the good with the bad antibiotic associated diarrhea (ADD). A.S.P.E.N. Clinical NutritionWeek, 2007.

Zillich AJ, Kuhn RJ, Petersen TJ: Skin discoloration with blue food coloring. Annals of Pharm 34:868-70,2000.

31Nutrition Support

Chapter Three:Parenteral Nutrition

Parenteral nutrition provides nutrients to a patient via vascular access. Parenteralnutrition can provide most necessary nutrients to patients unable to utilize their gas-trointestinal tracts effectively. In patients with non-functioning GI tracts, parenteralnutrition may make the difference between life and death. Because parenteral nutritionis much more complex and expensive than enteral nutrition therapies, its use must beclosely monitored. It should only be utilized in those patients who meet strict preestab-lished criteria.

CRITERIA FOR USE

A.S.P.E.N. guidelines for the use of parenteral nutrition are shown below.

• Massive small bowel resection

• Severe diarrhea (if unresponsive to other treatments)

• Intractable vomiting

• Diffuse peritonitis

• GI ischemia

• In previously healthy, well-nourished patients, only after the first 7 daysof hospitalization and only when enteral nutrition is available

• In patients with protein-calorie malnutrition and no feasibility of enteralnutrition, TPN should be initiated as soon as possible

Criteria for Total Parenteral Nutrition

32Nutrition Support

Patients who are unable to absorb nutrients through the gastrointestinal tractbecause of massive small bowel resection, certain diseases of the small intestine, severediarrhea, and intractable vomiting should have total parenteral nutrition as part of theirnutrition therapy. The parenteral route should also be considered in patients with acutepancreatitis.

Patients who are unable to utilize their gastrointestinal tracts over 5 to 7 days andwho are also severely malnourished or catabolic should also be treated with parenteralnutrition. The use of parenteral nutrition in these patients can help to alleviate nutritiondepletion and to aid in their recovery (Skipper, 1989). A VA study of 1250 patientsshowed a decrease in postoperative complications of 10 percent when severely mal-nourished patients were given TPN for 7 to 10 days prior to surgery (Buzby, 1991).

Total parenteral nutrition (TPN) should be considered in patients who have hadmajor surgery, who exhibit moderate stress caused by illness or injury and who cannotbe fed through the GI tract for 7 to 10 days. Patients with enterocutaneous fistulas thatpreclude enteral feeding may be considered candidates for bowel rest and parenteralnutrition. Other patients who might benefit include those with hyperemesisgravidarum, small bowel obstruction and inadequate enteral nutrition over 7 to 10 days.

The use of TPN should be limited to patients who truly require it and wouldbenefit from it. Those well-nourished patients with minimal injury or stress, or those inthe immediate postoperative period, are seldom benefited by TPN. A functional gas-trointestinal tract is a contraindication, and TPN should not be used when it is notdesired by the patient or when the patient has a very poor prognosis.

ACCESS

Total parenteral nutrition can be given through peripheral lines or through centralvenous access. Peripheral lines typically last up to 7 days, less in elderly patients,necessitating frequent tries at reestablishing venous access. Peripheral formulas must belimited in dextrose and electrolyte concentrations so as to reduce the osmolarity in orderto reduce the risk of thrombophlebitis (A.S.P.E.N., 1993).

Considerations for TPN

• Major stress or surgery (unable to use GI tract for 7 to 10 days)

• Enterocutaneous fistula

• Hyperemesis gravidarum

• Small bowel obstruction

• Inadequate enteral nutrition (for 7 to 10 days)

• Acute pancreatitis

33Nutrition Support

Central venous access can be attained via the subclavian, internal jugular andfemoral veins. Long-term TPN patients may require indwelling catheters placed underthe skin for a distance before the line enters the cephalic, external jugular, internaljugular subclavian vein. Catheters used in this manner include the Broviac, Hickman,and Groshong catheters. All require surgery for placement.

Peripherally inserted central catheter lines (PICC) can also be established and aremore readily placed than the more invasive indwelling catheters. PICC lines are oftenused for the patient who is receiving TPN or intravenous antibiotics at home and, moreand more, while hospitalized. PICC lines are inserted in the arm and the catheter is fedinto smaller peripheral veins to the superior vena cava or right atrium so that centralline concentrations can be used. PICC lines can be inserted by radiologists or trainednurses and, if cared for properly, can last up to two to three months.

TPN administered through a peripheral vein is, by necessity, less nutrient-dense.Because peripheral veins are more fragile and blood flow is less, the concentration ofdextrose, amino acids and electrolytes must be reduced so that the final osmolality ofthe solution is low enough to prevent thrombophlebitis.

Because solutions with osmolality greater than 900 mOsm/dl require administra-tion through a central line, the amount of nutrients provided in a peripheral vein islimited, unless the patient can tolerate large volumes of fluid. TPN administeredthrough a central vessel (subclavian, internal or external jugular veins) is usually moreconcentrated and can more easily provide adequate required nutrients.

FORMULA PREPARATION

Total parenteral nutrition is the admixture of carbohydrate, protein, fat, vitamins,minerals and electrolytes into a solution that can be administered through peripheral orcentral veins.

Total nutrient admixtures (TNA) are now utilized more frequently in the clinicaland home setting. TNA is a combination of all three nutrient (carbohydrate, protein, andfat) sources in contrast to the more traditional admixture of carbohydrate and proteinwith a piggybacking of the fat source.

TNA’s add convenience, reduce contamination and precipitation, and are easilyadministered. An added benefit to the patient is that continuous lipid infusion appearsto be better tolerated and may be less immunosuppressive.

Improper mixing of the additives in the solution can cause precipitation. It isimportant that each element of the solution be added and mixed at the proper time.Several components of the TPN can stabilize or destabilize the solution. A higher con-centration of amino acid and/or dextrose can be more stabilizing to the emulsion. Onthe other hand, a higher concentration of lipid can be less stabilizing. Increased concen-tration of the cations in the TPN can cause disruption of the emulsion as well (Driscoll,1996). Because TPN solutions must be sterile, they are mixed under the direction of apharmacist, utilizing a laminar flow hood. Many pharmacies utilize computerized mixmachines, which may reduce the incidence of precipitation. The 1.2 micron filtersprevent precipitates and emboli from being transmitted to patients (Driscoll, et al., 1996).

34Nutrition Support

TPN bags usually can hang for 24 hours without danger of precipitation or spoil-age. Any solution remaining after 24 hours should be discarded. Mixed bags can bestored safely, under refrigeration, for up to seven days. Lines for administration of TPNshould be changed every 24 hours for TNAs and every 72 hours for 2-in-1 solutions(HICPAC, 1996). Once vitamins are added to the admixture, the bag should be shelteredfrom light. At least 50 percent of vitamin A and 30 percent of vitamin E may be lost dueto light exposure. Additionally, there may be losses of vitamin C, vitamin K, thiamin,and riboflavin (Drott, et al., 1991).

ENERGY SOURCES

Dextrose solutions and lipid emulsions are the most frequently utilized energysources for TPN. Crystalline L-amino acid formulas supply the protein and an energysource, while electrolytes, minerals, vitamins and trace elements are added to completethe formula.

Dextrose can be compounded from base concentrations from 5 to 70 percent (witha final concentration of <35 percent), depending on the patient’s needs and ability totolerate the dextrose and osmotic load.

When peripheral parenteral nutrition is utilized, the final concentration of dextrosein solution must be kept at 5 to 10 percent. Since the hydrated form of dextrose is uti-lized, its caloric value is only 3.4 kcal/gm. Recommendations for carbohydrate adminis-tration are to give no more than 5 mg CHO/kg/minute, (Skipper, 1989; Buzby, 1989;Rosmarin, et al., 1996) because carbohydrate in excess of this amount can precipitatecholestasis, hyperglycemia, increased liver function tests, synthesis and storage of fatand increased carbon dioxide production.

Lipid emulsions are available in three forms. They provide 1.1 kcal/ml, 2.0 kcal/mland 3.0 kcal/ml. Lipid emulsions can be utilized as both a provider of essential fattyacids and as a calorie source. The 3.0 kcal/ml lipid emulsions are utilized only forcompounding.

Historically, lipid emulsions have been primarily utilized to prevent essential fattyacid deficiency, with the infusion of 500 ml of 10 percent lipid (1.1 kcal/ml) three timesper week. However, the use of lipid as a significant energy source has become moreprevalent. In stressed patients, lipid calories may be utilized as well as or better thandextrose calories.

No more than 2.5 gm lipid/kg/day should be given to adult patients, (Buzby, 1989)and no more than 60 percent of total calories from fat should be utilized. Administrationof 20 to 40 percent of calories from fat appears to improve nitrogen sparing and may beof use in the patient who has become glucose intolerant (Grant, 1985).

While lipid emulsions are an excellent way to provide increased calories to apatient, one must consider the possible deleterious effects to the immune system ofincreased amounts of linoleic acid. Linoleic acid is converted to arachidonic acid, anomega-6 fatty acid (Ω-6), in the liver and absorbed by the cells as such. They can act as aprecursor to eicosanoids, which stimulate the production of prostaglandins, one ofwhich — PGE2 — can be immunosuppressive.

35Nutrition Support

The literature suggests that the use of linoleic acid as a fat source should belimited in patients with a depressed immune system or those who have beenstressed by trauma, surgery or illness (Grant, 1985). Because of this, we have re-cently changed our standard TPN formulas to be lower in fat, attempting to provideapproximately 30 percent calories from fat in the central formula and a lower per-centage from fat in the peripheral formula. (For a more detailed discussion of fatsand immunity, see Nutrition Dimension courses Nutrition & Immunity, Part I and/orNutrition & Immunity Part II).

Since omega-6 fatty acids appear to negatively affect immunocompetence, possiblydue to the effects of arachidonic acid, a product of linoleic acid metabolism (Gottschlich,1985; Sax, 1990), the substitution of omega-3 fatty acids for at least a portion of theomega-6 fatty acids may be of benefit in enhancing immunocompetence.

While two to three fatty acid sources are available in most enteral formulas, theonly available parenteral lipid in the United States contains linoleic acid. Alternativesources, such as medium-chain triglycerides (MCT), or structured lipids (mixtures ofMCT and long-chain triglycerides [LCT]) are being studied and are available outsidethe US.

These alternatives hold promise. MCT are well tolerated when given intravenously,are rapidly cleared from the blood and appear to be just as protein-sparing as LCT(Jensen, et al., 1990). MCT appear less immunosuppressive than conventional lipidsources. MCT are more readily available for energy than LCT since they are rapidlycleared and are less carnitine dependent. However, MCT do not contain essential fattyacids and cannot be utilized as a sole fat source (Jensen, 1994). Currently the use of MCTin parenteral lipid emulsions has been approved in Europe.

Structured lipids can provide essential fatty acids and provide protection fromimmunosuppression which can occur with the exclusive use of LCT. Structured lipidsbehave like lipoproteins and are readily available for fuel (Jensen, 1994).

Carnitine transports carbon chains across cell membranes. Carnitine is endog-enously synthesized from methionine and lysine and is also provided throughintake of a normal diet (McCormick, et al., 1985). The TPN-fed patient (as well as thechronic hemodialysis patient) may become carnitine deficient, causing decreased

Structured Lipids

MCT +

C18C18C18

LCT =

C10C10C10

C10C10C18

C10C18C18

C18C10C18

Structured Lipid*

*Various fatty acids are used to make the structured lipids, including essential fatty acids

36Nutrition Support

nitrogen balance and decreased weight gain. Supplementation may help (Helms, etal., 1990). Because the metabolism of LCT is dependent upon carnitine, lipid clear-ance and associated high triglyceride levels may improve with carnitine supplemen-tation in depleted patients. However, carnitine is not currently available for usewith TPN in the clinical setting and appropriate levels of supplementation have notbeen determined.

PROTEIN

Protein can be supplied with crystalline L-amino acid preparations. These formulasare generally comprised of 40 to 50 percent essential amino acids and 50 to 60 percentnonessential amino acids.

Concentrations of amino acid formulas range from 3.5 percent to 15 percent for usein the treatment of a variety of illnesses: final concentrations rarely exceed 7.5 percent.For normal patients not highly stressed, a calorie-to-nitrogen ratio of 300 to 1 is accept-able to allow for adequate calories to spare protein. Critically ill patients require 100 to150 kcal/gm of nitrogen to assure that the protein provided is utilized for proteinsynthesis and not for energy.

For the patient who has no difficulty tolerating protein, protein requirements are0.8 gm/kg/day for the non-stressed patient with an increased requirement to 1.2 to 2.5gm/kg/day for the critically ill patient.

Disease-specific amino acid formulas have been developed for those patients withrenal and liver disease. High branched-chain amino acid formulas have also beendeveloped that, theoretically, aid in the treatment of the highly stressed patient. Thesespecific formulas will be discussed in more detail in later chapters.

VITAMINS AND MINERALS

Vitamins should be added to the parenteral solution to correct any existing defi-ciencies and to prevent their development. Because the absorption and utilization ofvitamins is altered when they are given parenterally, (Skipper, 1989) the recommendeddosages are greater than RDA levels.

The chart on the following page lists the American Medical Association’s recom-mended dosages for parenteral administration of vitamins. Vitamin K (12 to 14 mg/week) should be administered to patients on TPN, especially those without a func-tional GI tract.

Critical illness does not change the basic requirements for the electrolytes sodium,calcium and chloride, but the requirements for potassium, phosphorus and magnesiumchange dramatically during periods of stress and refeeding.

Existing deficiencies of these nutrients may become evident as the patient’srefeeding begins. Electrolyte administration must be individualized for each patient,and serum levels should be monitored closely throughout the course of parenteralnutrition administration.

37Nutrition Support

Zinc, copper, chromium, and manganese are routinely added to parenteral formu-las. Essential trace elements which may be added in long-term parenteral nutritioninclude selenium, iodine, molybdenum, fluorine and cobalt. Other trace elements, suchas vanadium, nickel, tin, silicon and arsenic, have not been shown to become deficientin those patients receiving long-term TPN, (Russell, et al., 1985) and so are not added toTPN formulas.

The chart below shows recommended dosages of trace elements.

Parenteral Vitamin Dosages

Vitamin AVitamin DVitamin E

Ascorbic AcidFolacinNiacin

RiboflavinThiamine

PyroxidineB12

Pantothenic AcidBiotin

3300 IU200 IU10 IU100 mg400 mcg40 mg3.6 mg3 mg4 mg5 mcg15 mg60 mcg

Parenteral Trace Element Dosages

CopperZinc

ManganeseChromiumSelenium

IodineMolybdenum

0.3 mg3 mg*0.7 mg20 mcg120 mcg120 mcg20 mcg

* higher in patients with diarrhea and higher GI losses

38Nutrition Support

FORMULAS

As mentioned above, peripheral formulas are less nutrient-dense than centralformulas. A final dextrose concentration of 10 percent or less is required, and the addi-tion of nutrients that contribute to osmolality must be closely monitored.

A peripheral formula mixture of dextrose and amino acids, along with electrolytes,etc., may be inadequate in calories and protein for most patients. A total nutrient admix-ture, which includes the lipid emulsion as well as dextrose and amino acids, may bebeneficial to the patient who requires feeding through a peripheral line. Total nutrientadmixtures have been shown to remain stable in solution and are generally fairly welltolerated through a peripheral line (Hoheim, et al., 1990).

A sample of a typical peripheral parenteral total nutrient admixture can be foundin Appendix #9.

A central line enables the use of more nutrient-dense formulas. Either a dextrose/amino acid formula or a total nutrient admixture can be utilized.

Advantages of a TNA include decreased cost, ease of administration and decreasedfat intolerance. Disadvantages may include increased risk for bacterial growth becauseof the limited use of in-line filters (larger and more porous filters have been developedand are being used). Very fine in-line filters remove microorganisms and other matterthat may contaminate the admixture. However, the larger filter is required in a TNA, toallow lipid particles to pass through. Also, the presence of fat creates an improvedmedium for bacterial growth.

Monitoring the formula for breakdown and other problems (i.e. calcium phosphateprecipitation) may also be difficult because the emulsion is more opaque. A sample of atypical central TPN total nutrient admixture is provided in Appendix #9.

The FDA alerted hospitals to a potential problem with the development of emboliin patients on TPN receiving a TNA. Strict compounding guidelines and the use of a 1.2micron filter in the delivery of the TPN will assist in minimizing this problem.

Total Nutrient Admixture

Advantages• Decreased cost• Decreased fat intolerance• Ease of administration

Disadvantages• Increased risk for bacterial growth• Difficult to monitor

39Nutrition Support

MONITORING THE TPN PATIENT

The status of the patient receiving parenteral nutrition support should be moni-tored carefully. Initial determination of weight, and serum values of electrolytes, glu-cose, BUN and creatinine should be made. Baseline serum magnesium, calcium, phos-phorus, cholesterol, triglycerides, albumin or transferrin and liver function tests shouldalso be determined (Lenssen, 1989). A summary of monitoring is shown below.

Electrolyte levels should be initially monitored twice a week and then weeklythroughout the course of TPN therapy. Electrolytes and glucose should be monitoreddaily initially, and every other day as the patient stabilizes. Monitoring of nitrogenbalance may help determine the adequacy of protein intake and demonstrate degree ofmetabolic stress and recovering.

Fluid balance should be monitored daily to determine if any weight gain is fromfluid overload or actual increase in body mass. A weight gain of more than 0.5 kg/daymay indicate fluid overload.

XXX

XXX

XXX

XX

XXX

weightelectrolytesglucose

BUNcreatininemagnesium

calciumphosphoruscholesterol

triglyceridesalbumin (or transferrin)

liver functionsfluid balanceaccess site

Values Initial 2X Daily Daily 2X Weekly Weekly

NOTE: When marks appear in two or more columns, values should bemonitored more frequently at first, then less frequently as patient stabilizes.

X

XX

XX

XXX

XXX

XX

X

XX

XXX

X

X

XX

X

X

TPN Monitoring

40Nutrition Support

Inspection of the patient’s intravenous access site for signs of infection and othercomplications noted in the next section should be made every day.

COMPLICATIONS

Complications of parenteral nutrition include phlebitis at the access site, pneu-mothorax during the insertion of the central line, thrombosis of the vein and infection ofthe venous access line. Treatment of occlusions includes urokinase for catheter thrombo-sis; hydrochloric acid for occlusions caused by mineral precipitate; and ethanol forocclusions related to lipids (Werlin, et al., 1995).

Metabolic complications are summarized in Appendix #10.A frequent complication of parenteral nutrition therapy associated with the criti-

cally ill patient is an alteration in glucose metabolism. Because of his illness, the patientmay be insulin-resistant or glucose-intolerant, and the introduction of a large dextroseload via TPN can exacerbate this problem. Hyperglycemia can be caused by overfeed-ing (excessive dextrose infusion) and is more likely to occur with diabetes, organ failureand stress.

To prevent the onset of a hyperglycemic, hyperosmolar, non-ketotic coma, glucoselevels should be monitored every 4 to 6 hours initially. Once insulin dosages have beendetermined and implemented and the hyperglycemia is under control, glucose levelsshould continue to be monitored closely and adjustments made as necessitated by thepatient’s condition.

Hypoglycemia may occur if TPN is discontinued too quickly; therefore, it shouldbe tapered off gradually over a 24-hour period (or by decreasing to 40 ml/hr for onehour, then discontinuing), with monitoring of glucose levels.

Hyperlipidemia may occur when lipid emulsions are given to a patient withexisting familial hyperlipidemia. A sedative called Diprivan (Propofol) maybe utilizedin ventilator-dependent patients. This medication is lipid based and must be consideredas a calorie and fat source. In patients receiving TPN with lipid and concurrent Propofolinfusions, serum triglyceride levels should be routinely monitored and adjustmentsshould be made to the amount of lipid in the TPN if serum levels are greater than 400mg/dl.

Septic and critically ill patients may also develop difficulty with fat metabolism,resulting in an increase in serum triglyceride levels.

How lipids are delivered in the TPN determines when blood should be drawn formeasurement of serum lipids. If the lipids are piggybacked, then blood should bedrawn prior to infusion or 6 hours post-infusion. If the lipids are part of a three-in-onemixture, it does not matter when the blood is drawn. If serum lipid levels are consis-tently high, over 400 mg, lipid emulsions may need to be limited to every other day oronce weekly, depending on the patient’s caloric needs and serum triglycerides level(Banks, 1997).

Electrolyte imbalances may occur during TPN. Hyperkalemia may occur withrenal insufficiency, while hypokalemia can occur due to protein anabolism and insuffi-cient potassium administration. The uptake of glucose into the cell occurs with theuptake of potassium into the cell, which may result in hypokalemia, common during

41Nutrition Support

refeeding and insulin therapy. Increased potassium losses may occur because of diar-rhea, vomiting and/or fistulas, and as side effects of such drugs as steroids, potassium-wasting diuretics and certain antibiotics. Adequate potassium levels can be maintainedthrough supplementation.

Malnourished patients frequently are at risk for the development of hypophos-phatemia. This occurs during refeeding due to inadequate phosphorus administration(because of the role phosphorus plays in glycolysis and synthesis of new cells). Othercauses are alkalosis, antacid use, hypomagnesemia and hypokalemia, and metabolicacidosis. Phosphorus can be given as needed.

Hyperphosphatemia, as well as hypermagnesemia, is typically seen only in pa-tients with renal insufficiency or failure. Decreased magnesium levels may come fromincreased losses and impaired absorption in the GI tract, as well as with aminoglycosidetherapy and chemotherapy (Skipper, 1989).

Phosphorus levels must be monitored and intake of phosphorus must be individu-alized to a patient’s requirements. Often, no phosphorus is given to these patients. Ifmagnesium levels are low, supplement to return levels to normal. Care should be takennot to oversupplement.

Elevation of liver function tests may occur with some patients on TPN after one totwo weeks of therapy. This increase may be a result of overfeeding or cholestasis.Generally, these levels return to normal once oral or enteral feedings are reinstituted,but they should be closely monitored to assure that liver failure does not ensue. Theetiology of TPN-related cholestasis is unknown. Treatment includes cyclic TPN, initia-tion of low rate enteral feedings, avoidance of overfeeding, and the elimination ofcopper and manganese from the TPN (Teitelbaum, 1997; Spiegel and Willenbucher,1999). If liver function is severely altered and/or changes in the liver have occurred,TPN may need to be discontinued or reduced.

An increase in carbon dioxide production may signify overfeeding with eithercarbohydrate calories or total calories. This may make ventilator weaning more difficultand could compromise patients with existing pulmonary disease. Care should be takenthat patients do not receive excessive calories and that a mix of calories from bothcarbohydrate and fat sources is provided.

A number of the following questions require computation of TPN solutions. Thevalues to be used are shown in Appendix #10.

REVIEW QUESTIONS

1. Your patient is 5’2" and weighs 99 lb (45 kg). She had a small bowel resection 5 daysago and shows no signs of a return in bowel function. Should TPN be utilized?Why or why not?

2. Your 35-year-old patient has had TPN ordered. A total nutrient admixture formula of400 ml dextrose 40 percent , 400 ml amino acid 10 percent, and 200 ml lipid 20percent was ordered (along with standard electrolytes, vitamins and minerals). Hehas no central venous access. What do you do?

3. Your 80-year-old female patient is intubated in the ICU. She has been diagnosed withsepsis based upon a fever of 101°F, an elevated WBC count, and a positive DISIDA

42Nutrition Support

scan (a nuclear medicine study to detect inflammation/possible infection). She hasbeen on TPN for 4 days. Her triglyceride level is 342, blood glucose is 240, andBUN is 40 with a creatinine of 2.0. What, if any, adjustments would you recom-mend for her TPN solution?

4. Your postoperative patient (10 days) on TPN has elevated liver function tests, whichwere not shown prior to the operation. There is no history of cirrhosis or other liverdisease. What do you do?

5. The pulmonologist has requested a consult from you to adjust the TPN on his intu-bated patient who has difficulty weaning from a ventilator. What do you suggest?

6. Figure the caloric content, nonprotein calorie content, protein content, percent caloriesfrom fat, and calorie: nitrogen ratio of the following TPN formula: 400 ml dextrose50 percent ; 400 ml amino acid 12 percent; 200 ml lipid 20 percent per liter. TotalNutrient Admixture at 80 ml/hr for 24 hours.

7. Figure the caloric content, nonprotein calorie content, protein content, percent caloriesfrom fat, and calorie: nitrogen ratio of the following TPN formula: 500 ml dextrose50 percent; 500 ml amino acid 10 percent at 50 ml/hr for 24 hours; 500 ml lipid 20percent given over 10 hours each day.

REFERENCES

Alexander JW: Arginine and lipids. A.S.P.E.N. 15th Clinical Congress, 1991.A.S.P.E.N. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN

17:4S, July-August, 1993.Banks P: Practice guidelines in acute pancreatitis. Am J Gastroenterol 92:377-386, 1997.Buzby G: Veterans Affairs Total Parenteral Nutrition Cooperative Study Group: Perioperative total

parenteral nutrition in surgical patients. N Engl J Med 325:525-532, 1991.Buzby KM and Neill L: Parenteral nutrition solutions and additives. In Dietitian’s Handbook of Enteral and

Parenteral Nutrition. Skipper A, Ed. A.S.P.E.N. Publications, Rockville, MD, 327-345, 1989.Daly JM, Reynolds J, Thom A, et al.: Immune and metabolic effects of arginine in the surgical patient. Ann

Surg 208(4):512-523, 1988.Driscoll DF: Total nutrient admixture update: physicochemical issues affecting parenteral nutrient safety.

Address at 5th Annual Nutrition Support Update, 1996, San Diego.Driscoll D, Bacon M, Bistrian B. Effects of in-line filtration on lipid particle size distribution in total

nutrient admixtures. JPEN 20:296-301, 1996.Drott P, Meurling P, and Meurling L. Clinical adsorption and photodegradation of the fat-soluble vitamins

A and E. Clin Nutr 10:348-351, 1991.Fish J: Amino acids and peptides. A.S.P.E.N. 18th Clinical Congress, San Antonio, 1994.Gottschlich MM and Alexander JW: Fat kinetics and recommended dietary intake in burns. JPEN 11:1:80-

85, 1985.Grant JP: Central venous hyperalimentation. In Hyperalimentation: A Guide for Clinicians. Kaminski MV, Ed.

Marcel Dekker, Inc., New York, 127-154, 1985.Helms RA, Mauer ED, Hay WW, et al.: Effect of intravenous L-carnitine on growth parameters and fat

metabolism during parenteral nutrition in neonates. JPEN 14:5:448-453, 1990.Hoheim DF, O’Callaghan TA, Joswiak BJ, et al.: Clinical experience with three-in-one admixtures adminis-

tered peripherally. Nutr Clin Prac 5:3:118-122, 1990.Hospital Infection Control Practices Advisory Committee (HICPAC). Guidelines for prevention of

intravascular device-related infections. Amer J Infect Control, 24:262-293, 1996.

43Nutrition Support

Jensen GL, Blackburn GL, Bistrian BR, et al.: Parenteral infusion of long- and medium-chain triglyceridesand reticuloendothelial system in man. JPEN 14:5:467-4717, 1990.

Jensen GL: Fats. A.S.P.E.N. 18th Clinical Congress, San Antonio, 1994.Kinsella JE, Lokesh B, Broughton S, et al.: Dietary polyunsaturated fatty acids and eicosanoids: potential

effects on the modulation of inflammatory and immune cells: an overview. Nutrition (supplement),6: 24-44, Jan./Feb. 1990.

Kirk SJ and Barbul A: Role of arginine in trauma, sepsis, and immunity. JPEN 14:5S:226S-229S, 1990.Lenssen P: Monitoring and complications of parenteral nutrition. In Dietitian’s Handbook of Enteral and

Parenteral Nutrition by Skipper, A, Ed. A.S.P.E.N. Publications, Rockville, MD, 1989.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition


McCormick DC, Knutsen CV, Griffen RE, et al.: Pharmaceutical aspects of parenteral nutrition. In:Hyperalimentation: A Guide for Clinicians. Kaminsky MV, Ed. Marcel Dekker, Inc., New York, 1985.

Paxton J and Williamson J: Nutrient substrates: making choices in the 1990s. Jour Burn Care & Rehab12:2:198-202, 1991.

Powers DE, and Moore AD: Food Medication Interactions, 6th ed. Food Medication Interaction Publishing,Phoenix, 1987.

Rosmarin D, Wardlaw G, Mirtallo J: Hyperglycemia associated with high, continuous infusion rates oftotal parenteral nutrition dextrose. Nutr Clin Prac 11(4):151-156, 1996.

Russell DM, Baker JP, and Jeejeebhoy KN: Trace elements and vitamins in parenteral nutrition. InHyperalimentation: A Guide for Clinicians. Kaminski MV, ed., Marcel Dekker, Inc., New York, 1985.

Sax HC: Practicalities of lipids: ICU patient, autoimmune disease, and vascular disease. JPEN 14:5S:223S-225S, 1990.

Skipper A: Parenteral nutrition. In Nutrition Support Dietetics. Shronts EP, Ed. A.S.P.E.N., Rockville, MD,1989.

Spiegel J and Willenbucher R: Rapid development of severe copper deficiency in a patient with Crohn’sdisease receiving parenteral nutrition. JPEN 23(3):169-172, 1999.

Teitelbaum D: Parenteral nutrition-based cholestasis. Current Opinion in Pediatrics 9:270-275, 1997.Werlin S, Lausten T, Jessen S, et al.: Treatment of central venous catheter occlusions with ethanol and

hydrochloric acid. JPEN 19:416-418, 1995.Young EA: Gut fuels; a roundtable. A.S.P.E.N. 15th Clinical Congress, 1991.

44Nutrition Support

Notes

45Nutrition Support

Chapter Four:Gastrointestinal Disorders

Gastrointestinal disease and its associated treatment, including surgery, can havea profound impact upon digestion, absorption and, eventually, nutritional status.Appropriate nutrition support should be implemented as quickly as feasible to lessenthe severity of nutritional depletion and enhance potential for recovery.

MOUTH

The mouth plays a small role in digestion, breaking down food through mastica-tion so that it can pass into the esophagus. Some initial digestion takes place here, withthe breakdown of carbohydrate by salivary amylase. Nutrition problems may resultfrom decreased intake caused by poor dentition, stomatitis and dysphagia. A solution tothese problems may be as simple as altering food consistency so that the food can beingested more readily. Foods of liquid consistency may be well tolerated and oralsupplements should be offered.

If stomatitis is so severe that no food can be ingested, a short period of enteralfeeding via a nasogastric tube may be indicated. Generally, any isotonic intact proteinformula is well tolerated in this case. Since stomatitis is related to chemotherapy orradiation therapy and is often short-lived, patients suffering from it should be able toresume oral intake once the therapy has ended.

Dysphagia (difficulty in swallowing) may be of longer duration — and may neverresolve — depending upon the severity and cause of the dysfunction. The assistance ofa speech pathologist is important in the treatment of patients with dysphagia, to helpdetermine whether it is caused by a neurological or muscular disease or related to asurgical procedure and in which phase of the swallow the problem lies — oral, pharyn-geal or esophageal.

46Nutrition Support

A modified barium swallow is valuable in determining the extent of a patient’sswallowing disorder and can be useful in determining prognosis. Diet may be modifiedto include very soft or pureed foods, and to restrict thin liquids. (Thick liquids, such asmilkshakes, puddings and custards, are more easily swallowed than thin liquids.)

If a patient is unable to protect his airway or cannot manage to swallow effectivelyenough for adequate nutrition intake, he may be a candidate for short- or long-termenteral support, via a nasogastric or gastrostomy tube.

Surgical procedures in the mouth may include glossectomy, surgical resection(usually for cancer) and jaw wiring after trauma, or for correction of abnormal forma-tions of the teeth or jaw.

Depending upon the ability of a patient to maintain oral intake, enteral feedingsmay be indicated until he can adapt to changes that have occurred. Normal masticationand swallowing is usually affected to the extent that semisolids or liquids are besttolerated. When a route for provision of adequate nutrition is found, patients with oralsurgery or disease are less at risk for nutritional depletion.

ESOPHAGUS

Strictures, varices and surgical resection can all affect feeding.Any problem involving the esophagus affects further digestion. A patient with a

complaint of difficulty in swallowing (“everything just sticks in my throat”) may bediagnosed as having esophageal strictures, which can narrow the esophagus so severelythat no food can pass through to the stomach.

Dietary modifications for this condition could include a trial period of a low-carbohydrate, low-protein, high-fat diet, because it could help decrease gastrin secretion(Lang, 1989). If this regimen does not work, and the physician advises that the strictureswill get worse, a regimen of liquid or pureéd foods or, perhaps, an enteral tube feeding

• Poor dentition• Stomatitis• Dysphagia• Swallowing disorders• Surgical procedures

glossectomysurgical resectionjaw wiringcorrective surgery

Guidelines for the use of enteral nutrition in the adult patient. JPEN 11:5,1993.

Mouth Problems Affecting Nutrition

47Nutrition Support

regimen with an isotonic formula delivered through a gastrostomy tube is indicated.The passage of a nasogastric tube could be difficult because of the strictures.

The treatment of esophageal varices is discussed in a later chapter on liver disease,since the varices are usually related to cirrhosis.

Esophageal resection (esophagogastrectomy) is often performed with the occur-rence of esophageal cancer. Replacement of the esophagus may be performed duringthe same surgery. This replacement may be accomplished by using a portion of theintestine or colon to take the place of the removed esophagus, or the esophagus may beleft drastically shortened. Other surgical interventions may include pulling the stomachto the remaining portion of the esophagus.

Obviously, either of these types of surgeries can cause significant problems withadequate intake of nutrition. These patients may have early satiety, symptoms of dump-ing (premature emptying of the stomach contents into the duodenum, which can causesuch symptoms as sweating, shakiness, and diarrhea), or difficulty in swallowing. Sincethe transition to oral intake may be a slow one, these patients should have enteralnutrition support via a jejunostomy tube or with low-volume feedings into the stomachduring the immediate postoperative period. TPN may be used in conjunction with theenteral feedings to provide adequate nutrition intake.

Isotonic feedings are generally well tolerated. Enteral feedings should continue aspatients relearn how to eat, and be tapered off and discontinued only when adequateoral intake can be maintained. An antidumping diet and small, frequent feedings maybe best tolerated during this relearning period.

STOMACH

Surgical resection, gastrectomy, gastroparesis and gastric outlet obstruction allimpact feeding.

Ingested food is further broken down in the stomach, where hydrochloric acid andenzymes such as pepsin and trypsin begin to act upon protein molecules in the food-stuffs. Intrinsic factor is made in the stomach and is necessary for the later absorption ofvitamin B12 in the ileum. Conditions affecting nutritional status include resection of thestomach, gastrectomy, gastroparesis, and gastric outlet obstruction.

The body can usually adapt to resection of the stomach, but the transitional periodmay be long and difficult. Resection necessitates B12 injections, since intrinsic factor willno longer be available and a B12 deficiency will occur in one to three years.

The elderly patient with decreased gastric acid secretions may also be at risk for B12

depletion, since the availability of intrinsic factor is dependent upon the presence ofadequate gastric acids. This population is also at risk for iron deficiency anemia becauseof the hypochlorhydria. These patients may require supplemental B12 and iron, or evenintramuscular injections of B12 and iron, if these levels are depleted.

One of the primary symptoms of gastrectomy is late dumping syndrome, whichoccurs because of the loss of the pyloric sphincter, resulting in quick release of carbohy-drate from the stomach to the small intestine, causing an increase in insulin release.These symptoms generally occur two to four hours after meals.

48Nutrition Support

Early dumping, which occurs because of fluid shifts, causes symptoms of nausea,flushing, and light-headedness within 30 minutes of a meal. (Kelly and Nehra, 2001).The traditional diet of limited concentrated sweets and fluids can be enhanced byadding pectin to slow the emptying of the stomach (Speth, et al., 1983).

The diet should be changed to small, frequent feedings which are low in carbohy-drate, high in protein and moderate in fat. Patients who cannot tolerate adequate oralintake may be supplemented with duodenal feedings, utilizing an isotonic formula atan appropriate volume to allow for tolerance. Tolerance may be assessed symptomati-cally: little or no residual, minimal diarrhea, minimal or no abdominal discomfort. Theamount that can best be tolerated will be different with individual patients. Gastro-paresis (paralysis of the stomach) is discussed in the later chapter on diabetes.

Gastric outlet obstruction may occur for a number of reasons, including stenosis ofthe pylorus and changes in gastric emptying time related to surgery. If it is severeenough to prevent oral or enteral intake for more than 5 to 7 days, and/or presents apotential long-term problem, patients with gastric outlet obstruction may requireenteral feedings into the jejunum or TPN if jejunal access is not possible.

It may be difficult to determine the best course of action for a patient with a gastricoutlet obstruction, because determination of when the obstruction will open (or ifsurgery will be required) is difficult. Some resolve within a few days; others may re-quire jejunal feedings for weeks or months.

DUODENUM

Digestion continues in the duodenum, with further breakdown of protein to aminoacids, fats to glycerol and fatty acids, and carbohydrates to mono- and disaccharides.

Enzymes for this digestion are released from the intestinal mucosal cells and fromthe pancreas. Hormones triggered by the presence of food in the stomach cause therelease of these enzymes, and alert the gall bladder to release bile for the absorption offat. Initial absorption of fatty acids, amino acids, and simple sugars begins in the duode-num. Vitamin A and thiamine are also absorbed through the duodenum.

If any portion of the duodenum is resected, the initial phases of digestion and thereadying of nutrients for absorption may be affected. However, as much as one-half ofthe small bowel can be resected without long-term negative affects (Bernard and Shaw,1993). The patient may have some problems, including symptoms of lactose intoleranceand/or dumping syndrome. Altered absorption of iron and calcium may also bepresent. If iron deficiency anemia occurs, oral or intramuscular iron supplementationmay be necessary, and calcium supplementation may be beneficial as well.

49Nutrition Support

JEJUNUM

The normally functioning jejunum is responsible for the absorption of glucose,galactose, amino acids, fatty acids and monoglycerides. The water-soluble vitamins (C,thiamine, folate, biotin, riboflavin, niacin, B6, and pantothenic acid), as well as the fat-soluble vitamins (A, D, E, and K), are all absorbed through the jejunum. Minerals, suchas copper, zinc, iron, iodine, calcium, magnesium, phosphorus, chromium, manganese,and molybdenum are absorbed here as well.

Because the jejunum is the site for many digestive and absorptive functions, it isoften selected for placement of feeding tubes. Either needle catheter jejunostomies orregular jejunostomies can be placed in patients requiring short- or long-term enteralfeedings who cannot utilize gastric or duodenal feedings.

Jejunostomy feedings are beneficial because they utilize the digestive and absorp-tive capacities of the GI tract. Elemental, peptide, predigested or intact nutrient formu-las can be utilized if the tube is placed 6 to 8 inches distal to the ligament of Treitz(Lang, 1989). A jejunostomy tube placed lower in the jejunum may necessitate the use ofelemental or peptide products if intact formulas are not tolerated (as indicated byincreased diarrhea, cramping and/or abdominal discomfort.)

If the jejunum must be resected because of small bowel disease, cancer, trauma oradhesions, the ileum is usually able to expand its role so that absorption is not affectedgreatly. Initially, however, patients with a resected jejunum may experience malabsorp-tion of lactose, fat, and protein. Decreased transit time through the gut may also precipi-tate symptoms similar to those experienced with dumping syndrome.

Because ileal adaptation may take some time, patients should be followed closelyand advised to choose a low-residue, lactose-free diet in small frequent feedings. Multi-vitamin/mineral supplementation should be considered. Eventually, a more normaldiet can be resumed, depending upon the patient’s tolerance (Beyer, 1989).

Should enteral feedings be necessary, care should be taken to assure continuousfeedings at a well-tolerated volume. Depending on the site of resection, elemental orpeptide formulas may be necessary, especially if the resection has involved a largeportion of the jejunum. Intact nutrient isotonic formulas may be well tolerated in thosepatients with more distal resections.

Lactose intolerance

Dumping syndrome

Impaired iron and calcium absorption

Alterations in absorption of phosphorus, magnesium, copper

Alterations in absorption of thiamin, riboflavin, niacin, folate, and biotin

Alterations in absorption of Vitamins A, D, E, and K

Consequences of Duodenal Resection

50Nutrition Support

Patients with jejunostomies may lose up to 3 liters of fluid and 90 mEq/L of so-dium per day (Nightingale, et al., 1990). Since calcium (duodenum and jejunum) andmagnesium (jejunum and ileum) are absorbed in the small intestine, significant lossescan occur with resection.

ILEUM

The ileum is the only site of absorption of bile salts and vitamin B12. It is also the siteof absorption of chloride, sodium, potassium and disaccharides, as well as many nutri-ents absorbed by the jejunum. Vitamins C, D, and K are also absorbed via the ileum.

Any disease or resection of the ileum may cause severe malabsorption and steator-rhea (passage of large amounts of fats in the feces). The maldigestion and malabsorptionof fat is caused by the inability to absorb bile salts. The unabsorbed bile salts cause thecolonic cells to increase sodium and water secretion, thus increase diarrhea (Ladefoged,1996). Parenteral or intramuscular B12 supplementation is necessary.

Should the ileocecal valve be removed as well, significant bacterial overgrowth canoccur. Because there is no barrier between the ileum and the colon, bacteria normallyfound in the colon can migrate into the ileum. This overgrowth may precipitate diarrheaor steatorrhea, and result in malabsorption of carbohydrate, protein, fat and fat-solublevitamins.

Loss of the ileocecal valve can also decrease transit time, with resulting malabsorp-tion (Ladefoged, et al., 1996). Absorption of all nutrients, especially the macronutrients,calcium, iron, zinc, magnesium and fat-soluble vitamins, is affected.

Nutritional treatment may include total parenteral nutrition to maintain adequatenutritional status and allow time for the remaining intestine to adapt. Once a patientcan tolerate feedings into the gut, enteral or peptide-based formulas with medium-chaintriglycerides as a fat source are best tolerated, since medium chain triglycerides do notrequire bile for absorption. These allow for healing and growth of villi. Once oralfeedings can be reimplemented, small, frequent meals should be used.

Fat probably will not be well tolerated, at least initially, and should be restricted.Increased amounts of complex carbohydrate and protein should be provided. Often,disaccharides (maltose, lactose, and sucrose) are limited because of the limited ability ofthe gut to absorb these nutrients. Lactose intolerance may occur; increased amounts ofhigh fiber foods may precipitate diarrhea or discomfort.

Oral intake should be introduced and advanced slowly to allow for adaptation andbetter availability for absorption.

Massive small bowel resection may be necessary because of Crohn’s disease, smallbowel infarct or ischemia, trauma, etc. This terminology usually refers to resections ofmore than two-thirds of the small bowel, with less than 100 cm of small bowel remain-ing. Malabsorption of nearly all nutrients occurs (depending upon which portions of thesmall bowel have been resected).

Total parenteral nutrition is vital for patients who have undergone such a resectionand may be necessary for the rest of the patient’s life. If enteral nutrition is imple-mented, elemental low fat formulas should be given via a continuous drip system (toenhance absorption of nutrients). If a patient is eventually able to tolerate oral feedings,small, frequent feedings can be initiated and individualized to patient tolerance.

51Nutrition Support

Transition to enteral or oral feeding is often frustrating for the patient and thedietitian. I’ve had highly motivated patients who become extremely disheartened attheir inability to quickly resume eating whatever they want. One of the greatest serviceswe can provide these patients is counseling to help them understand their condition.Exercise patience.

COLON

The primary role of the colon is the reabsorption of water and electrolytes, and theproduction of biotin and vitamin K. Diseases that may require a colon resection includecolon cancer, diverticulitis, ulcerative colitis and Crohn’s disease.

Total parenteral nutrition may be of use in patients with severe ulcerative colitis orCrohn’s disease. Generally, Crohn’s disease patients respond better to TPN and bowelrest than patients with ulcerative colitis (Beluzzi, et al., 1995). Parenteral steroid admin-istration appear to be effective with Crohn’s patients, regardless of nutrition regimen(Hanauer, 1997). Patients with significant colon resection may require supplementationwith biotin and vitamin K. Generally, however, patients can gradually tolerate a low-residue or low-fiber, low-lactose diet and should eventually be able to resume a normaldiet after adapting to the surgical changes.

MALABSORPTION

Malabsorption of nutrients can also be related to diseases such as cancer, sprue,Crohn’s disease, ulcerative colitis, AIDS and infectious diseases of the GI tract. Malnu-trition may result because of this malabsorption related to inflammatory bowel disease(IBD) and may manifest itself with hypoalbuminemia, anemia, and weight loss(Fleming, 1995). Deficiencies of protein, folate, B12, and calories may occur because ofdiminished nutrient intake, malabsorption from the small bowel because of resection ordisease, maldigestion of fat and fat-soluble vitamins after ileal resection, and drug-nutrient interactions (Fleming, 1995).

Nutrition Problems & GI Diseases

Protein deficiency Carbohydrate deficiencyFat malabsorption/deficiency Weight lossAnorexia DiarrheaVitamin C deficiency Fat-soluble vitamin deficiencyVitamin B12 deficiency Folate deficiencyZinc deficiency Magnesium deficiencyCopper deficiency Iron deficiencyCalcium deficiency

52Nutrition Support

Commonly prescribed drugs for IBD include sulfasalazine, corticosteroids, andcholestyramine. all of which can cause significant nutrient deficiencies (sulfasalazineinterferes with folate absorption; corticosteroids interfere with calcium absorption; andcholestyramine interferes with fat and fat soluble vitamin absorption) (Fleming, 1995).

Fat malabsorption —steatorrhea — is commonly observed, and fat-soluble vita-mins are affected. The primary symptom of malabsorption is diarrhea. Normal stoolcolor is present with malabsorption of carbohydrate, lactose, fluid and electrolytes. Thestool may become yellow or silver with fat malabsorption; its consistency may becomeoily or floating and it may have an offensive odor. Lactose malabsorption often causeswatery diarrhea (Hermann-Zaidins, 1989). Diarrhea and fistula drainage cause losses ofelectrolytes and trace elements.

Zinc deficiency is quite common in patients with IBD and other diarrhea relatedillnesses. The deficiency of zinc appears to be related to decreased absorption rather thanto increased demand for the nutrient (Fleming, 1995). Other nutrients that may becomedeficient include selenium, vitamin D, vitamin C, vitamin A, folate, and magnesium.

Debate continues over the optimal treatment for fat malabsorption. Typically, totalfat intake has been restricted and medium-chain triglycerides have been used to en-hance absorption and reduce diarrhea. However, recent studies suggest that no benefitis served by limiting the fat in the diet and that, in fact, the higher calorie intake from fatis of more benefit. This is one of those “whatever works best for the patient” situations,where a moderate- or low-fat diet may be appropriate.

Carbohydrate malabsorption is relatively uncommon (except disaccharide intoler-ance). It may result in decreased transit time, diarrhea, abdominal discomfort, andassociated nutritional ramifications. The type of carbohydrate that is not absorbedeffectively should be identified and restricted in the diet. Protein malabsorption isuncommon, but may require using elemental or peptide formulas or supplements.Intact nutrient formulas may be more beneficial than defined-formula diets for patientswith Crohn’s disease, ulcerative colitis, and inflammatory bowel disease (Ginsberg andAlbert, 1989; Afdhal, et al., 1989). Others (O’Morain, et al., 1984; Saverymuttu, et al.,1985) suggest that elemental diets are more efficacious for IBD patients.

Reasons for positive outcomes with patients fed elemental diets may include theincreased glutamine content of elemental diets and/or the lower fat content of theelemental diet (Fleming, 1995). Other studies suggest that patients with IBD have abetter response to steroids than to enteral feedings (Lindor, Fleming, et al., 1992;Fernandez-Banares, et al., 1995).

TPN may often be required for the patient with IBD as either an adjunctive orprimary therapy. TPN and bowel rest appears to be more beneficial for the patient withCrohn’s disease than for the patient with ulcerative colitis.

Nutrient requirements for patients with gastrointestinal disease and/or followinggastrointestinal surgery are generally increased. With significant malabsorption aftermajor GI surgery, enteral calorie needs are increased by 150 to 200 percent. Protein needsare also increased by 150 to 200 percent. Generally, 30 to 35 kcal/kg/day and at least 1.5gm protein/kg/day is required. Vitamin and mineral supplementation should be consid-ered as well, based on each patient’s specific needs and the extent of the resection.

53Nutrition Support

SHORT BOWEL SYNDROME

Short bowel syndrome (SBS) occurs when greater than 50 percent of the smallbowel is resected or bypassed (Bernard and Shaw, 1993). Several factors are importantin determining how severe symptoms will likely be: the remaining length and site of thesmall bowel; whether the stomach and/or colon has been resected; whether the ileoce-cal valve has been resected; and the presence of remaining disease in the bowel(Rombeau, 1995; Ladefoged, et al., 1996; Purdum and Kirby, 1991). This syndrome ischaracterized by significant malabsorption of fluid, electrolytes and other nutrients as aresult of chronic diarrhea, frequent dehydration and electrolyte disturbances. As aresult, the patient experiences progressive weight loss and malnutrition (Wilmore, et al.,1994). A more positive outcome may be seen in the patient with less than 70 percent ofthe small bowel removed: if the ileum is present; if the ileocecal valve is present; and ifthe remaining colon is not diseased (Rombeau, 1995; Carbonnel, et al., 1996).

In order to determine the most effective method of nutritional treatment, we mustbe aware of the portions of the small bowel that are remaining: whether the ileocecalvalve is present; the presence or absence of the colon; and the adaptive capacity of theremaining gut (dependent upon the presence of disease, such as Crohn’s disease orulcerative colitis) (Espat, 1994).

Resection of the ileum of greater than 100 cm and/or the loss of the ileocecal valvewill cause significant steatorrhea and decreased B12 absorption; the absence of theileocecal valve may also result in significant bacterial overgrowth (Kudsk, et al., 1990).The resection of the colon may result in increased incidence of diarrhea and oxalateurinary stones and decreases in water and electrolyte reabsorption (Wilmore, et al., 1994;Stralovich, 1993; Simko, 1980). Because the duodenum, ileum, jejunum, and, to a lesserextent, colon are where minerals, trace elements, and vitamins are absorbed, deficien-cies of these nutrients may occur.

After extensive bowel resection, adaptation does occur, but this period of adapta-tion may take as long as one to two years. TPN is necessary during this period to pro-vide adequate nutrient intake and, in essence, keep the patient alive. Early initiation ofenteral feedings into the remaining bowel or even oral intake can be of benefit becauseof the advantages of enteral feedings in preventing mucosal atrophy, stimulating intesti-nal adaptation, and decreasing the risk of bacterial translocation (Byrne, et al., 1996).

Often, TPN and enteral/oral feedings must continue simultaneously for anywherefrom one month to several years. The type of enteral formula utilized is dependent onthe patient’s individual needs. Patients with less than 100 cm of bowel left will usuallyrequire TPN on a long-term basis. If the patient has only 110 cm of bowel left with nocolon, defined-formula diets are of benefit; patients with more bowel remaining, espe-cially with the presence of the colon, may well tolerate an intact nutrient formula (Ber-nard, et al., 1993). Intact nutrient formulas may be beneficial because of their isotonicityand stimulation of the intestinal tract (Stralovich, 1993; Simko, 1980; Rombeau, 1995).

Oral intake, once initiated, should consist of small frequent feedings consisting ofhigh protein, complex carbohydrate, and low fat foods. Restriction of disaccharides(lactose, maltose, and sucrose) is often necessary. Because calcium and magnesium mayhave formed soaps with unabsorbed long chain fatty acids, oxalate absorption is altered

54Nutrition Support

and increased (normally the calcium and magnesium bind the oxalates) (Ladefoged, etal., 1996). High oxalate foods may require restriction if the colon has been resected.Supplemental vitamins and minerals are usually required (Bernard, et al., 1993). Zincmay be lost in the stool at a rate of 12 to 16 mg/liter (Fleming, 1989).

Success has been recently reported in treating short-bowel syndrome patients withspecific nutrients that appear to stimulate the gut, glutamine, fiber, and short-chain fattyacids, along with growth factor (Wilmore, et al., 1994). The addition of these nutrients toan oral diet resulted in weaning of TPN in several long-term TPN patients with SBS.

Growth hormone appears to increase mucosal hyperplasia and colonic massfollowing resection. It also increases water and sodium in the small bowel and colonand may increase amino acid transport (Wilmore, et al., 1994; Byrne, et al., 1996).Glutamine increases hyperplasia as well, while enhancing glucose and sodium absorp-tion (Byrne, et al., 1996).

A high-carbohydrate, low-fat, high-fiber diet may be beneficial (Byrne, et al., 1996)because of the possibility that any malabsorbed carbohydrate and fiber that passes intothe colon will be fermented to short-chain fatty acids, thereby enhancing sodium andwater absorption.

PANCREAS

The pancreas, though not part of the gastrointestinal tract, is important to digestionand absorption. Hormones secreted by the pancreas include glucagon and insulin.Pancreatic juice, containing enzymes such as amylase, trypsin and lipase, is secretedinto the duodenum when chyme is present. Pancreatic and duodenal enzymes are vitalfor the adequate digestion and later absorption of nutrients. Pancreatic cancer, severeacute pancreatitis and pancreatitis with associated abscess, fistula or pseudocyst have amarked effect on nutritional status.

Acute pancreatitis is characterized by hypermetabolism and hypercatabolism(Seidner and Fish, 1998). Negative nitrogen balance is common, as is alterations inglucose metabolism (Shaw and Wolfe, 1986). As is the case in sepsis, elevations incatecholamines, insulin, glucagon, tumor necrosis factor, and other hormones occur(Seidner, Fish).

Most patients with mild or moderate pancreatitis do not require nutrition support(JPEN, 1993). Those patients who do require nutrition support may benefit fromparenteral nutrition. Absolute indications for TPN are acute necrotizing pancreatitis,pancreatic fistulae, pancreatic pseudocyst, and pancreatic abscess. Gastrointestinalfeedings had been contraindicated because of the associated gastric atony, ileus, intesti-nal obstruction and malabsorption due to the alteration in release of pancreatic enzymes(Espat, 1994; Grant, et al., 1984).

Recent studies have indicated that fat given parenterally is well tolerated in patientswith pancreatitis, with no increase in serum triglyceride levels or worsening of thepancreatitis as long as pancreatitis is not caused by hypertriglyderidemia (Kudsk, 1990).

However, Espat recommends that, in acute pancreatitis, IV fat should be limited tothe severely malnourished or those patients with severe glucose intolerance because ofthe stimulation of the pancreas by the fat infusion. Patients with pancreatic disease

55Nutrition Support

receiving TPN typically require insulin supplementation but otherwise appear to toler-ate support. However, the incidence of glucose intolerance may be lower in enterallyfed patients with severe acute pancreatitis (Kakfarentzos, et al., 1997).

Peptide or elemental feedings into the jejunum below the ligament of Treitz causesome secretion of hormones and pancreatic activity; however, the enzymes released arelow in concentration. The feedings were safely tolerated in some studies of mild andmoderate pancreatitis and the expected problems of stimulation of the pancreas withelevated serum amylase levels, ileus, and leakage around the jejunostomy tube did notoccur (Kudsk, 1990). It appears that the adynamic ileus that occurs with pancreatitis islimited to the stomach and colon and does not affect the small bowel.

Patients with severe acute pancreatitis may also be fed into the stomach (McClave,et al., 2009). Pancreatitis is associated with a high degree of hypermetabolism (Gran, etal., 1984; Bouffard, et al., 1989).

The goal of nutrition support in pancreatic disease is to replete nutrition stores andto maintain these stores throughout the course of the illness. Calorie needs in acutepancreatitis are estimated at 1.3 to 1.5 times BEE. During chronic pancreatitis, the esti-mated needs are lowered to 1.0 to 1.3 times BEE. Suggested protein requirements are 1.0to 1.3 gm protein/kg/day for chronic pancreatitis, with an increase to 1.5 to 2.0 gmprotein/kg/day for acute pancreatitis (Aalyson, 1989).

CASE STUDY #1: GASTROINTESTINAL DISEASE

Note: Nothing can replace experience in nutrition support. The judgment of thedietitian, physician and pharmacist is of paramount importance. Accordingly, I’veincluded case studies to illustrate how cases progress, what twists and turns occur andhow the nutrition support team must constantly make adjustments. It is hoped thatthese studies will help the material come alive, and that the student taking the coursewill give each one his or her close attention.

Case study #1: GB was a 32-year-old male who was admitted to the medical surgi-cal floor with a diagnosis of inflammatory bowel disease that was thought to be ulcer-ative colitis. His symptoms of severe bloody diarrhea and an associated 25 lb weightloss over three months resulted after he had consumed water from a trout stream. Hehad been treated as an outpatient with prednisone and 5 aminosalycilate (an analgesic).When this therapy became ineffective, his therapy changed to an increased dosage ofprednisone along with sulfasalazine and metronidazole (Flagyl). He was admitted tothe hospital after further weight loss and was started on TPN. His colonoscopy revealeddisease from the rectum to the left half of the transverse colon.

His TPN regimen was a peripheral formula of final concentration of dextrose 8percent, amino acid 4 percent and lipid 3 percent at a volume of 2500 ml/day. The TPNwas administered through a PICC line and provided approximately 1830 kcal and 100gm protein. He also continued to consume a full liquid diet. His anthropometrics in-cluded a height of 5’9” and a weight of 71.4 kg. His needs were assessed to be 1800 to2100 kcal/day and 70 to 105 gm protein/day. His albumin was 2.3.

Six days after admission, he had increased cramping and bloody stools.Colonoscopy revealed a normal right colon and severe left-sided colitis with extensive

56Nutrition Support

ulcerations. Surgery (colectomy) was considered vs treatment with continued TPN anda change in drug regimen to methotrexate and cyclosporin. Two days later, his symp-toms lessened and he was started on cyclosporin (an immunosuppressant thought to beeffective because of the autoimmune component of the disease). The TPN continuedand his diet was advanced to low residue bland. His symptoms continued to decreaseand he tolerated the diet and TPN well. His complaints changed from problems with hisGI tract to “knee pain” and other arthralgias (possibly associated with increased hydra-tion). He continued to tolerate the TPN and diet and regained approximately tenpounds. His TPN was tapered until it was discontinued and he continued on his POdiet. A follow-up colonoscopy revealed marked improvement in his colon with fewulcerations and reduced colitis.

The TPN and nutrition support provided to this patient enabled his nutritionalstatus and GI symptoms to improve. Surgery was avoided and he was discharged homewithout a colostomy as he had feared.

REVIEW QUESTIONS

1. The patient has had esophageal resection. Formulate a nutrition care plan.2. What nutrition concerns are vital in a post-total gastrectomy patient?3. How would you support a patient with a small bowel resection (the resection in-

cluded the duodenum, jejunum, and a small portion of the ileum)?4. What would you do for a patient with acute alcoholic pancreatitis and an associated

enterocutaneous fistula?

REFERENCES

Aalyson M: Nutrition support in pancreatic disease. Nutrition Support Dietetics. Shronts EP, Ed. A.S.P.E.N.,Silver Spring, MD, 1989.

Afdhal NH, Kelly J, McCormick PA, et al.: Remission induction in refractory Crohn’s disease withnonelemental formula diet. Dig Dis Sci 34:1624-1628, 1989.

A.S.P.E.N. Board of Directors. Guidelines for the use of parenteral and enteral nutrition in adult andpediatric patients. J Parenter Enteral Nutr 17 (4suppl):1SA-52SA, 1993.

Belluzi A, Brignola C, Campieri M, et al.: New fish oil derivative for preventing clinical relapses in Crohn’sdisease: A double blind placebo controlled randomized trial. Gastroenterology 108(4):A781, 1995.

Bernard DKH and Shaw MJ: Principles of nutrition therapy for short-bowel syndrome. Nutr Clin Prac8:153-162, Aug, 1993.

Beyer PL: Short-bowel syndrome. Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A, Ed.A.S.P.E.N. Publications, Rockville, MD, 1989.

Bouffard YH, Delafosse BX, Annat GJ, et al.: Energy expenditure during severe acute pancreatitis. JPEN13:1:26-27, 1989.

Byrne TA, Morissey TB, Nattakom TV, et al.: Growth hormone, glutamine, and a modified diet enhancenutrient absorption in patients with severe short bowel syndrome. JPEN 19:4:296-302, 1995.

Byrne T, Nompleggi D, Wilmore D: Advances in the management of patients with intestinal failure.Transplantation Proc. 28:2683-2690, 1996.

Byrne TA, Browning B, Tu N, et al.: A new treatment option for patients with short bowel syndrome:bowel rehabilitation with growth hormone, glutamine, and a modified diet. Support Line XVIII:1:1-7,February, 1996.

57Nutrition Support

Carbonnel F, et al.: The role of anatomic factors in nutritional autonomy after extensive small bowelresection. JPEN 20:4:275-279, 1996.

Espat J: Pancreatitis. A.S.P.E.N. 18th Clin Congress, San Antonio, TX, 1994.Fernandez-Banares F, Cabre E, et al.: How effective is enteral nutrition in inducing clinical remission in

active Crohn’s disease? A meta analysis of the randomized clinical trials. JPEN 19:5:356-361, 1995.Fleming C: Trace element metabolism in adult patients requiring total parenteral nutrition. Am J Clin Nutr.

49:573-579, 1989.Fleming CR: Nutritional considerations in inflammatory bowel disease. A.S.P.E.N. 5th Annual Advances

and Controversies in Clinical Nutrition. Scottsdale, AZ, 1995.Ginsberg AL and Albert MB: Treatment of patient with severe steroid-dependent Crohn’s disease using a

high calorie whole diet. Dig Dis Sci 34:1624-1528, 1989.Grant JP, James S, Grabowski V, and Trexler KM: Total parenteral nutrition in pancreatic disease. Ann Surg

11:627-631, 1984.Hanauer S and Meyers S: Management of Crohn’s disease in adults. Am J Gastroenterol 92:559-566, 1997.Hermann-Zaidins MG: Malabsorption. Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A,

Ed. A.S.P.E.N. Publications, Rockville, MD, 1989.Howard L, Michalek AV, and Alger SA: Enteral nutrition and gastrointestinal, pancreatic, and liver

disease. Clinical Nutrition: Enteral and Tube Feeding. Rombeau JL and Caldwell MD, Ed. WBSaunders, Philadelphia, 1990.

Kakfarentzos F, Kehagias J, Mead N, et al.: Enteral nutrition is superior to parenteral nutrition in severeacute pancreatitis. Results of a randomized prospective trial. Br J Surg 84:1665-1669, 1997.

Kelly DG, NehraV. Gastrointestinal disease. In Gottschlich MM, Fuhrman MP, Hammond KA, et al. (Eds.)The Science and Practice of Nutrition Support. A Core-Based Curriculum. Dubuque, IA. Kendall/Hunt Publ Co, 2001.

Kudsk KA, Campbell SM, O’Brien T, and Fuller R: Postoperative jejunal feedings following complicatedpancreatitis. Nutr Clin Prac 5:1:14-17, 1990.

Ladefoged K, Hessov I, Jarnum S: Nutrition in short-bowel syndrome. Scand J Gastroenterol. 31 Suppl216:122-131, 1996.

Lang CE: Nutrition support in gastrointestinal disease. Nutrition Support Dietetics. Ed. Shronts EP, Ed.A.S.P.E.N., Silver Spring, MD, 1989.

Lindor KD, Fleming CR, Burnes JU, et al.: A randomized prospective trial comparing a defined formuladiet, corticosteroids, and a defined formula diet plus corticosteroids in active Crohn’s disease. MayoClin Proc 67:328-333, 1992.

McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutritionsupport therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) andAmerican Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) JPEN 33(3): 277-316, 2009.

Nightingale J, Lennard-Jones J, Walker E, et al.: Jejunal efflux in short bowel syndrome. Lancet 336:765-768,1999.

O’Morain C, Segal AW, Levi AJ: Elemental diet as primary treatment of acute Crohn’s disease; a controlledstudy. Br Med J 288: 1895-1862, 1984.

Peth PA, Jansen JB, Lammers CB. Effect of acarbose, pectin, a combination of acarbose with pectin, andplacebo on postprandial reactive hypoglycemia after gastric surgery. Gut 24:798-802, 1983.

Purdum P and Kirby D: Short-bowel syndrome: A review of the role of nutrition support. JPEN 5:93-101, 1991.Rombeau JL: Nutritional-metabolic treatment — short bowel syndrome. A.S.P.E.N. 5th Annual Advances

and Controversies in Clinical Nutrition. Scottsdale, AZ, 1995.Saverymuttu S, Hodgson JGF, Chadwick VS: Controlled trial comparing prednisolone with an elemental

plus non-absorbable antibiotics in active Crohn’s disease. Gut 26:994-998, 1985.

58Nutrition Support

Seidner DL, Fish JA. Nutritional management of patients with feeding-induced pain: acute pancreatitis.Semin Gastrointest Dis 9:200-209, 1998.

Shaw HF, Wolfe RR. Glucose, fatty acid, and urea kinetics in patients with severe pancreatitis. Ann Surg204:665-672, 1986.

Simko V: Short bowel syndrome. Gastroenterology 78:170,1980.Stralovich A: Gastrointestinal and pancreatic disease. Nutrition Support Dietetics, 2nd ed. Gottschlich MM,

Matarese LE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.Van Gossum A, Lemoyne M, Greig PD, et al.: Lipid-associated total parenteral nutrition in patients with

severe acute pancreatitis. JPEN 12:3:250-255, 1988.Wilmore DW, Ziegler TR, and Byrne TA: Is long-term TPN essential in the short bowel patient? A.S.P.E.N.

18th Clinical Congress Symposium #4, San Antonio, TX, Jan, 1994.

59Nutrition Support

Chapter Five:Stress and Sepsis

This chapter will discuss sepsis and surgery, how the body reacts to these stres-sors, and the nutrition support requirements of patients subjected to such stress. (An-other Nutrition Dimension course, Nutrition & Immunity, Part I, deals with the dietaryand nutritional effects of stress in greater detail.)

The stressed or septic patient is unique in that nearly all of his metabolic pathwaysmay be altered. Determining the optimal method and mode of feeding to meet hisindividual requirements is quite a challenge. The additional factor of individual ormultiple organ failure must also be considered, and may prevent adequate provision ofcalories and, especially, protein.

Sepsis is defined as a systemic inflammatory response to infection. Systemic In-flammatory Response Syndrome (SIRS) is much like sepsis but is an inflammatoryresponse to various types of insults, i.e. pancreatitis. Severe sepsis is defined as sepsisaccompanied by organ dysfunction, hypoperfusion, and/or hypotension. Septic shockis sepsis with hypotension that is unresponsive to fluid resuscitation with resultantperfusion abnormalities.

So what happens from a nutrition perspective when a patient is admitted withsepsis? The patient is hypermetabolic; there is increased production of glucose withincreased uptake at the cellular level; and protein and fat are broken down at a fasterrate.

THE STRESS RESPONSE

The body reacts to stress (or threats), whether emotional or physical, with a mes-sage sent from the brain to the hypothalamus to initiate the “flight or fight” response.This response is said to be undifferentiated — that is, the physical reaction is essentially

60Nutrition Support

the same, whether the perceived threat is physical or emotional. Only the duration andintensity varies.

During the stress response, stimulation of the autonomic nervous system causes anincreased production of catecholamines (epinephrine and norepinephrine). This de-creases the release of insulin into the blood, and increases glucagon release to allow asudden burst of energy for action. These increased catecholamines, along with glucocor-ticoids, may be a factor in the insulin resistance seen in stressed or septic patients (Kline,1999).

Secretion of adrenocorticotropic hormone (ACTH) is increased due to stimulationof the pituitary and adrenal glands.

Sympathetic AutonomicNervous System

PITUITARY GLAND

Hormones ACTH

Pancreas

InsulinGlucagon

AdrenalMedulla

• Growth hormone• Prolactin• Vasopressin

GlucocorticoidsAldosterone

Mineralocorticoids

TSH

ThyroidGland

AdrenalCortex

ThyroxineEpinephrine

Norephinephrine

The Stress Response

CRF

BRAIN/RAS

HYPOTHALAMUS

(reticular activating system)

(corticotropin-releasing factor)

61Nutrition Support

Glucocorticoids (cortisol, cortisone, and deoxycorticosterone) and mineralocorticoids(aldosterone and deoxycorticosterone) also increase, but typically return to their normallevels rather quickly. Glucocorticoids act to increase the synthesis of glucose by the liverthrough their action of increasing breakdown of protein and fat stores in the body (Moore,et al., 1989). The action of these hormones is summarized in the chart below.

The increased synthesis and decreased utilization of glucose during stress andsepsis causes hyperglycemia. In fact, the rate of glucose synthesis is increased by 200percent in septic patients (Nelson, et al., 1989). This is made possible because of anincrease in glucagon production by the pancreas, mobilization of fatty acids fromadipose tissues and the oxidation of branched-chain amino acids (leucine, isoleucineand valine) for gluconeogenesis. Protein stores may be utilized for as much as 25 per-cent of the energy required in the stressed or septic state (Gray and Kaminski, 1985).

Effect of Hormones on Metabolism

GlucocorticoidsIncreases: protein breakdown

fat breakdownglucose mobilization

Decreases: insulin action

AldosteroneConserves: sodium

potassium

Growth hormoneIncreases: protein breakdown

fat breakdown

CatecholaminesIncreases: fat breakdown

protein synthesisglucose synthesis

InsulinDecreases: protein synthesis

fat synthesis

GlucagonIncreases: protein synthesis

glucose synthesis

Glucose

Tissue repair Albumin

AMINO ACIDPOOL

LIVER(Protein synthesis)

Urea(Stress level

indicator)

Gut(enzymes,

secretory IgA)

MusclesSkin(collagen)

FibrinogenComplementRetinol-binding proteinPrealbumin

Acute PhaseProteins

Protein Metabolism During Stress and Sepsis

62Nutrition Support

The liver is very active during stress; its primary purpose is the production ofglucose for energy. The amino acid pool in the body is increased by pulling amino acidsfrom the intestinal tract, muscles, skin and serum albumin. These amino acids are usedby the liver for gluconeogenesis and production of the acute phase proteins, albuminand transferrin.

Ketosis may occur during stress and sepsis, possibly related to decreased insulinavailability and increase in fatty acid synthesis. This results in reduced nitrogen loss andmore efficient utilization of energy sources. However, this adaptation does not occurreadily in stress or sepsis, for reasons that have yet to be determined.

Because the immune system of a stressed or septic patient may be impaired, pro-longed stress may precipitate multi-system organ failure, which can cause furtherchanges in carbohydrate, protein and fat metabolism.

These alterations, summarized above, may be recognized by increased serumtriglyceride levels (resulting from increased mobilization of fatty acids), increased bloodurea nitrogen levels (caused by decreased protein synthesis and reduced utilization ofaromatic amino acids) and progressive reduction in serum glucose levels (caused by thereduced ability for gluconeogenesis) (Shronts and Fish, 1989). Adequate nutritionsupport of the stressed or septic patient is critical to enhance the body’s ability to re-cover from the stressed state.

STRESS

GLUCOSE

STRESSHORMONES

Carbohydrate

Alterations in Metabolism During Stress and Sepsis

Cholesterol steroid hormonesproduction

InsulinBlood Sugar

Fat

Protein

blood sugarglycosuriasensitivity of tissues

fat breakdownfatty liver / cirrhosisarterial plaque

proteolysisprotein synthesisprotein for immune organs & cells

glycogen breakdowngluconeogenesis

63Nutrition Support

NUTRITION REQUIREMENTS

• Energy. During the acute phase of a septic episode, focus should be on metabolicsupport or maintenance. Recommendations are to feed “hypocalorically” at a rate of 25kcal/kg and 1.5 to 2.0 gm protein/kg in an effort to preserve lean body mass (Wolley,2007). During the recovery or repletion stage, calorie needs increase to 25 to 35 kcal/kgwith 1.5 to 2.0 gm protein/kg, taking care to avoid overfeeding.

When available, indirect calorimetry, utilizing a metabolic cart, should be used todetermine caloric requirements. Indirect calorimetry will be discussed further in Chap-ter Seven: Respiratory Failure. Calorie requirements can be provided with a mix ofcarbohydrate and fat sources.

It’s important to avoid overfeeding, since hyperglycemia causes cellular disfunc-tion, an increased risk of infection, and intracellular shifts of electrolytes. Overfeedingcan also result in increased CO2 production.

• Fat. No more than 30 to 40 percent of calories, but at least 4 percent, should beprovided by fat to meet essential fatty acid needs. The type of fat is of importance instressed or septic patients, since certain fats are known to inhibit immune function.

Omega-6 (Ω-6) fatty acids, including linoleic acid, are precursors to arachidonicacid — itself a precursor to types of prostaglandins, thromboxanes, prostacyclins, andleukotrienes that can have a deleterious effect on immune functions, as shown below.

Omega-3 (Ω-3) fatty acids, on the other hand, are metabolized to forms of prostag-landins, thromboxanes, prostacyclins and leukotrienes that have a lesser effect on theimmune system. Omega-3 fatty acids may mitigate the deleterious effects of Ω-6 fattyacids on the immune system, when given in adequate amounts. The chart on the follow-ing page outlines the effects of Ω-3 and Ω-6 fatty acids on immunity.

To increase the amount of Ω-3 fatty acids available to the enterally fed patient,formulas containing canola oil or fish oils (including eicosapentaenoic acid (EPA) anddocosahexaenoic acid (DHA)), should be used. The lipid emulsions for TPN currentlyavailable contain linoleic acid (so that essential fatty acids are available to the patient ontotal parenteral nutrition).

Caloric Requirements in Stress & Sepsis

Metabolic support25 kcal/kg/day with 1.5 to 2.0 gm protein/kg/day

Nutrition support (repletion)25 to 35 kcal/kg/day with 1.5 to 2.0 gm protein/kg/day

Source: Wooley, 2007.

64Nutrition Support

The efficacy of adding Ω-3 fatty acids to TPN lipid emulsions is currently beingstudied, but no alternative is presently available. Perhaps in the immunocompromisedpatient on TPN, care should be taken to limit the total calories from fat to less than 30percent of total calories.

However, we must again weigh what is best for the individual patient. Whileincreased fat intake may alter immunocompetence, it may also enable the patient to beweaned from the ventilator. We can’t make a blanket statement about fat calories inTPN. Once the composition of lipid emulsions can be altered to contain fewer Ω-6 fattyacids, this subject may not be as controversial.

• Carbohydrate. Since hyperglycemia and insulin resistance are part of the stressresponse, the provision of calories from carbohydrate may require limitation and closemonitoring for patient tolerance. In the glucose-intolerant patient, glucose should belimited to 4 mg/kg/minute.

• Protein. Obviously, protein requirements increase during stress and sepsis.Protein needs during sepsis as well as through recovery or repletion are determined as1.5 to 2.0 gm protein/kg/day.

Renal and liver function should also be considered when assessing protein require-ments. The immunocompromised, septic or stressed patient also may have renal insuffi-ciency or acute renal failure. Care of acutely ill renal patients and patients with hepaticinsufficiency or failure is discussed in later chapters.

While arginine is not an essential amino acid in the healthy individual, it appearsto become essential during periods of stress and sepsis (Kirk and Barbul, 1990). Argin-ine increases secretion of growth hormone, prolactin, insulin, glucagon and insulin-likegrowth factor 1 (IGF-1). Through the actions of these hormones, it appears that nitrogenbalance and wound healing are improved during periods of stress as these hormonesimprove cellular growth. Arginine also appears to enhance the immune response byimproving T cell production (Kirk and Barbul, 1990). Peripheral lymphocytes are in-creased in number by arginine and the mitogenic response of immune cells to antigensCon A and PHA is improved (Daly, et al., 1988).

Fatty Acids and Immunity

Potent inflammatory agentPotent platelet aggregator and vasoconstrictorWeak vasodilatorPowerful inducer of chemotaxis, adherence

of cells & inflammation

Weak inflammatory agentWeak platelet aggregator and vasoconstrictorActive vasodilator & inhibitor of platelet aggregationWeak inducer of chemotaxis, adherence of cells

& inflammation

PGE2TXA2PGI2LTB4

PGE3TXA3PGI3LTB5

Ω-6

Ω-3

65Nutrition Support

ARGININE AND GLUTAMINE

• Arginine appears to increase synthesis and the release of growth hormone,prolactin, and insulin (Kirk, et al., 1990; Alexander, 1988). Growth hormone is a power-ful stimulator of immunity and wound healing, while prolactin is a stimulator of anabo-lism or cellular growth. These factors result in decreased weight loss and increasedwound healing (Young, 1991; Kirk, 1990). Arginine also appears to play a role in increas-ing insulin release.

Arginine accelerates wound healing and improves immunity The mechanisms arenot clearly understood, but are believed to be related to arginine’s chemical makeupand metabolism, as shown in the chart on the following page.

Arginine may be of benefit to the critically ill patient by improving or preservingimmune function (Daly, et al., 1988). Supplemental arginine has been added to someenteral formulas; they contain approximately 5 percent (7 to 20 gm/1500 kcal) of totalprotein as arginine. The addition of arginine via an enteral formula may be beneficial topatients with blunt torso trauma and in malnourished patients who will undergoelective gastrointestinal surgery. Arginine can be added to TPN at levels of 5 to 12.5 gmarginine/100 gm amino acid (Fish, 1994). The addition of enteral arginine to formulasfor the septic patient is not effective and may be harmful (VanWay, 2007).

Pontes-Aruda has extensively studied the effects of enteral nutrition witheicosapentanoic acid, glutamine and antioxidants when utilized during critical illnessand sepsis. His studies, published in Critical Care Medicine, suggest that using thesespecialized formulas appear to reduce incidents of organ failure, ventilator days, ICUdays, and mortality (by 60 percent)(Pontes-Aruda, et al., 2006, 2007).

Arginine

• Formed as part of the urea cycle

• Generated from citrulline by kidney

• Conditionally essential during stress

• Precursor of nitrites, nitrates and nitric oxide (used by immune cells to destroy antigens)

• Converted back to ornithine (used to synthesize glutamine)

• Promotes cellular growth

ArginineNH3 + CO2 + 2 ATP

Ornithine

66Nutrition Support

• Glutamine, while generally described as a non-essential amino acid, becomes anessential amino acid during periods of catabolism or extreme stress. Glutamine comprises61 percent of the amino acid pool in skeletal muscle and, along with alanine, is the pri-mary mode of transport for nitrogen from muscles to organs (Lacey and Wilmore, 1990).

During periods of stress, the skeletal muscle increases the release of glutamine at agreater rate, thereby depleting intracellular glutamine by more than 50 percent. Duringstress, glutamine synthesis increases. The gut appears to play a role in the metabolismof glutamine by converting skeletal muscle glutamine to nitrogen and alanine; these arethen used by the liver for gluconeogenesis, acute phase protein synthesis and urea.

Since glutamine is a glucogenic amino acid (i.e. it can be converted to energy in theKrebs cycle) — it is a preferential fuel source for the gut, kidney and lung during stress.In the gut, glutamine is utilized for energy and synthesis of other amino acids. Replicat-ing cells such as fibroblasts, lymphocytes and epithelial cells avidly consume glutamine(Jensen, et al., 1996).

Glutamine is the most important substrate for ammoniagenesis in the kidneys andis important for gluconeogenesis in the liver (Long, et al., 1995). Glutamine’s otherfunctions include transport of ammonia between tissues; regulation of glycogen synthe-sis in the liver; and acting as a precursor in the formation of purine and pyrimidinerings (Zaloga, unpublished; Smith and Wilmore, 1990).

Glutamine is stored in the muscles of the body and released when the demandincreases. Without an exogenous supply of glutamine during stress and sepsis, themuscles shrink and glutamine can become depleted. When glutamine is not available orthe supply is limited, as is the case in patients receiving TPN, the gut is “starved”.Depletion of glutamine is not inhibited by TPN standard amino acid solutions (Laceyand Wilmore, 1990).

During a catabolic or stressed state, levels of glutamine in the blood fall 20 to 30percent, indicating that glutamine may be vital to the body’s response to stress. Re-duced protein synthesis, atrophy of intestinal mucosa and impaired immune responseresult (Lochs and Hubl, 1990).

In animal studies, stressed animals supplemented with glutamine showed im-provement in the quality of the gut wall and reduced incidence of weight loss andinfection and increased nitrogen retention (Fox, et al., 1988; Jacobs, et al., 1988; Klimberg,et al., 1990; Jensen, et al., 1996). Glutamine may play a role in decreasing bacterial trans-location and may help to improve patient outcome (Jensen, et al., 1996).

Bacterial translocation is defined as the “passage of viable indigenous bacteriafrom the gastrointestinal lumen, through the epithelial mucosa to mesenteric lymphnodes and visceral organs as liver, spleen, and lung” (Berg and Garlington, 1979).

Bacteria which may translocate include: Escherichia coli, enterococcus, proteus species,Klebsiella pneumoniae; enterobacteriaceae, and Pseudomas aeruginosa (Hermann, 1995).

Several factors (sepsis, shock, and trauma; altered immune function; bacterialovergrowth; and endotoxemia) (Hermann, 1995) contribute to translocation. The inci-dence of bacterial translocation is lower when the gut is utilized for feeding (Moore andJones, 1986). Glutamine is metabolized in the gut and then serves as energy for theenterocyte. During stress, glutamine uptake by the GI tract increases (Austgen, 1991).

67Nutrition Support

When glutamine is supplemented, plasma and muscle glutamine levels increase; intesti-nal cell integrity and villous height are better maintained; and mucosal DNA activity ismaintained.

Glutamine is available in all enteral formulas, primarily as glutamic acid, but mustbe supplemented in free amino acid formulas.

Generally, glutamine content ranges from 5 to 8 gm per 16 gm of nitrogen. Thiscorresponds to from 3.8 to 7.8 gm of glutamine per day. In critically ill patients,glutamine supplementation has been suggested in the range of 10 to 20 gm/day (Kuhn,et al., 1996) and later recommendations have suggested that stressed patients mayrequire up to 40 gm of glutamine/day (Brantley, 2007). Glutamine is not typically stablein an aqueous solution or at room temperature for longer than 24 to 48 hours; thus,supplementation to TPN is not often accomplished. When glutamine was added toTPN, however, translocation decreased (Souba, et al., 1990).

Glutamine can be given at levels of 20 to 40 gm/day (0.285 to 0.571 gm/kg) or atlevels of 30 percent of total protein given in TPN (MacBurney, 1994; Ziegler, et al., 1990).If supplemental IV glutamine is not possible, very low rate (less than 25 ml/hr) enteralfeedings can be started to stimulate the gut mucosa and prevent gut atrophy. Glutaminecan also be added to enteral formulas by mixing 10 gm glutamine with 30 ml water andinfusing three times per day with the enteral formula or by itself. (MacBurney, 1994).

VITAMINS AND MINERALS

No specific vitamin and mineral requirements for stressed patients have beenestablished, but we do know that the need for certain vitamins and minerals increases.The chart below summarizes the vitamins and minerals required for each metabolicprocess.

Nutrients Needed for Metabolic Processes

Carbohydrate metabolismThiamine, riboflavin, niacin, B6, B12, biotin, pantothenic acid, sulfur,phosphorus, potassium, magnesium, manganese, copper, chromium

Protein metabolismNiacin, B6, folic acid, biotin & pantothenic acid, phosphorus,potassium, sulfur, magnesium, zinc & copper

Fat metabolismThiamine, riboflavin, niacin, panthothenic acid, biotin, phosphorus,magnesium, iron, copper & sulfur

Steroid synthesisRiboflavin, niacin, pantothenic acid & magnesium, cholesterol assubstrate

Catecholamine synthesisB6, C, iron, magnesium & copper, tyrosine as substrate

68Nutrition Support

The stressed state and resulting decrease in lean body mass causes losses of potas-sium, magnesium, phosphorus, zinc and sulfur. Generally, follow the RDA/RDI guide-lines for the orally or enterally fed patient (or the AMA guidelines for use duringparenteral nutrition) to determine vitamin/mineral needs.

NUTRITIONAL REPLETION

Nutritional repletion of the critically stressed or septic patient should begin when thepatient has been fluid resuscitated and is hemodynamically stable. If at all possible, earlyenteral nutrition support should be initiated. Hypoperfusion to the gut can occur with amean arterial pressure below 60; enterally feeding a patient who is significantly hypoten-sive may result in injury to the gut, resulting in bowel ischemia or infarction.

If at all possible, the gastrointestinal tract should be utilized to provide nutritionsupport. The gut appears to influence the production of cortisol, glucagon and norepi-nephrine (Alexander, 1988; Kudsk, 1988). When the GI tract is utilized, the gut wallappears to be maintained and the levels of “stress hormones” appear to be decreased. Adecrease in septic complications in trauma patients has been shown to occur when thesepatients are fed enterally (Minard and Kudsk, 1994).

When the GI tract is not utilized, the intestinal villi atrophy. This causes a break-down in the intestinal wall mucosal integrity, which can allow translocation of gutbacteria into the lymphatic and portal circulation. In an already immunocompromised,critically ill patient, this can be a deciding factor in the patient’s outcome.

Enteral feedings should be initiated slowly into the small bowel if possible. Whilean ileus may persist for several days in the colon, the small bowel does not develop anileus until it has not been utilized for 3 to 5 days (Zaloga and MacGregor, 1990).

Early feeding into the gut, and especially into the duodenum, ileum or jejunum,appears to play a role in preserving the gut mucosal lining and to decrease the hypermeta-bolic response to stress. Feedings into the small bowel can also reduce the risk for aspiration.Once initiated, the rate of feeding can be increased every 8 to 12 hours (Gray and Kaminski,1985) until a volume adequate to provide the patient’s nutrition needs is attained.

While enteral feedings are the nutrition support method of choice in the stressed orseptic patient, the use of total parenteral nutrition is warranted in some instances, asdiscussed in Chapter Three. Adjunctive parenteral nutrition can be of use in patientswho can’t meet their nutritional requirements with enteral feedings alone.

The stressed or septic patient is often the patient in the ICU who never seems toimprove, then suddenly everything kicks in and he recovers. There are times, too, whennothing works for these patients, and they eventually die after long and expensive treat-ment. Nutrition support is important for these patients, but we must remember that it isonly one of many therapies they’re receiving. Sometimes it seems there is little we can do.

69Nutrition Support

CASE STUDY #1: STRESS AND SEPSIS

PK was a 35-year-old female admitted to the ICU with meningococcus bacteremia/sepsis with disseminated intravascular coagulation (DIC) and early adult respiratorydistress syndrome (ARDS). Her medical and surgical history was benign except for a 10-year history of bulimia and anorexia. Upon admission, she was 5’4" and weighed 100 lb(which may not have been accurate). Her albumin level was 1.2, hemoglobin was 9.7,glucose was 879, cholesterol was 18, and triglycerides were less than 30.

Her needs were assessed to be 1500 to 1800 kcal and 50 to 90 gm protein/day. Shewas immediately started on standard TPN at 40 ml/hr and Fibersource™ at 40 ml/hr,providing a total of 2343 kcal and 79 gm protein. Recommendations were made todecrease caloric intake to prevent overfeeding and TPN was discontinued when theenteral feeding was increased to 50 ml/hr (1440 kcal, 64 gm protein). She continued totolerate the feeding. Enteral feedings gradually increased to 65 ml/hr (1560 ml, 1872kcal, 82 gm protein). Enteral feedings continued to be well tolerated and were furtherincreased to 80 and then to 100 ml/hr (utilizing the old “if some is good, more is better”adage), contrary to our recommendations. Her weight increased to 64 kg and she wasedematous.

She stabilized and came out of the acute septic stage but had suffered ischemia ofboth lower extremities, all of her fingers and her nose because of the DIC. She facedbilateral amputations of her legs (first BKA, then AKAs) and amputation of her fingers.Grafts were done on her buttocks as well because of breakdown there. Lab values hadimproved: albumin 2.5; prealbumin showed mild depletion and transferrin showedmoderate depletion. Enteral feedings resumed at 60 ml/hr (1440 ml, 1728 kcal, 62 gmprotein) and oral intake was initiated. Needs were reassessed to be 1500 to 1900 kcal/day and 70 to 90 gm protein/day.

Oral intake diet began with full liquids (PK was lactose intolerant), which weretolerated well. Oral intake resulted in between 300 to 500 kcal/day and 30 gm protein/day; enteral feedings were increased to 75 ml/hr. Oral intake continued to improve andenteral feedings were changed to 11 hours at night at 100 ml/hr (1320 kcal/47 gmprotein). She was taking 60 to 75 percent of a regular diet, but continued to exhibitsymptoms of an eating disorder as she consistently avoided certain food groups andconcentrated only on increasing her intake of high protein foods. Enteral feedings werechanged to a more nutrient-dense formula at 50 ml/hour over 12 hours (900 kcal, 33 gmprotein). Oral intake remained at about 700 kcal, 40 gm protein. Her weight was 42.8 kg(after bilateral AKAs) and albumin was 3.8 (had received IV albumin).

PK continued to improve and began to participate in physical and occupationaltherapies. Her oral intake improved and revealed adequate intake to allow discontinu-ing her enteral feedings. Albumin stabilized at 3.4 to 3.8. Multivitamins were given (shehad supplemental zinc, vitamin C, and vitamin A in her enteral feeding). Weightdropped to 39 kg with an IBW of 39 to 47 kg. Needs were assessed at 1700 to 2100 kcal/day and 50 to 75 gm protein/day. PK was discharged to a rehabilitation unit.

PK’s devastating illness was likely related, in part, to her immunocompromisedstate caused by a combination of her anorexia/bulimia and an acute illness. She becamevery septic and developed DIC, an unusual coagulopathy that results in disturbed

70Nutrition Support

blood flow to extremities. As a result, she was lucky to survive, but will have to con-tinue on with bilateral AKAs and reduced usage of her once dominant hand. PK hasreturned to the hospital to visit on multiple occasions. While she is confined to a wheel-chair because of bilateral AKA’s, she has rehabilitated well and lives as normal a life aspossible. Luckily, PK had early nutritional support and was able to tolerate enteralfeedings from the beginning.

CASE STUDY #2LG was a 50-year-old female admitted to the ICU after surgery to repair a dissect-

ing ascending aorta that extended all the way to her renal arteries. Post-operatively shedeveloped respiratory failure and ARDS and acute renal failure. Other problems includeobesity (5’4”, 94 kg) and anemia, as well as coronary artery disease (CAD).

LG was started on CRRT (continuous renal replacement therapy) post op day 2 andwas started on TPN the same day. Her TPN formula was: amino acid 5 percent, dextrose18 percent, and lipid 2 percent at 70 ml/hr (1700 kcal and 84 gm protein). Her needswere assessed to be 1700 to 1900 kcal per day and 65 to 100 gm protein per day. HerBUN was 46, Cr 4.3, glu 364, and albumin 2.4. Insulin was given for the increasedglucose — this may have been elevated because of the dextrose load of the TPN becauseof the stress response, and/or because of a predisposition for glucose intolerance.

Four days later, LG’s condition had not improved; she was now pharmacologicallyparalyzed; her albumin was 1.5 (further evidence of a highly catabolic state), BUN was36 and Cr 3.2 and glucose was 231. TPN increased to 80 ml/hr (1943 kcal and 96 gmprotein). Her course continued much the same with little improvement in lab values.She had a tracheostomy and was converted to hemodialysis. Nutrition status remainedstable but did not improve. After two weeks of intensive medical and nutrition therapy,LG expired.

REVIEW QUESTIONS

1. What metabolic changes occur with stress?2. What mix of calories should be provided to septic patients?3. Calculate protein requirements for a severely septic 40-year-old male, 5’8”, 160 lb

(72 kg).

REFERENCES

Alexander JW: Influence of feeding route on metabolic response to injury. The Gastrointestinal Response toInjury, Starvation, and Enteral Nutrition. Ross Laboratories, Columbus, OH, 1988.

Austgen TR, et al.: The effects of endotoxin on the splanchnic metabolism of glutamine and relatedsubstrates. J Trauma 11:742-752, 1991.

Berg RD and Garlington AW: Translocation of certain indigenous bacteria from the gastrointestinal tract to themesenteric lymph nodes and other organs in a gnotobiotic mouse model. Infect Immun 23:401, 1979.

Bower RH, et al.: BCAA-enriched solutions in the septic patient. Ann Surg 203:1:13-19, 1986.Brantley SL. Glutamine metabolism: nutritional and clinical significance. A.S.P.E.N. Clinical Nutrition

Week, 2007.

71Nutrition Support

Cerra FB: Pocket manual of Surgical Nutrition. CV Mosby Co., St. Louis, 1984.Cerra FB, et al.: Branched chain metabolic support. Ann Surg 199:3:286-291, 1984.Chiarla C, et al.: Inhibition of post-traumatic septic proteolysis and ureagenesis and stimulation of hepatic

acute-phase protein production by BCAA TPN. Journ Trauma 28:8:1145-1170, 1988.Daly JM, Reynolds J, Thom A, et al.: Immune and metabolic effects of arginine in the surgical patient. Ann

Surg 208(4): 512-523, 1988.Fish J: Amino acids and peptides. Lecture at A.S.P.E.N. 18th Clinical Congress, Jan, 1994.Fox AD, Kripke SA, DePaula J, et al.: Effect of a glutamine-supplemented enteral diet on methotrexate-

induced enterocolitis. JPEN 12:325-31, 1988.Freund H, et al.: The role of BCAA in decreasing muscle catabolism in vivo. Surgery 83:6:611-617, 1978.Gray DS and Kaminski MV: Stress. Hyperalimentation: A Guide for Clinicians. Kaminski MV, Ed. Marcel

Dekker, Inc, New York, 1985.Hasselgren P, et al.: Infusion of a BCAA-enriched solution and alpha-ketoisocaproic acid on septic rats:

effects on nitrogen balance and liver protein synthesis. JPEN 14:2:156-161, 1990.Hermann VM: The gut barrier translocation and rationale for enteral nutrition. A.S.P.E.N. 5th Annual

Advances and Controversies in Clinical Nutrition, Scottsdale, AZ, 1995.Iwasawa, et al.: Nutritional effects of branched-chain amino acids on injured rats in total parenteral

nutrition. JPEN 14:2:156-161, 1990.Jacobs DO, Evans DA, Mealy K, et al.: Combined effects of glutamine and epidermal growth factor on the

rat intestine. Surgery 104:356-364, 1988.Jensen GL, Miller RH, Talabiska DG, et al.: A double-blind, prospective, randomized study of glutamine-

enriched compared with standard peptide-based feeding in critically ill patients. Am J Clin Nutr64:615-621, 1996.

Kawamura I, et al.: Optimum branched-chain amino acids concentration for improving protein catabolismin severely stressed rats. JPEN 14:4:398-403, 1990.

Kirk SJ and Barbul A: Role of arginine in trauma, sepsis, and immunity. JPEN 14:5:226S-229S, 1990.Kirvela O and Takala J: Postoperative parenteral nutrition with high supply of BCAA: effects on nitrogen

balance and liver protein synthesis. JPEN 10:6:574-576, 1986.Klimberg VS, Souba WW, Dolson DJ, et al.: Prophylactic glutamine protects the intestinal mucosa from

radiation injury. Cancer 66:1:62-68, 1990.Kline DA: Nutrition & Immunity, Part II: Diet and Diseases of Immunity. Nutrition Dimension, Inc., Eureka,

CA, 1999.Kudsk KA: Influence of feeding route on morbidity and mortality in animals. The Gastrointestinal Response

to Injury, Starvation, and Enteral Nutrition. Ross Laboratories, Columbus, OH, 1988.Kuhn KS, Stehle P, and Furst P: Glutamine content of protein and peptide-based enteral products. JPEN

20:4:292-294, 1996.Lacey JM and Wilmore DW: Is glutamine a conditionally essential amino acid? Nutr Reviews 48:8:297,

1990.Lochs H and Hubl W: Metabolic basis for selecting glutamine-containing substrates for parenteral

nutrition. JPEN 14:4S:114S-117S, 1990.Long CL, et al.: Glutamine supplementation of enteral nutrition: impact on whole body protein kinetics

and glucose metabolism in critically ill patients. JPEN 19:6:470-476, 1995.MacBurney M: Administering glutamine in clinical setting. 2nd Master Clinical Dietitians Meeting. San

Antonio, TX, 1994.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition


72Nutrition Support

Minard G and Kudsk K. Effect of route of feeding on the incidence of septic complications in critically illpatients. Sem Resp Inf 9:228-231, 1994.

Moore EE and Jones TN: Benefits of immediate jejunostomy feeding after major abdominal trauma. JTrauma 26:874-881, 1986.

Moore F, Moore E, Jones T, et al.: TEN vs. TPN following major abdominal trauma-reduced septic morbid-ity. J Trauma 29:916-923, 1989.

Nelson KM and Long CL. Physiological basis for nutrition in sepsis. Nutr Clin Prac 4:1:6-15, 1989.Pontes-Aruda A, et al.: Effects of enteral feeding with eicosapentaenoic acid, alpha-linoleic acid, and

antioxidants in mechanically ventilated patients with severe sepsis and septic shock. Crit Care Med34(9): 2006.

Pontes-Aruda A, DeMichele S, Seth A, et al.: The use of an enteral diet with EPA, GLA and antioxidants incritical illness. Crit Care Med, 2007.

Shronts EP and Fish JA: Surgery, sepsis, and trauma. Dietitian’s Handbook of Enteral and Parenteral Nutrition.Skipper A, Ed. A.S.P.E.N. Publ., Inc., Rockville, MD, 1989.

Shronts EP and Lacy JA: Metabolic support. Nutrition Support Dietetics (2nd ed.). Gottschlich MM,Matarese LE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.

Smith RJ and Wilmore DW: Glutamine nutrition and requirements. JPEN 14:4S:94S-99S, 1990.Souba WW, Herskowitz K, Salloum RM, et al.: Gut glutamine metabolism. JPEN 14:4S:45S-50S, 1990.Vanderwoude, et al.: Addition of BCAAs. Crit Care Med 8:685-688, 1986.Wooley J. The role of nutrition during the metabolic response to sepsis. A.S.P.E.N. Clinical Nutrition Week,

2007.Young EA: Gut fuels, a roundtable. A.S.P.E.N. Fifteenth Clinical Congress, 1991.Zaloga GP: Parenteral vs enteral nutrition in the critically ill. Unpublished.Zaloga GP and MacGregor DA: What to consider when choosing enteral or parenteral nutrition. J Crit Ill

5:11:1180-1200, 1990.Ziegler TR, et al.: Safety and metabolic effects of L-glutamine administration in humans. JPEN 14:4S:137S-

146S, 1990.

73Nutrition Support

Chapter Six:Obesity and Diabetes Mellitus

The nutrition care of the diabetic or obese patient is really no different from thecare of any other critically ill patient. Care should be taken that the patient is not over-fed; intentional underfeeding of the critically ill obese patient requires close monitoringand remains controversial. The existence of additional illnesses, including renal, cardiac,and/or respiratory disease should be evaluated and appropriate adjustments in thenutrition support regimen should be made to optimize nutrition care and status.

The nutritional monitoring of the diabetic patient should include awareness ofchanges in weight, laboratory data and clinical condition.

DETERMINING NUTRIENT NEEDS

Nutrition support of a critically ill obese patient is a challenge, partly because theprecise determination of caloric and protein needs is difficult. The percentage of leanbody mass in obese patients is difficult to determine. We know that as a person becomesmore obese, total lean body mass increases. But, due to excessive fat stores, the percentof lean body mass in relation to total body weight decreases. In fact, because of thisdecrease in percent of lean body mass, a very obese patient may have caloric expendi-tures as low as 16 to 18 kcal/kg of body weight.

Permissive underfeeding or hypocaloric feeding is recommended for critically illpatients with a BMI greater than 30. This means that these patients should be fed atlevels not exceeding 60 to 70 percent of estimated energy requirements (or 22 to 25 kcal/kg ideal body weight, or 11 to 14 kcal/kg actual body weight)(McClave, et al., 2009).

The REE of an obese person can be determined as follows:REE = 1.44 x [(3.9 x VO2) + 1.1 x CO2)].

74Nutrition Support

The obese patient may not appear malnourished because of his weight, but may, infact, have depleted protein and lean body mass stores. When this type of patient becomescritically ill, he is at equal or greater risk for nutritional depletion than a normal-weightpatient. Careful determination (or estimation) of nutrition needs should be made toprevent nutritional depletion.

NUTRITION ASSESSMENT

Nutrition assessment of an obese patient is difficult because his fat stores makedetermination of lean body mass by conventional methods nearly impossible. There-fore, we must consider laboratory data, including the parameters for evaluating proteinstores:

• Serum albumin• Serum transferrin• Serum prealbumin• Serum retinol-binding protein• Total lymphocyte count

Important factors to monitor in the ongoing assessment of nutritional status in-clude: weight changes not associated with changes in fluid status, adequacy of nutrientintake and the patient’s clinical condition.

The most optimal method of determining caloric requirements in the critically illobese patient is with indirect calorimetry, utilizing a metabolic cart. A study of obesepatients (who were not critically ill) using indirect calorimetry revealed that theirenergy expenditures were much higher than those of patients who were not obese(Ireton-Jones, 1989). No such studies have been conducted on critically ill obese pa-tients, but their needs are likely to be increased to at least the same degree.

While the Harris-Benedict equation can be utilized in the determination of caloricrequirements in the non-obese population, its use for the obese patient is limited. If thepatient’s ideal body weight (IBW) is utilized in this equation, its use may seriouslyunderestimate actual requirements. Some practitioners increase the determined restingenergy expenditure (REE) by 120 to 150 percent to allow for higher requirements causedby increased fat stores and, to a lesser extent, increased lean body mass (Baron, 1986).Others adjust the patients’ IBW to account for the approximate 25 percent increase inlean body mass, as shown below.

Determining Adjusted Ideal Body Weight

[(actual weight – IBW) x .25] + IBW = adjusted IBW

Example: actual weight = 90 kgIBW = 50 kg90 – 50 = 40 x .25 = 10 + 50 = 60 kg adjusted IBW

75Nutrition Support

Caloric needs can also be determined by utilizing a factor of 22 to 25 kcal/idealbody weight or 11 to 14 kcal/kg actual body weight. After determining caloric require-ments, the patient should be closely monitored to assure that he is not being over- orunderfed.

Protein requirements should be determined by using the patient’s ideal bodyweight. In order to allow for protein sparing and to reduce the risk for protein deple-tion, a factor of 2.0 to 2.5 gm of protein per kilogram of IBW should be applied (Baron,1986; Pasulka and Kohl, 1989; McClave, et al., 2009). Continue monitoring the patient’snutritional status with nitrogen balance studies and laboratory data. Nitrogen balancestudies may be of limited value in the critically ill patient. However, they do provide abaseline and can be used to show that nutrition support is not working to improvenutritional status. Remember that a high protein intake can increase nitrogen output.

Requirements for trace elements, vitamins, minerals, and electrolytes are the sameas for other critically ill non-obese patients. These requirements have been outlined inearlier chapters.

LONG-TERM CARE

Because the obese patient may be at risk for associated cardiac and respiratoryproblems, he may often be critically ill for extended periods of time. Some researchershave suggested that the use of hypocaloric nutrition support in the obese patient maybe of benefit (Baxter and Bistrian, 1989). Obese patients are often insulin-resistant andglucose-intolerant. Use of a hypocaloric formula (approximately 60 percent of predictedenergy expenditure) may be of use in improving glucose tolerance.

In the critically ill obese patient, the need for some nonprotein calories, in additionto protein calories, appears necessary to improve nitrogen balance. While hypocaloricnutrition support is not appropriate for all obese patients, it may be of use in some,especially those who have stabilized and are recovering.

When indirect calorimetry is used, the determination of calories for hypocaloricfeedings can be made by subtracting 300 to 500 kcal from the REE, up to a limit of 2000kcal/day. Protein needs remain the same, utilizing the estimate at the upper end of therange described earlier (about 1.0 to 1.7 gm protein/kg/day adjusted body weight)(Baxter and Bistrian, 1989).

DIABETES

Diabetes mellitus is estimated to be present in 16 million persons in the UnitedStates (Mahler and Adler, 1999). Diabetics comprise approximately 10 percent of hospi-tal discharges; their length of stay is 30 to 50 percent longer than their nondiabeticcounterparts. Approximately 100,000 diabetics receive TPN on an annual basis; aboutthe same number receive enteral nutrition support annually (Holdy, 1995).

Diabetes mellitus involves not only an alteration in the metabolism of carbohy-drate, but also an alteration in the metabolism of protein and fat.

Alterations of carbohydrate metabolism include: a decrease in peripheral glucoseuptake, an increase in exogenous glucose production; a decrease in the ability to sup-press hepatic glucose production; and a decrease in the ability to oxidize infused glucose.

76Nutrition Support

Alterations in fat metabolism include: a increase in lipolysis with resultant in-creases in free fatty acid, triglyceride and lipoprotein levels, a increase in fat oxidation,an increase in glycerol turnover, an increase in ketogenesis, and a reduced ability tosuppress lipolysis.

Alterations in protein metabolism include: an increase in the breakdown of protein,a decrease in the synthesis of protein, an increase in the catabolism of protein, a de-crease in the uptake of branched chain amino acids by the muscle tissue, and an in-crease in the release of amino acids from muscle tissue (Ziegler and Smith, 1994).

Diabetes mellitus also causes primary or secondary disturbances in the secretionand/or sensitivity of insulin, glucagon, catecholamines, growth hormone, and cortisol(Felig and Bergman, 1995).

Glycemic control is very important in the diabetic patient, whether the diabetes incaused by diabetes mellitus, occurs with pregnancy, or occurs with stress or sepsis.Elevated glucose levels impair leukocyte function and complement function. Both ofthese complications can impair immune function. Growing evidence suggests thathyperglycemia increases the risk of nosocomial infection (Holdy, 1995; McMahon, 1995).

Several studies have shown that the rate of central catheter-related infections is fivetimes higher in diabetic patients on TPN and that hyper-glycemia is the most commonrisk factor for the development of Candida albicans infection in the hospitalized patient(McMahon, 1995). Baxter, et al., (1990) studied 100 diabetic patients and found that thenosocomial infection rate was five times greater than what would have been expected.

Clearly, tight glucose control is important in all patients, not just the diabeticpatient. Glycemic control can be improved. Serum glucose should be maintained atbetween 80 to 110 mg/dL in cardiac surgery, and possibly other surgical patients.Glucose levels in critically ill patients should be maintained at between 110 to 180 mg/dl (Amer Diab Assoc., 2006; McClave, et al., 2009).We should not exceed a glucoseadministration of greater than 2 mg/kg/min. until glycemic control is achieved (Holdy,1995). The diabetic patient should be limited to a level of no more than 4 mg/kg/min.of glucose administration. Most diabetics require insulin coverage to maintain glycemiccontrol. The insulin can be included in the TPN at a level of approximately 0.1 units pergram of dextrose (Holdy, 1995; McMahon, 1995).

Subcutaneous insulin may be given as needed to maintain a serum glucose level ofless than 180 mg/dL. If the glucose levels consistently remain higher than 200 mg/dL,insulin can be increased by 0.05 units/gm of dextrose to a maximum of 0.2 units of insulinper gram of dextrose. Insulin drips may also be utilized to maintain tight glucose control.Insulin is compatible with total nutrient admixtures although there may be as much as a10 percent loss of insulin bioavailability when mixed with TPN (Marcuard, et al., 1990).

Elevations of glucose in the serum that do not respond to even relatively highlevels of insulin may indicate that the patient has become insulin resistant. Insulinresistance can occur with stress, sepsis, medications (i.e. glucocorticoids), or overfeeding(McMahon, 1995). This circumstance necessitates using ever increasing levels of insulin.

Patients with diabetes mellitus may be overweight or obese and may also be atincreased risk for depletion of protein stores. They should be monitored closely forchanges in nutritional status.

77Nutrition Support

Laboratory data of importance are:• BUN• Creatinine• Potassium• Glucose• Liver function tests• Albumin• Triglyceride• Nitrogen balance studies

Adequate protein should be given to the diabetic patient. Infusion of 4 mg/kg/minute of dextrose decreases net catabolism of protein by 11 percent (Holdy, 1995).Generally, if the patient can tolerate the protein load, intake of protein should be set at1.5 to 2.0 gm/kg/day. Keep in mind that the diabetic patient may have renal compro-mise and may not tolerate this level of protein intake.

Nutrition support should be initiated as quickly as possible. Because of the intoler-ance to glucose and the goal of improving control of serum glucose, enteral feedings orTPN of both glucose and fat sources should be utilized.

Enteral feedings can be utilized fairly readily in diabetic patients. Blenderizedformulas and high fiber formulas may be better tolerated in these patients because of theeffect of soluble fiber on glucose control. However, the amount and type of fiber in mostenteral formulas appears to have little impact on serum glucose levels. Little researchexists to support the use of high fiber formulas for glycemic control (Charney, 1993).

Diabetic gastroparesis (delayed gastric emptying time) may occur in 45 to 75 per-cent of patients with insulin dependent diabetes mellitus (IDDM) (Charney, 1993).Symptoms include nausea, early satiety, postprandial vomiting, and epigastric pain(Kim, et al., 1991). The patient with delayed gastric emptying or gastroparesis will likelybenefit from the use of formulas that are isotonic or nearly so. However, the patient withgastroparesis may better tolerate jejunal feedings because of the delayed gastric empty-ing and small bowel dysmotility (Kim, et al., 1991).

If the patient with gastroparesis is fed into the stomach, a high fiber intake mayfurther delay gastric emptying (Charney, 1997), as can formulas containing free aminoacids (Charney, 1997). Formulas that are restricted in carbohydrate and higher in fat maybe beneficial in controlling blood glucose levels, especially in patients with difficulty inattaining tight control. Generally, isotonic feedings run continuously are best tolerated,especially initially. Monitor glucose levels closely, adjusting additional administration ofinsulin as needed.

The avoidance of overfeeding is the most important factor in the nutrition supportof the diabetic patient. Specialty formulas containing lower levels of carbohydrate andhigher levels of fat have been developed in the hope that the formulas could aid in thelevel of glycemic control. However, the clinical significance of studies performed withthese formulas is unclear. The avoidance of overfeeding appears to be far more benefi-cial than the use of specialized “diabetes” formulas (Charney, 1997; McMahon, 1995).

78Nutrition Support

REVIEW QUESTIONS

1. A female patient has been admitted with sepsis and respiratory distress. She is 5’2"and weighs 220 lb (100 kg). Determine her protein/calorie requirements.

2. A diabetic patient, 6’2", 198 lb (90 kg) was admitted to the CCU for an acute myocar-dial infarction and has subsequently been through surgery for a coronary arterybypass and graft. Postoperative complications include acute renal failure and aninability to wean from the ventilator. What are his needs and what mode of nutri-tion support would you choose?

REFERENCES

American Diabetes Association. Standards of medical care in diabetes. Diabetes Care 28: S4, 2006.Baron RB: Nutrition support of the critically ill obese patient. Topic in Clin Nutr 1:4:71-78, 1986.Baxter JK and Bistrian BR: Nutrition support of the stressed obese patient. Nutr Clin Prac 1:4:133-135, 1989.Baxter JK, Babineau TJ, Apovian CM, et al.: Perioperative glucose control predicts increased nosocomial

infection in diabetics. Crit Care Med 18:5707,1990.Charney PJ: Diabetes mellitus. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese LE,

Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.Charney PJ: Diabetes Specialty tube feeding formulations: use in clinical practice. Address at A.S.P.E.N.

21st Clinical Congress, San Francisco, 1997.Hoban P, Burge J, Flanebaum L. Nutrition support of obese hospitalized patients. Nutr Clin Prac 12:149-

154, 1997.Felig P and Bergman M: The endocrine pancreas: diabetes mellitus. Endocrinology and Metabolism. 3rd ed.

Felig P, et al. Eds. McGraw-Hill, 1995.Holdy K: Metabolic and nutrition support of the diabetic patient. Address at Advances in Clinical

Practice: Disease-Specific Nutrition Support. San Diego, 1995.Ireton-Jones CS: Evaluation of energy expenditures in obese patients. Nutr Clin Prac 4:4:127-129, 1989.Kim C, Kennedy F, Camilleri M, et al.: The relationship between clinical factors and gastrointestinal

dysmotility in diabetes mellitus. J Gastrointest Motil 3:268-272, 1991.Marcuard S, et al.: Availability of insulin from total parenteral nutrition solutions. JPEN 14:262, 1990.Mahler RJ, Adler ML. Type II diabetes mellitus: Update on diagnosis, pathophysiology, and treatment. J

Clin Endocrinol Metab 84:1165-1171, 1999.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition

support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) andAmerican Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) JPEN 33(30: 277-316, 2009.

McMahon MM: Nutrition support of the hospitalized patient with diabetes mellitus. Address at 5thAnnual Advances and Controversies in Clinical Nutrition, Scottsdale, AZ, 1995.

Pasulka PS and Kohl D: Nutrition support of the stressed obese patient. Nutr Clin Prac 4(4):130-132, 1989.Ziegler T and Smith R: Parenteral nutrition on patients with diabetes mellitus. Clinical Nutrition: Parenteral

Nutrition, 2nd ed. Rombeau J and Caldwell M, Eds. WB Saunders, 1994.

79Nutrition Support

Chapter Seven:Respiratory Failure

As many as 19 percent to 74 percent of patients with COPD are malnourished(Schols, et al., 1989; Laaban, et al., 1993). Respiratory disease and/or ventilator-depen-dent patients are often the sickest patients in the ICU. They are at great risk for malnu-trition and resulting complications, especially pneumonia. The early initiation of nutri-tion support is vital in the care of this type of patient.

ENERGY REQUIREMENTS

As many as 40 percent of patients with chronic obstructive pulmonary disease(COPD) have lost 10 percent or more of their body weight (Weissman and Askanazi,1985). The cause of this weight loss is not clearly understood but may be related, in part,to inadequate caloric intake. However, it has been shown that often caloric intake isadequate, and, therefore, other reasons for weight loss must be examined.

The normal, healthy person uses 36 to 72 kcal/day for breathing. A patient withCOPD, however, may expend 430 to 720 kcal/day to breathe (Wilson, et al., 1985).COPD patients thus have a higher REE (as much as 15 percent to 20 percent) than theirhealthy counterparts (Gray-Donald, et al., 1996; Donahoe, et al., 1989; Schols, et al., 1991).

This increase in calories expended may be related to increased airway resistance anddecreased respiratory muscle efficiency (Rothkopf, 1989). Impaired gas exchange withsubsequent inadequate oxygen delivery to organs and tissue may also contribute tomalnutrition (Sridhar, et al., 1994). The hypermetabolic state may be related to the in-creased work of breathing and may be accompanied by inadequate intake, thereby result-ing in weight loss (Wilson, et al., 1985; Schols, et al., 1991). Whatever the cause, pulmonarydisease presents a set of challenges and problems to the nutrition support dietitian.

If a COPD patient subsequently becomes acutely ill and develops anorexia anddecreased intake, he loses weight more rapidly than a person without respiratorydisease. The malnourished COPD patient has a higher incidence of respiratory mortal-

80Nutrition Support

ity than a well nourished person with COPD (Gray-Donald, et al., 1996). Since his caloricrequirements are so high, the patient may have difficulty regaining, or even maintain-ing, weight. This weight loss may be associated with a decrease in muscle mass, includ-ing respiratory muscle mass. The diaphragm loses muscle mass and strength, and, sincenormal muscle mass is necessary for normal lung function, any weakening makes thelungs less efficient.

Impaired pulmonary function may necessitate intubation, or complicate weaningthe patient from the ventilator. The respiratory patient is at a greater risk for atelectasis(collapse or incomplete inflation of the lung) due to a decrease in minute ventilation(the amount of air taken in per minute).

The lungs are profoundly affected by malnutrition, as shown above. The immuneresponse is also affected: the rate of surfactant production decreases, immunoglobulinlevels drop and the production of new cells in the epithelial lining slows. Decreasedsurfactant levels can contribute to atelectasis and possibly pneumonia. Alteration of theepithelial lining impairs the lung’s ability to fight off infection.

Macrophages in the lining defend against the invasion of foreign materials andbacteria. If the number of macrophages is reduced, immune function is compromised.Hypoalbuminemia can cause pulmonary edema because of decreased oncotic pressuresand fluid shifts (Schwartz, 1993).

Pulmonary disease affects immunocompetence to the extent that a patient who isalso malnourished is at greater risk for infection. Once an infection sets in, the patientmay begin a downward spiral in which he becomes more nutritionally depleted due topoor appetite and intake, leading to further weakening and loss of respiratory musclemass. Clearly, early nutrition support of pulmonary patients is warranted.

ASSESSING NUTRIENT NEEDS

As mentioned earlier, energy expenditure is increased in patients with respiratorydisease. In order to determine nutritional requirements, indirect calorimetry can give anaccurate estimation of actual needs, but other measures can be utilized if a metaboliccart is unavailable or not appropriate for use. REE is determined by the followingformula when a metabolic cart is utilized:

REE = (3.94 x VO2) + (1.11 x VCO2) - (2.17 x UUN)

Effects of Malnutrition

Respiratory rate Tidal volume Muscle mass Muscle strength

Minute ventilation Response to hypoxia Immune responseAffects pulmonary metabolism

81Nutrition Support

In the completion of an indirect calorimetry measurement, a 24-hour urine collec-tion for UUN (urinary urea nitrogen) is necessary. Those patients receiving enteralnutrition support or TPN should have a constant intake for 12 hours before the test is tobegin (McClave and Snider, 1992). The patient should then be kept NPO for greater thantwo hours; the room must be quiet and thermoneutral; and the patient should be keptquiet (Compher, 1993).

Indirect calorimetry can be determined with either the open-circuit method or theclosed-circuit method. The more accurate open-circuit method allows the patient tobreathe room air. Actual volumes of expired gas are measured; the fractions of oxygenand carbon dioxide are then ascertained. From these measurements, oxygen consump-tion and carbon dioxide production are calculated and energy expenditures are deter-mined. Patients who cannot remove supplemental oxygen to breathe room air andpatients who are intubated on high pressure support with low measured oxygen levelsare not candidates for metabolic cart measurements. The easier-to-perform closed-circuit method requires that the patient breathe from a controlled air system, allowingus to know volume and oxygen concentration. Continuous 24-hour metabolic monitorshave recently become available and may reflect actual energy expenditure and respira-tory quotient. The monitor reflects actual requirements for the patient and no formulasare required.

Oxygen consumption is determined by milliliters of oxygen utilized in one minute.O2 consumption = (volume inspired/minute x FIO2) - (volume expired x FEO2). FIO2 isthe fractional concentration of O2 in inspired gas and FEO2 is the fractional concentra-tion of O2 in expired gas.

CO2 production is the milliliters of CO2 produced in one minute. CO2 production =expired minute volume (FECO2 - FICO2). FECO2 is the fractional concentration of CO2 inexpired gas and FICO2 is the fractional concentration of CO2 in inspired gas.

Metabolic measurement carts measure oxygen consumption and carbon dioxideproduction. Many factors influence metabolic rate, including activity, posturing, hyper-thermia, disease states, dialysis, hyperthyroidism, and surgery. Several factors (musclerelaxants, sleeping, starvation, narcotics, hypothermia, and hypothyroidism) decreasemetabolic rate. Metabolic monitoring cannot be completed on patients with chest tubesor tracheal cuffs with significant leaks; patients receiving more than 60 percent oxygen;or patients undergoing dialysis.

Caloric requirements for the ventilator-dependent patient are recommended to beno more than 1.25 to 1.3 times the estimated REE, utilizing total calories (Talpers, et al.,1992). Overfeeding should be avoided, especially in patients on ventilator support or inpatients who are unable to increase ventilatory drive to compensate for excess carbondioxide production (Jolly, 1997). The Vencor (a national chain of hospitals for ventdependent patients) metabolic studies showed that an estimation of 25 kcal/kg is oftenappropriate; in fact, 67 percent of patients on the study had measured energy expendi-tures of less than 25 kcal/kg (McClave and Snyder, 1996).

Increased protein intake can cause increased minute ventilation and oxygen con-sumption and can increase ventilatory response to hypoxia and hypercapnia. In otherwords, the increased protein can cause the lungs to work harder and consume more

82Nutrition Support

oxygen. They overcompensate in response to the low oxygen in the blood. The patienthas to breathe harder and faster. The patient with respiratory disease generally requires1.2 to 1.5 gm protein per kg.

Pulmonary patients should never be overfed! Patients overfed with a high carbo-hydrate formula produce more carbon dioxide and show increased blood carbon diox-ide levels, putting them at risk for worsening respiratory failure. Increased carbondioxide production results in increased minute ventilation (Rothkopf, et al., 1989;Schwartz, 1993) which can exacerbate respiratory failure.

An important consideration in the nutrition care of pulmonary patients is theirrespiratory quotient (RQ), the ratio of carbon dioxide production to oxygen consump-tion. This can be determined using a metabolic cart. RQ increases with the oxidation ofcarbohydrate (as shown below), so carbon dioxide production increases with highcarbohydrate intake. This increases the lungs’ workload (to expel the additional carbondioxide), thereby increasing minute ventilation.

In the patient who already has impaired pulmonary function, any increase inworkload can result in respiratory distress. Septic or stressed patients have a higherlevel of oxygen consumption and carbon dioxide production, and so become at risk forrespiratory distress.

Respiratory Quotient

RQ =carbon dioxide production

oxygen consumption

Oxidation of fat: RQ = 0.7Oxidation of protein: RQ = 0.8Oxidation of carbohydrate: RQ = 1.0

Nutritional Requirements

Calories Protein

Maintenance 1.2 - 1.3 X BEE 1.2 - 1.5 gm/kg/day25 - 30 kcal/kg/day

Anabolism 1.4 - 1.6 X BEE 1.5 - 2.0 gm/kg/day20 - 30 kcal/kg/day

83Nutrition Support

Respiratory distress is defined as increased dyspnea, pO2 level below 90, pCO2

level above 50 and the inability to maintain normal respiration without support. Respi-ratory distress is usually a physician’s diagnosis, and is so indicated on the patient’schart.

TREATMENT MODALITIES

Respiratory failure can affect patients with existing pulmonary disease, and alsomay occur in patients who have experienced septic shock, trauma or major surgery.If a patient is intubated at some point, he is at risk for atrophy of the respiratorymuscles and for infection in the lung caused by aspiration of gastric contents or fluidsthrough unprotected airways (Miller, 1986).

Therefore, the feeding route for these patients is very important. As a rule, enteralfeedings are the method of choice. The benefits of enteral feeding often outweigh therisks, especially if care is taken to avoid complications. The feeding tube should beplaced in the duodenum or jejunum, if possible, and the patient should be positioned sothat his head is at a 45-degree angle to the rest of his body in order to reduce the risk ofaspiration of gastric contents.

However, if circumstances preclude the use of enteral feedings, TPN can be uti-lized effectively. TPN may be a better choice for the patient who cannot be fed enterallybecause of altered gastrointestinal function (perhaps from surgery or trauma) or whoseGI function is slowed because of medications, like narcotics (which “paralyze” thesympathetic nervous system to calm the patient and make ventilator treatment moreeffective).

FORMULAS

Because of the increase in carbon dioxide production with high carbohydrateintake, it has been suggested by nutrition support companies that the patient whonormally is a carbon dioxide retainer be treated nutritionally with a high-fat, low-carbohydrate formula. In clinical practice, however, the use of these formulas is rarelywarranted (Jolly, 1997). I have found that these formulas may be of limited use in apatient who is a CO2 retainer, rather than in all patients on ventilators. A.S.P.E.N. andSCCM do not recommend the use of high-lipid, low-carbohydrate formulas designed tomanipulate respiratory quotient (McClave, et al., 2009).

A more important consideration is that the patient should not be overfed orunderfed. Hypocaloric intake can decrease metabolic rate, minute ventilation, andresponse to hypoxia. Overfeeding can increase CO2 production, minute ventilation, andresponse to hypoxia. By the avoidance of overfeeding, excess carbon dioxide produc-tion will not occur.

High-fat formulas often cause gastrointestinal side effects, such as belching, ab-dominal distention and diarrhea (Kuo, 1993). Abdominal distention can increase pres-sure on the diaphragm and may contribute to delays in ventilator weaning. Delayedgastric emptying and high residuals can also occur with high fat formulas; high residu-als can increase the risk of aspiration, already a risk in the ventilator dependent patient.

84Nutrition Support

Elemental enteral formulas which are extremely low in fat (about 4 percent), cancause elevated carbon dioxide levels and metabolic acidosis (Schwartz, 1993), increasingthe lungs’ workload. A formula high in fat (60 percent calories from fat) and low incarbohydrate may therefore benefit patients who are known carbon dioxide retainers orwho have difficulty weaning from the ventilator. Again, it varies from individual toindividual and the key issue is not to overfeed.

Many pulmonary patients, including most intubated patients (especially if wean-ing is not imminent or difficult) can be managed effectively on more conventional,balanced formulas with 20 to 50 percent calories from fat. Considering the adverseeffects of a high-fat-content formula on gastrointestinal function and immune function, Irecommend the use of conventional formulas for most patients.

Recommendations for provision of glucose in TPN solutions vary from a limit of 2to 4 gm glucose/kg/day (Rothkopf, et al., 1989) to a provision of 50 percent of non-protein calories from carbohydrate (Wilson, et al., 1985; Miller, 1986; Schwartz, 1993)with the remainder of required calories provided from fat and protein. A limitation oncarbohydrate can result in a decrease in carbon dioxide production and may enhanceweaning from the ventilator. A more important consideration, again, is to ensure thatthe patient is not overfed.

While the provision of protein to the patient with respiratory disease or failure mayincrease the respiratory workload, the benefits (in terms of nutrition support) of itsprovision in appropriate amounts outweigh the drawbacks. A high protein intake mayresult in increased minute ventilation and increased oxygen consumption in the respira-tory-compromised patient.

Requirements for protein in the pulmonary patient are 1.2 to 1.5 gm/kg/d, rangingup to 2.0 gm/kg/d in the severely stressed patient. Response to the provision of proteinshould be closely monitored, and changes made if symptoms of worsening respiratorydistress, such as increased metabolic rate and minute ventilation, develop. Proteinintake should then be reduced to levels sufficient to meet the lower ends of estimatedneeds, or at higher levels if respiratory distress lessens.

Fluid balance should be closely monitored in the pulmonary or ventilator-depen-dent patient. These patients are at increased risk for fluid retention and may developpulmonary edema (accumulation of fluid in the lungs caused by depressed cardiac andpulmonary function), which further increases the work of breathing. Fluid restrictionmay often be indicated. Symptoms of edema are shortness of breath and worseningrespiratory distress.

Adequate phosphorus is vital to these patients. Low serum phosphorus altersoxygen transport and appears to reduce the strength of the diaphragm (Rothkopf, et al.,1989; Schwartz, 1993). Phosphorus levels, therefore, must be closely monitored (at leastonce or twice a week), with appropriate supplementation to achieve normal serumvalues provided as needed. Changes in phosphorus, potassium, and magnesium levelsmay occur with refeeding.

Provision of vitamins and minerals in RDA amounts is sufficient for most patients.The guidelines for vitamin and mineral supplementation for the parenterally fed patientin Chapter Four can be used as well.

85Nutrition Support

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)ARDS is the onset of severe acute lung injury resulting in acute hypoxemic respira-

tory failure (Bernard, et al., 1994). Triggers of ARDS include sepsis, infection, aspiration,and trauma. Nutritional status, which may already be compromised due to COPD,stress, and/or sepsis, may be further impacted by ARDS. The inflammatory response, asdiscussed earlier, is implemented with ARDS, with the same sequellae as exists in otherstressed states. Just as in the patient with COPD or who is ventilator dependent, thepatient with ARDS should not be overfed, especially with carbohydrate calories. Calorieand protein requirements are similar to the those recommended in COPD (25 to 30kcal/kg and 1.5 to 2.0 gm protein/kg) (Schwartz, 1998; Freund, 1991; Hudson,Steinberg, 1998; Mcclave, et al., 2009).

Formulas supplemented with omega-3 fish oils, borage oil and antioxidants maybe of benefit. While enteral feedings are preferred, parenteral nutrition may be utilizedwhen enteral feedings are not well tolerated or in the presence of gut failure.

ASSESSMENT AND MONITORING

Nutrition assessment and monitoring during nutrition support are much the samefor the respiratory patient as for any other patient. An accurate admission weight andknowledge of any recent weight considering fluid status changes are important tools inthe determination of nutrient requirements.

During nutrition support, laboratory data, such as albumin, transferrin,prealbumin, total iron-binding capacity and total lymphocyte count should be periodi-cally monitored to assess improvement in nutritional status. Other laboratory data ofuse in determining tolerance to nutrition support should also be monitored. Theseindicators have been discussed in earlier chapters. Clinical improvement in conditionshould be considered as well.

Once a patient is able to begin oral feedings, small, frequent feedings are of benefit.High-calorie liquid supplements are often well tolerated, in part because their con-sumption does not interfere as much with the actual act of breathing. (Solid foodsexpand the stomach, causing it to press against the diaphragm, making it difficult toboth eat and breathe.) Be sure that the patient continues to maintain adequate oralintake once he is tapered off TPN or enteral feedings.

Laboratory values of use in determining changes in respiratory status may or maynot be of use in determining appropriate nutrition support. Indirect calorimetry isuseful in determining respiratory quotient; this information can help you determine theoptimal method of feeding.

CASE STUDY #1: PULMONARY DISEASE

JM was a 60-year-old male who presented with a GI bleed. He weighed 81 kg uponadmission. He presented with an accompanying history of alcoholism, staph pneumo-nia, COPD and developed acute renal failure.

On Day 3 of his stay, TPN was initiated with a formula of 400 ml D50, 400 ml 10percent amino acids, and 200 ml of 20 percent lipid emulsion, to run at 60 ml/hr.

86Nutrition Support

On Day 5, TPN was increased to 80 ml/hr, providing 2073 nonprotein calories(2381 total calories) and 77 gm protein. Lab values included: BUN 95, Cr 5.3, Na 141, K3.3, glucose 153, albumin 1.6, PO4 6.3, WBC 13.8, and Hgb 10.8 with Hct 32.4. Needswere assessed to be 2000 to 2400 kcal/day and 80 to 95 gm protein/day. Factors toassess needs were 30 to 35 kcal/kg/day and 1.0 to 1.2 gm protein/kg/day. Acute renalfailure continued as evidenced by increased BUN, creatinine and phosphorus. (Thedecreased albumin level likely was secondary to sepsis, decreased intake and possibleliver disease due to alcohol intake.)

By Day 6, TPN was increased to 90 ml/hr (2333 nonprotein kcal, 2678 total and 87gm protein), meeting his needs. On Day 10, weight had increased to 85.1 kg, BUN was112 and Cr was 6.2. Albumin levels had increased to 2.1 and hemoglobin and hematocritlevels had improved. Dialysis was initiated at this point, with resulting improvementsin lab values.

On Day 17, pCO2 levels were noted to be elevated and the patient continued torequire high levels of ventilatory support. Recommendations were made to change theTPN formula in order to lower the carbohydrate load and increase the fat contentprovided in the hopes of improving RQ. The TPN was subsequently changed to aformula consisting of: 300 ml D50, 400 ml 10 percent amino acids, and 300 ml 20 percentlipid emulsion. This provided (at 90 ml/hr) 2398 nonprotein calories, 2744 total caloriesand 87 gm protein. Percentage of calories from fat was increased to 57 percent. Thepatient was also given 25 percent IV albumin to assist with dialysis.

By Day 19, improvement in response to ventilatory support was noted and pCO2levels had decreased. Serum albumin levels had fallen to 1.8 secondary to increasedlevels of stress and slow response to therapy caused by the long half-life of albumin. Allother lab values remained stable, in an acceptable range for this patient with ARF. OnDay 22, the patient was stabilized well enough to allow him to be transferred to anotherfacility.

CASE STUDY #2JW was a 71 year old male admitted with respiratory failure. His history included

COPD, obesity, hypertension, and IDDM. He had experienced compression fracturesbecause of chronic steroid therapy. He also had a permanent pacemaker inserted. Hefollowed a 1700 kcal ADA diet at home and was allergic to milk, pork, and soy. He was5’8” and weighed 83.8 kg (109 percent of IBW). His needs were assessed to be 2100 to2500 kcal/d and 85 to 110 gm protein/day.

He was intubated on his second hospital day and was started on a polymeric,isotonic feeding at 25 ml/hr on hospital day 3. The goal rate for the enteral feeding was75 to 85 ml/hr (the feeding was 1.2 kcal/ml and 53 gm protein/liter). The followingday, he developed increasing levels of agitation, which prevented a ventilator wean. Theenteral feeding was increased to 40 ml/hr. On the following day, the feeding was in-creased to 60 ml/hr; his blood glucose level rose to 437 mg/dl. Insulin was increased.The feeding was then changed to a fiber-containing formula. On day #7, ventilatorsupport was decreased, steroid administration was decreased, and insulin administra-tion was increased. His glucose level remained elevated.

87Nutrition Support

He continued to tolerate the enteral feeding, which was increased to his goal rate of85 ml/hr. He was gradually weaned from the ventilator and transitioned back to an oralADA diet. JW appeared to benefit from early enteral feedings. His weight and proteinparameters remained stable through his admission and he was weaned from ventilatorysupport.

CASE STUDY #3CL was a 71 year old male admitted with a GI bleed secondary to Coumadin

therapy and CHF. His history included COPD, paroxysmal atrial fibrillation, hyperten-sion, CVA, a decubitus ulcer on his foot secondary to peripheral vascular disease,alcohol abuse, and smoking. He was intubated with respiratory failure. He was 6’1” andweighed 106.3 kg (115 percent of IBW). His needs were assessed to be approximately2100 kcal/day and approximately 105 gm protein/day.

He was pharmacologically paralyzed because of his agitation on the ventilator. Anesophagogastroduodenoscopy (EGD) revealed gastritis and an ulcer. He then developedencephalopathy and delirium tremens and his anemia worsened. He was started onenteral feedings at 40 ml/hr. His albumin remained stable at 2.8, as did his weightremain stable. He developed high residuals with the enteral feedings, likely related tothe pharmacologic agent utilized to paralyze him. As the drug was decreased, he be-came able to tolerate the feeding and the rate was increased to meet his needs. Hisalbumin level improved and his weight remained stable. Although his nutritional statusremained stable, he was not readily weanable from the ventilator and his ventilatordependency became prolonged, not uncommon with patients with COPD.

REVIEW QUESTIONS

1. Can an intubated patient be nutritionally supported with enteral feedings?2. What is the most important thing to remember in feeding the patient with pulmonary

disease (especially with one who is ventilator-dependent and weaning is beingattempted)?

3. A 5’4", 100 lb female patient is admitted with adult respiratory distress syndrome.Determine her requirements and suggest a method of nutrition support.

REFERENCES

Bernard G, Artigas A, Brigham K, et al.: The American-European consensus on ARDS: Definitions,mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 149:818-824, 1994.

Compher C: Calorimetry, body composition, nitrogen balance, labs. Address at A.S.P.E.N. 17th ClinicalCongress, San Diego, 1993.

Donahoe M, Rogers R, Wilson D, et al.: Oxygen consumption of the respiratory muscles in normal andmalnourished patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 140:385-391,1989.

Freund HR: Nutritional support in cardiac and pulmonary disease. IN: Fischer JE (ed). Total ParenteralNutrition. 2nd ed. Boston: Little Brown; 203-216, 1991.

Gray-Donald K, Gibbons L, Shapiro S, et al.: Nutritional status and mortality in chronic obstructivepulmonary disease. Am J Respir Crit Care Med 153:961-966, 1996.

88Nutrition Support

Hudson LD, Steinberg KP: Acute respiratory distress syndrome; clinical features, management and out-come. In Fishman AP (ed). Pulmonary Diseases and Disorders. New York: McGraw-Hill; 2549-2565, 1998.

Jolly AF: Pulmonary-specific tube feeding formulations: use in clinical practice. Address at A.S.P.E.N. 21stClinical Congress, San Francisco, 1997.

Kuo CD, Shiao GM, and Lee JD: The effects of high-fat and high-carbohydrate loads on gas exchange andventilation in COPD patients and normal subjects. Chest 104:189, 1993.

Laaban JP, Kouchakji b, Dore MF, et al.: Nutritional status of patietns with chronic obstructive pulmonarydisease and acute respiratory failure. Chest 103:1362-1368, 1993.

McClave S: Clinical application of indirect calorimetry. Address at 5th Annual Nutrition Support Update.San Diego, 1996.

McClave SA and Snider HL: Use of indirect calorimetry in clinical nutrition. Nutr Clin Prac 7:207-221, 1992.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition


Miller MA: A practical approach to eating and breathing in respiratory failure. Top Clin Nutr 1:4:61069,1986.

Rothkopf MM, Stanislaus G, Haverstick L, et al.: Nutrition support in respiratory failure. Nutr Clin Prac4:166-172, 1989.

Schols A, Mostert R, Soeters, et al.: Inventory of nutritional status in patients with COPD. Chest 96:247-249,1989.

Schols Am, Soeters PB, Mostert R, et al.: Energy balance in chronic obstructive pulmonary disease. Am RevRespir Dis 143:1248-1252, 1991.

Schols AMWJ, Soetes PB, Dingemans AMC, et al.: Prevalence and characteristics of nutritional depletionin patients with stable COPD eligible for pulmonary rehabilitation. Am Rev Respir Dis 147:1151-1156,1993.

Schwartz D: Pulmonary Failure. In: Matarese LE, Gottschlich MM (eds.) Contemporary Nutrition SupportPractice: A Clinical Guide. WB Saunders; 395-408, 1998.

Schwartz DB: Pulmonary failure. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese LE,Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.

Sridhar MK, Carter R, lean ME, et al.: Resting energy expenditure and nutritional state of patients withincreased oxygen cost of breathing due to emphysema, scoliosis and thoracoplasty. Thorax 49:781-785, 1994.

Talpers SS, Romberger DJ, Bunce SG: Nutritionally associated increased carbon dioxide production:excess total calories vs. high proportion of carbohydrate calories. Chest 102:551:1992.

Weissman C and Askanazi J: Parenteral nutrition, malnutrition, and the respiratory system. Nutr SuppServ 5:9:46-48, 1985.

Wilson DO, Rogers RM, and Hoffman RM: Nutrition and chronic lung disease. Am Rev Respir Dis132:1347-1365, 1985.

89Nutrition Support

Chapter Eight:Renal Disease

The kidneys maintain the normal homeostatic condition of the body. Their pri-mary function is to regulate extracellular fluid through the formation of urine, whichinvolves regulation of serum sodium and potassium concentrations and maintenance ofan appropriate-base balance (Fox, 1987). The kidney is also involved in the regulation ofcalcium in the blood by decreasing phosphate reabsorption when extracellular calciumlevels decrease. This increases calcium reabsorption (Liftman, 1989).

When patients with renal disease or acute renal failure lose these primary func-tions, a wide variety of metabolic changes occur, making nutrition support a challeng-ing task.

The primary effects of altered renal function, shown on the following page, arefluid retention, increased serum levels of potassium, magnesium, and phosphate, andincreased protein catabolism. Blood urea nitrogen levels increase with the catabolism ofprotein stores and decreased filtering of waste products, such as urea. BUN levels canincrease with gastrointestinal bleeding and dehydration as well.

Serum creatinine rises as renal function deteriorates. In fact, serum creatinine levelsincrease by 200 percent with each 50 percent decline in glomerular filtration rate(Liftman, 1989). Patients with very little muscle mass have lower than normal serumcreatinine levels. Therefore, renal deterioration may be missed or diagnosed late in thepatient with reduced muscle mass.

Phosphate levels increase with as little as a 30 percent decrease in glomerularfiltration rate (GFR). Because phosphorus and calcium maintain a balance, this causes adecrease in serum calcium. The general picture, then, is of a system severely out ofbalance, making even basic nutrition assessment more complex.

Effects of reduced renal runction inlcude increased fluid retention, serum potas-sium, serum magnesium, serum phosphate, BUNand serum creatinine, as well asdecreased serum calcium.

90Nutrition Support


Malnutrition occurs in as many as 40 percent of patients with renal disease (Kopple,1999). Patients often are anorectic or may have gastroparesis; dietary restrictions (protein,phosphorus, sodium, potassium, fluid) may result in decreased intake.

Since fluid retention and edema can make determination of actual weight of anacute or chronic renal failure patient difficult, obtaining a “dry” weight is important inassessing his nutritional requirements. Dry weight is post-dialysis weight. From this, anestimation of lean body mass can be made, utilizing anthropometric measurements.

Changes in weight are often due to fluid shifts and changes, so once this baselineweight is established, weight should be monitored daily. Weight gain of more than 0.5to 1 kg per day usually represents fluid gain rather than an increase in lean body mass.The presence or absence of fluid gain is of critical importance in determining the treat-ment of existing renal disease. With excess fluid gain or retention, the need for dialysisor other means of fluid removal increases.

A patient’s protein status can be estimated from serum albumin, serum transferrinor total lymphocyte count. Because of albumin’s half-life of about 20 days and the factthat it is profoundly affected by fluid shifts, its use as a nutrition indicator of proteinstores is limited. Albumin is not uncommonly given during dialysis and may tran-siently become elevated.

Transferrin’s shorter half-life of 8 days makes it a more accurate indicator. How-ever, transferrin levels are affected by hydration (to a lesser degree), surgery, sepsis andiron deficiency, which is often present in patients with renal failure. Iron deficiencycauses a false elevation in transferrin levels. Total lymphocyte count is used as anindicator of overall nutritional status, and can be an indicator of protein deficiency orimmunocompetence.

Other acute phase proteins, such as prealbumin and retinol-binding protein, are oflimited use in renal failure patients. Prealbumin is normally degraded by the kidney, solevels may be abnormally elevated by renal failure. Retinol-binding protein is filteredand metabolized by healthy kidneys, so these levels are elevated in kidney failurepatients. This elevation does not, however, reflect actual protein status.

Obviously, the assessment of protein status in the patient with renal failure is quitedifficult and frustrating. Taking all of the above factors into consideration and weighingbenefits and drawbacks of each, you must develop through experience the ability tojudge protein status well. The best thing to do is to estimate needs based upon clinicaljudgement, give adequate protein and calories, and follow the clinical course.

Nitrogen balance studies are of limited value in renal patients; however, determina-tion of protein catabolic rate and urea kinetic modeling can be of use in determiningprotein requirements. (See Nutrition Assessment: Tools and Techniques and another Nutri-tion Dimension course, Renal Nutrition). Urea kinetic modeling, though, is difficult to do.

91Nutrition Support

CHRONIC RENAL FAILURE

The chronic renal failure (CRF) patient has probably already started on dialysis bythe time nutrition assessment and treatment is begun. Because of the changes in kidneyfunction, he requires controlled intake of protein, potassium, sodium, phosphorus andfluids. He likely requires supplementation with calcium and water-soluble vitamins(because of vitamin loss in the dialysate), as shown below.

Heavier supplementation of folate (1 mg/day), and vitamin B6 (10 mg/day), andvitamin C (100 mg/day) is indicated. Care should be taken with lengthy vitamin Csupplementation during CRF, since oxalate deposition can occur (Liftman, 1989).

Vitamin A supplementation should be avoided or restricted to prevent toxicity, andtrace elements should not be supplemented because they cannot be cleared effectively.The potential for developing toxic levels is very real. Symptoms of vitamin A excessinclude headaches, nausea, hepatomegaly and hypercalcemia.

The chronic renal patient is often already protein-depleted because of losses in theearly stages of renal disease, poor intake, etc. This existing malnutrition places thepatient at increased risk for infection in the hospital.

Once a CRF patient is admitted with a critical illness, he usually has a very poorappetite or may be unable to take any nutrients by mouth. The early initiation of nutri-tion support in this patient is important. If the gut is functional, enteral feedings shouldbe initiated as soon as possible.

ENTERAL FEEDINGS

Generally, a critically ill patient with CRF can tolerate a conventional or standardenteral formula. The use of dialysis allows for the removal of excess protein, potassium,sodium, phosphorus and fluid. A patient needing fluid restriction can usually tolerate amore nutrient-dense formula.

If a patient does not receive dialysis, a formula which is nutrient-dense (2 kcal/ml),

Nutrition for Chronic Renal Failure

Limit

ProteinPotassiumPhosphorusFluidsSodium

Supplement

CalciumFolateVitamin B6Vitamin C (limit duration)Water-soluble vitamins

Do not supplement

Vitamin A , trace elements (not dialyzed)

92Nutrition Support

with reduced protein (30 gm/L) can be utilized. The mineral content has been altered tomeet the needs of patients with chronic renal failure. Protein content may be too low;thus, additional protein may be supplemented, utilizing modular components.

Nutrient dense formulas specifically designed for renal failure may be appropriatefor the patient who has higher protein requirements and/or who has already starteddialysis. These formulas are also nutrient-dense but are higher in protein and aresupplemented with vitamins and minerals that may be lost with dialysis.

Depending upon the patient’s acute illness, he may require a more defined for-mula, such as a peptide or elemental formula. Peptide and/or elemental formulas areoften necessary after severe bowel resection, other surgery or trauma that prohibitsnormal bowel function. Peptide formulas are often better tolerated in the acutely illpatient who is severely hypoalbuminemic.

Enteral formulas provided into the stomach are usually well tolerated, but theduodenum is generally the preferred site, to reduce the risk of aspiration for the patientwho is intubated or has an altered level of consciousness.

TPNShould TPN be required, the chronic renal failure patient can usually tolerate a mix

of essential and non-essential amino acids (Matarese, 1993; Matarese, 1997). Individual-ization of electrolytes, calcium and phosphorus is necessary, using a baseline level andclinical judgment. A combination of calories from glucose and lipid can be utilized if thepatient does not have impaired triglyceride metabolism.

As mentioned earlier, water-soluble vitamins are supplemented (with additionalsupplementation of folate, B6 and C). Trace elements are generally given every day if thepatient is being dialyzed but avoided if the patient is not on dialysis (Matarese, 1997).

Calorie requirements for the acutely ill CRF patient are much the same as for anyother acutely ill patient. A factor of 25 to 30 kcal/kg (dry weight)/day can be utilized. Ifthe Harris-Benedict equation is used, factors appropriate for the acute illness should beapplied (See Chapter Five). Indirect calorimetry can be used if available (Matarese, 1997).

Nutrition for Critically ill CRF Patients

CaloriesStarvation/mild stress 1.0 - 1.3 x BEEModerate stress 1.2 - 1.5 x BEESevere stress 1.4 - 1.8 x BEESepsis 1.4 - 1.8 x BEE

ProteinHemodialysis 1.0 - 1.2 gm/kg/dayPeritoneal dialysis 1.2 - 1.5 gm/kg/day

93Nutrition Support

In acute and critical illness, nitrogen balance often becomes negative because ofcatabolism and decreased protein synthesis during stress. With the additional stress ofdialysis, the patient may lose an additional 9 to 12 gm of protein during hemodialysisand 12 to 13 gm during peritoneal dialysis. Generally, protein requirements for thesepatients are 1.0 to 1.2 gm protein/kg/day for hemodialysis patients; 1.2 to 1.5 gmprotein/kg/day for peritoneal dialysis patients if BUN is stable (<100). If BUN levelsare not well controlled, protein restriction should be continued.

Protein requirements can also be determined via the glomerular filtration rate(GFR). Protein is restricted according to the level of glomerular filtration per minute,with more protein being allowed with a higher GFR.

Many hemodialysis patients develop malnutrition because of poor dietary intake,decreased absorption, increased catabolism, and losses of nutrients into the dialysate(Wolfson and Foulks, 1996). This malnutrition has been shown to be associated with anincrease in mortality risk (Goldwasser, et al., 1993). Prevention of this malnutrition isimportant and may be achieved with aggressive use of supplements, etc. The use ofintradialytic parenteral nutrition (IDPN) has been studied to a small extent. This processallows for the provision of calories and protein during dialysis. IDPN can be expensiveand, to date, no scientific evidence exists that shows that it is indicated or even optimalin the provision of additional nutrients to the malnourished CRF patient (Wolfson andFoulks, 1996; Charney, 1995).

ACUTE RENAL FAILURE

Acute renal failure (ARF) can occur in a previously healthy individual as a result ofmany different factors. Among the most common factors is acute tubular necrosis(ATN), which occurs in some patients subjected to nephrotoxic agents or a decrease inrenal perfusion — a decrease in blood flow to the kidneys. This can occur during sur-gery, with injury or infection, and after myocardial infarction.

Catabolism increases in the ARF patient, caused in part by the increase in therelease of catecholamines, corticosteroids and glucagon during the stress response(Feinstein, 1988). The increased catabolism causes a rapid increase in BUN, loss ofmuscle mass, and decreased albumin and transferrin. During acute renal failure, ureaand glucose production from amino acids increases as well. In some patients with ARF,net protein catabolism can be as much as up to 150 gm/day (Kopple, 1996).

Protein Restriction

GFR Protein allowed

25 - 70 0.7 - 0.8 gm/kg/day< 25 0.6 gm/kg/day< 5 1.0 - 1.2 gm/kg/day (with dialysis)

94Nutrition Support

Postoperative renal failure is associated with a 40 to 60 percent chance of survival(Liftman, 1989). Early initiation of appropriate nutrition support may help to reducecomplications and improve survival rates.

Nutrition goals for ARF are: limit protein catabolism and wasting of lean bodymass; prevent fluid overload; reduce accumulation of nitrogenous waste in the blood;and facilitate healing of the injured kidney (Freund, et al., 1987).

PROTEIN

The optimal type of protein for the ARF patient remains controversial. Theorysuggests that patients should be given a higher percentage of essential amino acids toallow for decreased urea synthesis and a more rapid decrease in BUN levels. However,some studies have shown that no differences in BUN, nitrogen balance or urea appear-ance were seen in patients given essential amino acid vs. a standard amino acid formula(Feinstein, 1988; Freund, et al., 1987). In fact, Kopple (1996) found that giving onlyessential amino acids was hazardous, resulting in hyperammonemia, coma, and evendeath, with marked derangements in the plasma amino acid pattern. Nonessentialamino acids are vitally important in the synthesis of proteins and other biologicallyvaluable compounds (Kopple, 1996). Thus, nonessential amino acids should also begiven to the patient with ARF.

It appears that the quality of protein provided in ARF does not affect renal recov-ery. However, the amount of protein does. Excessive protein intake can be directlyrelated to decreased weight gain, a progressive increase in BUN and a decrease inglomerular filtration rate (GFR). Current recommendations for provision of protein toARF patients are a combination of essential and nonessential amino acids at moderatelevels (see amounts on the following page).

Because patients with ARF are often hypercatabolic, when protein is given at levelsbelow 1.5 gm/kg/day, the patient may remain in significant negative nitrogen balance(Macias, et al., 1996). Lower levels of calories provided appear to be associated withimproved nitrogen retention and balance (Macias, et al., 1996). The optimal energy andprotein level for the ARF patient is as yet unknown. Macias suggests that to achievenitrogen balance in the ARF patient, protein requirements are between 1.5 and 1.8 gm/kg/day.

Nutrition Goals for Acute Renal Failure

• Limit protein catabolism• Limit wasting of lean body mass• Prevent fluid overload• Reduce accumulation of nitrogenous waste• Facilitate healing of injured kidney

95Nutrition Support

Caloric requirements appear to be 25 to 30 kcal/day. Protein requirements are thesame as in any critically ill patient. The patient on continuous renal replacement therapy(CRRT) can receive 1.1 to 2.5 gm/kg/day.

CRRT may involve continuous arteriovenous hemofiltration (CAVH) or continuousveno-venous hemofiltration (CVVH) with or without dialysis. The use of CRRT mayreduce the risk of fluid and electrolyte disorders and hypotension during dialysis, andallow for the provision of greater amounts of nutrients to the patient (Kopple, 1996).CRRT removes large amounts of fluid, electrolytes, and other compounds in a slow,methodical fashion. Fluid and other waste products are removed on a regular basis,thus, greater amounts of protein and fluid can be given. The need for hemodialysis maybe avoided altogether (Kopple, 1996).

Protein losses into the dialysate are about 4 to 7 gm/day with CVVHD. TheCAVHD patient may lose from 9 to 12 gm/day. These losses are easily replaced withoral, enteral, or parenteral nutrition.

The use of TPN is sometimes required during ARF because of the patient’s otheracute problems. A very concentrated base solution of 70 percent dextrose may be neces-sary to compound TPN solution in those patients requiring fluid restriction. Concen-trated lipid emulsions (20 percent) can provide additional calories. Approximately 50percent of ARF patients require insulin supplementation because of glucose intolerancecaused by diabetes mellitus, sepsis or steroid therapy.

Standard amino acid formulas can be utilized; however, total protein should not belimited. Water-soluble vitamins, with additional folate, B6 and C, should be supple-mented. Vitamin K may require supplementation weekly. Supplementation of other fat-soluble vitamins is usually not recommended. Vitamins A and E are not dialyzable andpatients supplemented with vitamin A may develop hypervitaminosis (Wolk, 1993).

Trace elements are generally limited because of clearance of zinc and chromium bythe kidney. Electrolytes, calcium and phosphorus should be individually monitored andlimited or supplemented as needed. A decline in serum potassium and phosphorus mayoccur with nutrition repletion, requiring supplementation of adequate amounts toreturn levels to normal.

Nutrition for ARF Patients

Calories

25 - 30 kcal/kg/day

Protein

1.2 - 2.0 gm/kg/day

96Nutrition Support

If possible, the gut should be utilized for provision of nutrients. Nutrient-denseformulas are often necessary because of fluid restriction. A standard enteral formulashould be utilized for optimal nutrition care; specialty formulations can be utilized if/when significant electrolyte abnormalities occur (McClave, et al., 2009).

Enteral feedings are usually given continuously to these patients. Continuousfeedings are better tolerated in the critically ill patient and can be monitored moreeffectively. As the ARF patient recovers and regains function of his kidneys, nutritioncare can be modified.

Eventually, patients who regain renal function can return to a normal diet withoutrenal restrictions. If they do not regain normal renal function, however, they will requirethe same restrictions as any CRF patient.

CASE STUDY #1TL is a 37-year-old female admitted to the ICU with systemic lupus erythematosus

(SLE), gastrointestinal bleed, chronic renal failure, non-insulin dependent diabetesmellitus, and anemia. She is 5’4” and weighs 129 lb. Her admitting labs included a BUNof 88, Cr of 4.9, albumin of 2.6, triglycerides of 263, and Hgb of 8.7. Her medicationsincluded prednisone, IV albumin, Os-Cal, Lasix, and sliding scale insulin coverage. Onadmission, she was tolerating a prescribed 4 gm Na diet.

The next day, her diet was changed to NAS, 800 mg PO4, 70 meq K, 70 gm proteinand 1500 ml fluid per day. Her BUN rose to 107, Cr to 5.4, and her weight was 143.5 lb,signifying that her renal failure was worsening. She was not yet on dialysis. By Day 4,she was made NPO for placement of a vascular access for use with dialysis. Pulmonaryinfiltrates were noted on x-ray, indicating that she had developed an infection. Dialysiswas initiated later that day.

On Day 6, she was intubated as respiratory distress worsened, likely precipitatedby the presence of pulmonary infiltrates. She was diagnosed by the consultingpulmonologist with pulmonary hypertension and Serratia (a type of infection). She wasstarted on full strength Suplena™ at 40 ml/hr. This provided 960 ml, 1920 kcal, 28 gmprotein. Her needs were assessed to be 1700 kcal/day (based upon a factor of 30 to 40kcal/kg with increased levels of stress) and 35 to 50 gm protein/day (based on a factorof 0.6 to 0.8 gm protein/kg/day).

On Day 7, the tube feeding was decreased to 25 ml/hr since she was not tolerating theformula, as evidenced by high residuals (greater than 300 ml) of gastric contents. Unfortu-nately, placement of a feeding tube into the duodenum was not attainable at this time.

On Day 9, tube feedings were discontinued and TPN was initiated with a formulaof 400 ml D50, 400 ml amino acid 8.5 percent, and 200 ml 20 percent lipid at 60 ml/hour.All concentrations listed were prior to compounding. MVI-12 was added each day andtrace elements were added every other day. (Long-term TPN was not anticipated, butwe continued to monitor for problems associated with vitamin A toxicity. It was felt thatthe benefits of trace element supplementation outweighed the drawbacks.) The TPNprovided 1440 ml, 1751 total calories, and 48 gm protein.

97Nutrition Support

Recommendations were made to increase the TPN as tolerated to 70 to 80 ml/hourto approach estimated needs. On Day 11, TPN was increased to 70 ml/hr, providing1680 ml, 2043 total calories, and 57 gm protein. Her albumin had decreased to 2.5 (likelyrelated to the level of sepsis and other problems this patient is experiencing). BUN was81 and Cr was 7.5 (improved with dialysis) and her glucose level was 199 (patient wasreceiving steroids - Solumedrol - and was also being covered with sliding scale insulinand an insulin drip as needed). She was receiving dialysis every other day and wasdiagnosed as having multi-system organ failure, secondary to failure of her kidneys,lungs, and gut.

On Day 13, an inflammatory process was noted to be present in the bowel, butnothing was seen on CAT scan. Her amylase was 790 and she was diagnosed withpancreatitis, adult respiratory distress syndrome, and with CMV (cytomegalovirus).Her albumin level remained constant at 2.6 and her BUN and Cr levels remained stable.

On Day 15, she received a tracheostomy and all other care continued as the same.Her antibiotics included Flagyl, ganciclovir, ciprofloxacin, nystatin, and another thirdgeneration cephalosporin for treatment of her multiple problems. On Day 16, she com-plained of increased abdominal pain. A differential diagnosis of:

(1) spontaneous perforation of the sigmoid colon secondary to steroids, vs.(2) diverticulitis with a perforation or abscess, vs.(3) pancreatitis secondary to lupus or steroids, vs.(4) infarcted bowel secondary to lupus or pancreatitis.

Her nutrition support continued the same, as she tolerated her TPN and laboratoryvalues remained stable.

On Day 16, a 13 cm abscess was detected on her small bowel by CAT scan. Theabscess was drained and an exploratory laparotomy was scheduled for the followingday. TPN increased to 80 ml/hr and we continued to follow the available lab values tomonitor her tolerance to TPN and for improvement in nutritional status. Her albuminlevel dropped with the surgery and because of the abscess. However, she continued toreceive IV albumin to assist with dialysis and to maintain oncotic pressures. Slowenteral feedings were resumed over the next few weeks. TL improved and was able tobe weaned from the ventilator and TPN and was slowly transitioned to enteral (fullstrength 50 ml/hr) and then oral feedings.

CASE STUDY #2LA was a 68 year old woman admitted with ischemic cardiomyopathy, IDDM,

ARDS (adult respiratory distress syndrome) and a history of acute renal failure that hadprogressed to chronic renal failure. Her surgical history included a CABG (coronaryartery bypass graft) and a redo CABG. Her needs were estimated to be 1700 kcal/dayand 70 to 80 gm protein/day. (She was 5’4” and weighed 68 kg.)

Her left leg wound (from the CABG) had never healed well and required debride-ment. A Barium swallow study revealed frank aspiration (because of vocal cord paraly-sis from intubation with the previous surgery). A PEG (percutaneous endoscopic gas-trostomy) tube was placed. Her stormy course continued as she developed sepsis,required intubation, and started hemodialysis.

98Nutrition Support

Two days after extubation, LA started on a cardiac diet with supplements but hadpoor PO intake. Her ejection fraction (a measurement of the strength and effectivenessof the heart) was noted to be only 10 percent. TPN was initiated with 6 percent aminoacid, D10, and lipid 4 percent (1647 kcal, 101 gm protein) final concentration. The higherlevel of protein was possible because she was placed on CRRT (continuous renal re-placement therapy); this treatment provided an additional 550 kcal.

PO intake remained poor; TPN continued. One month after admission, LA wasstarted on enteral feedings of Nepro 40 ml/hr (1728 kcal, 79 gm protein) due to electro-lyte disturbances and TPN was decreased to one liter with dialysis. LA’s lab valuesremained stable throughout. Two weeks later, her repeat modified Barium swallowrevealed that it was safe for her to attempt PO intake; she was able to consume approxi-mately 1000 kcal/day and about 60 gm protein/day (with supplements). Enteralfeedings were thus reduced to one can of Nepro each day.

Her course continued until she had a bout of emesis and aspirated and becameintubated. TPN was restarted (amino acid 4 percent dextrose 20 percent and lipids 4percent at 70 ml/hr) which provided 2083 kcal and 67 gm protein. She required athrombectomy and developed pulmonary edema and was ventilator dependent. Threedays later, CVVHD (a type of CRRT) resumed and provided an additional 550 to 855kcal/day. She was meeting her needs, assessed now to be 1600 to 2200 kcal/day and 65to 95 gm protein/day. Her albumin was 2.3; LFT’s were elevated; and her weight was64.1kg.

The CVVHD was successful in removing excessive fluid. However, LA becameseptic and required pressor support to maintain her blood pressure. Her lab valuesremained stable. She continued to deteriorate and it appeared that she would be ventila-tor dependent and continue to require dialysis and other heroic measures to stay alive,with little hope of ever improving. The decision was made to extubate LA, continueCRRT, and allow her to move out of the ICU. Her diet advanced from CL to FL; POintake was poor. Two days later, LA expired.

REVIEW QUESTIONS

1. What nutrition parameters are best used to assess the renal failure patient?2. What vitamins and minerals should be supplemented in renal failure?3. Determine a mode of support for a 65-year-old male patient with chronic renal failure

who presents with ventilator dependency following surgery for an abdominalaortic aneurysm. At two days post-op, he exhibits no bowel sounds as yet. Patientis 6’1”, 171 lb (78 kg). Lab results were: BUN 50, creatinine 5.6, potassium 4.8,sodium 131, albumin 2.3, phosphate 8.2.

4. Recommend nutrition support for a 73-year-old female post-coronary artery bypassgraft patient who now exhibits acute renal failure. BUN 111, creatinine 10.2, potas-sium 5.0, sodium 150, albumin 2.7, phosphate 8.0, cholesterol 139, triglycerides 90,glucose 252. She is 5’4”, 154 lb (70 kg).

99Nutrition Support

REFERENCES

Charney DI: Intradialytic parenteral nutrition: a critical review of the literature. Support Line XVII:6:1-5,1995.

Feinstein EI: Total parenteral nutritional support of patients with acute renal failure. Nutr Clin Prac 3:1:10-13, 1988.

Fox SI: Physiology of the kidneys. Human Physiology, 2nd ed. Wm. C. Brown Publ., Dubuque, IA, 1987.Freund HR, et al.: The effect of different intravenous nutritional regimens on renal function during acute

renal failure in the rat. JPEN 11:6:556-559, 1987.Goldwasser P, Mittman M, Antignani A, et al.: Predictors of mortality on hemodialysis. J Am Soc Nephrol

3:1613-1622, 1993.Kopple JD: The nutrition management of the patient with acute renal failure. JPEN 20:1:3-12, 1996.Kopple JD, et al.: J Nutr 31: 247S, 1999.Liftman C: Renal function. In: Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A, Ed.

A.S.P.E.N. Publ, Rockville, MD, 1989.Macias WL, Alaka KJ, Murphy MH, et al.: Impact of the nutritional regimen on protein catabolism and

nitrogen balance in patients with acute renal failure. JPEN 20:1:56-63, 1996.Matarese LE: Renal failure. In: Nutrition Support Dietetics, 2nd ed. Ed. Gottschlich MM, Matarese L,

Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.Matarese L: Acute renal failure. Roundtable presentation at A.S.P.E.N. 21st Clinical Congress, San Fran-

cisco, 1997.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition


Wolfson M and Foulks CJ: Intradialytic parenteral nutrition: a useful therapy? Nutr Clin Prac 11:5-11, 1996.Wolk R. Micronutrition in dialysis. Nutr Clin Prac 8:267-276, 1993.

100Nutrition Support

Notes


Chapter Nine:Liver Disease

The liver has a vast number of responsibilities in the body, including detoxifica-tion of the blood, carbohydrate metabolism, lipid metabolism, protein synthesis andsecretion of bile (Fox, et al., 1987).

Most nutrients must pass through the liver, where they are stored, used for energyor processed into other substances. All essential amino acids, except the branched-chainamino acids, are broken down in the liver. Lipid is primarily metabolized in the liver,through oxidation or fatty acid synthesis. Carbohydrates are metabolized in the liverand glucose levels are maintained at a reasonably constant level through its actions.

It is obvious that any disease of the liver has a profound effect on nutritional status.Liver disease and/or damage can occur with viral infections, such as hepatitis, Epstein-Barr, and cytomegalovirus. Ischemic damage to the liver can occur after trauma orsurgery, while the liver can also be damaged with alcohol and/or drug abuse, by au-toimmune diseases, and by cancer.

Nutrition therapy, while sometimes difficult, is of primary importance in thetreatment of the patient with diseases affecting the liver and will likely have an impacton the patient’s final outcome.

Care of liver failure patients requires careful assessment of their nutritional re-quirements and provision of appropriate levels of nutrients to allow anabolism butprevent complications from overfeeding. Assessment is difficult because damage to theliver affects the metabolism, transport and synthesis of many nutrients.


CARBOHYDRATE METABOLISM

In the normal liver, carbohydrate metabolism occurs without problems. Afteringestion, glucose and other simple sugars are converted into glycogen. If there is toomuch simple carbohydrate for the liver to store, it converts the excess to fat. When thebody requires more glucose (as might happen several hours after a meal), the liverinitiates the process of glycogenolysis, and the resulting glucose is released into thebloodstream. If the glycogen stores are depleted, as might happen overnight, gluconeo-genesis begins, forming glucose from amino acids, lactate and glycerol.

The injured or diseased liver is often unable to maintain normal carbohydratemetabolism. This is most often manifested as hypoglycemia in acute liver failure, andhyperglycemia in chronic liver disease. The cause of these changes remains unclear, butfactors may include the inability of the liver to undergo glycogenesis and a reducedability for gluconeogenesis (Shronts and Fish, 1989, Guenter and Slocum, 1983; Wong, etal., 1998).

FAT METABOLISM

The healthy liver secretes bile, which is transported to the gastrointestinal tract toassist in the absorption of fats and fat-soluble vitamins. Triglycerides are transported tothe liver and are converted to fatty acids and glycerol. These substances are then oxi-dized for energy, reformed into triglycerides for transport and storage, or transformedinto other compounds, such as cholesterol and phospholipids (Shronts and Fish, 1989;Guenter and Fischer, 1983).

Injury or diseases of the liver can affect the normal metabolism of fat and, thus, thenutritional status of the patient. Without the normal production and secretion of bilesalts, malabsorption of fats and fat-soluble vitamins may occur. If normal fat metabo-lism does not occur, short-chain fatty acids accumulate in the liver, causing “fatty liver.”

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 deficiencyThiamine deficiency B6 deficiencyFolate deficiency Niacin deficiencyIron deficiency Copper deficiencyManganese deficiency Zinc deficiency


The causes of this alteration in fat metabolism are many and include increased amountsof fat produced by the liver, reduced transport of these fats out of the liver, and reducedoxidation of fats.

The steatorrhea that occurs with liver disease may cause as much as 30 to 60 percent of fat to be malabsorbed (Sokol, 1995).

PROTEIN METABOLISM

The liver plays a significant role in the normal metabolism of protein. Absorbedprotein passes through the portal system to the liver. Nonessential amino acids andother important compounds, including albumin, are formulated there. Urea, made inthe liver, is vital to the removal of ammonia formed in the body. Fibrinogen and pro-thrombin — vital blood clotting factors — are also synthesized in the liver (Wong, Klein,et al., 1998).

A diseased or injured liver requires increased protein to repair damaged cells.However, it is often unable to utilize (or even tolerate) levels of protein adequate forhealing. Several functions are impaired, as shown in the following chart.

Decreased production of urea decreases ammonia removal, thus boosting the levelof serum ammonia, which is toxic to the brain. This may contribute to the developmentof hepatic encephalopathy. In severe liver disease, the increase in serum ammonia iscaused from secretion of glucagon and its stimulus of gluconeogenesis from aminoacids. The increased use of protein for calories results in diminished plasma levels ofbranched chain amino acids. Serum levels of aromatic amino acids (AAA) rise when theliver decreases metabolism of AAA. The elevation in blood ammonia results in in-creased uptake of ammonia by the brain. Influx of AAA increases into the brain — theAAA substitute for norepinephrine and dopamine to form octopamine andphenylethanolamine. These altered compounds cause encephalopathy and resultantconfusion and reduced levels of consciousness (Sokol, 1995).

Liver Dysfunction

Decreased urea production

Increased serum ammonia levels

Increased AAA Levels

Decreased BCAA levels

Production of“false neurotransmitters”

Confusion, reduced consciousness


MICRONUTRIENTS

The liver normally plays a significant role in the storage, synthesis, and transportof many vitamins and minerals. Vitamins A, D, thiamine, riboflavin, B6, B12, niacin,folate, and pantothenic acid are all stored in the liver to some extent. Minerals that arestored in the liver include iron, copper, and cobalt. Thiamine, B6, and vitamin D areconverted to their active forms in the liver. Transport of vitamin A is dependent uponnormal liver function, as well. The steatorrhea that may occur with liver disease maycause malabsorption of calcium, magnesium, zinc, and fat-soluble vitamins.

As mentioned earlier, liver disease or failure can result in decreased absorption offat-soluble vitamins. Deficiency of vitamin A may occur due to a decrease in the amountof transport proteins available, while vitamin D levels may fall because of alterations inconversion of vitamin D to its active form. The inability of the diseased liver to convertthiamine and B6 to their active forms may result in deficiencies of these vitamins. Asignificant decrease in folate stores may also occur, especially in liver disease associatedwith alcohol intake.


Nutrition assessment may be difficult because of the wide variety of effects of liverdisease or injury. The patient may be edematous with ascites or anasarca or dehydrateddue to diuretic therapy, making determination of weight difficult. Weight may befurther impacted by increased interstitial fluid associated with hypoalbuminemia andby the potential for increased size and weight of the liver and spleen (Sokol, 1995).

The incidence of protein-energy malnutrition ranges from 27 to 87 percent(McCollough, 1997); this malnutrition is associated with reduced survival and an in-creased risk of complications, such as peritonitis. Factors contributing to this malnutri-tion include anorexia with poor intake, maldigestion and malabsorption, and thechanges in metabolism associated with liver disease.

Since many of the serum proteins (including albumin, transferrin, prealbumin, andretinol-binding protein) are synthesized by the liver, their use in nutrition assessment isinvalid. Although only 25 percent of normal liver function is required to maintain nor-mal albumin production (Shronts and Fish, 1989), its extended half-life (about 20 days)makes it a less-than-optimal measure of protein status.

Creatinine-height index (CHI) can be used to some extent to assess the amount oflean body mass, but its use may be limited because CHI can be affected by age, malnutri-tion and hepatorenal syndrome (failure of the hepatic and renal systems) (Shronts andFish, 1989; Shronts, 1988).

Thus it is difficult to accurately assess the nutritional status of the patient withsevere liver disease. Laboratory values will likely be skewed with liver disease. Totalbilirubin will increase and liver function tests (aspartate aminotransferase [SGOT],alanine aminotransferase [SGPT], alkaline phosphatase) will increase dependent uponthe severity of the disease and type of disease (Shronts and Fish, 1993). Prothrombintime will likely be lengthened.


Liver disease patients have increased energy requirements for anabolism andhealing of the injured liver. Adequate calories to allow for protein sparing should beprovided — perhaps as much as 25 to 35 kcal/kg/day (utilizing the estimated dryweight) (Shronts and Fish, 1993; Kondrup and Muller, 1997).

Needs can also be determined with utilization of the Harris-Benedict equation,applying a factor of 1.3 (Shronts, 1988). If the patient can tolerate fat, 25 to 40 percent ofthe non-protein calories should be given as fat. Since overfeeding of calories may exac-erbate fatty liver, care should be taken to provide the appropriate level of calories.

Protein requirements vary with the severity of the disease and presence or absenceof symptoms. The patient with acute and chronic liver failure should have no proteinrestriction — protein should not be restricted in an effort to manage hepatic encephal-opathy (McClave, et al., 2009; Plauth, et al., 2006; Florea and Aranda-Michel, 2006).Patients should receive a protein level of 1.5 gm protein/kg/day, with or withoutencephalopathy.

Several studies have shown that the supplementation of protein with BCAA maybe of benefit in the treatment of encephalopathy (Hiyama and Fischer, 1988; Cerra, et al.,1985; O’Keefe, et al., 1987; Sokol, 1995; Flores and Aranda-Michel, 2006; Horst, et al.,1984; Yoshida, et al., 1989; Marschesini, et al., 2003; Muto, et al., 2005; Sato, et al., 2005).Some showed that supplementation with BCAA resulted in improved nitrogen balance,as well as improvement in mental status, and slowed progression of disease, especiallywith long term use. In refractory hepatic encephalopathy, use of BCAA formulas mayimprove coma grade.

MICRONUTRIENTS

Because of alterations in vitamin and mineral absorption, metabolism and trans-port in liver disease, supplementation is often warranted. However, the liver may beunable to metabolize or transport certain vitamins and minerals, and toxicities maydevelop, especially in end-stage liver disease. Any supplementation should be judiciousand closely monitored. Fat-soluble vitamin status should be evaluated regularly andsupplemented when deficiency occurs. Water-soluble vitamin E can be given at a doseof 15 to 25 IU/kg/day; vitamin D can be supplemented at a level of 2 to 4 mcg/kg/dayif the patient is also exposed to sunlight.

Calorie Requirements

25 - 35 kcal/kg/dayor

1.3 - 1.5 X BEE(25 to 40% as fat)


Vitamin K can be given as a 2.5 to 5 mg oral dose twice per week. Vitamin A canbecome toxic if supplemented.

Other nutrients that may require supplementation include zinc, magnesium,phosphorus, and calcium (Sokol, 1995). Copper and manganese should not be supple-mented in patients with liver disease who are receiving TPN. Copper may be storedexcessively in the diseased liver; both copper and manganese are excreted in bile (excre-tion via bile would be decreased with cholestasis) (Fell, et al., 1996).

Individual dosages should be based upon the patient’s symptoms of clinical defi-cits and subsequent evidence of deficiency, through biochemical measurements. In otherwords, in end-stage liver disease, vitamin-mineral supplementation — especially fat-soluble vitamins stored in the liver — should be limited. Supplementation of water-soluble vitamins is less risky and often warranted, such as 25 to 50 mg thiamine, 400 to800 mg folate and the RDA for vitamin C.

NUTRITION SUPPORT

The patient with hepatitis, either acute or chronic, can usually be maintained on anormal diet, with 25 to 35 kcal/kg/day and 1.0 to 1.5 gm protein/kg/day. The cirrhoticpatient especially needs adequate calories and protein (needs can be determined fromrecommendations above).

If esophageal varices from cirrhosis prevent oral intake or placement of anasogastric tube, TPN is indicated. Enteral nutrition support is recommended over TPNif the patient is unable to ingest nutrients orally and has a functional gastrointestinaltract. Small-bore feeding tubes should be used to prevent irritation of varices andsubsequent hemorrhage (Shronts and Fish, 1989).

Most patients with esophageal varices can tolerate a normal diet. The presence ofascites or edema may indicate the need for sodium (2 gm Na/day) and fluid restriction(1000 to 1500 ml/day). Several BCAA-enriched formulas are available forencephalopathic patients. Most standard enteral formulas may be well tolerated.

Often, a calorie-dense formula is recommended because of the need for fluidrestriction. Since these types of formulas are often hypertonic, they should be welltolerated if initiated and advanced slowly.

Initially, the formula should be given continuously at a low rate, with gradualincrease as tolerated by the patient (Shronts and Fish, 1989). Certain medications, suchas lactulose®, given to bring down serum ammonia levels, will cause diarrhea; thisshould not be attributed to the enteral feedings.

TPN support can be used in the patient with a nonfunctioning GI tract. It may alsohelp a patient with encephalopathy who has difficulty protecting his airway, and whotherefore may be at risk for aspiration.

As mentioned previously, 25 to 30 percent of nonprotein calories should be pro-vided as fat, with additional calories from carbohydrate in the form of 50 to 70 (initialconcentration) percent dextrose concentrations. Should fat intolerance become apparent,with the occurrence of hypertriglyceridemia or lipemia, limit lipids to twice a week(only allow for provision of essential fatty acids) (Shronts and Fish, 1993).


As mentioned earlier, any supplementation of vitamins and minerals should bemonitored carefully to prevent toxicities (especially copper and manganese).

The liver failure patient presents many challenges to those responsible for nutritioncare. There is often a fine line as to the level of protein a patient can tolerate. Findingthat level is challenging and frustrating. Because of varices, enteral feedings may benext to impossible, unless a G-tube is placed. TPN is not always well tolerated becauseof the complex role of the liver in metabolism. And, once the patient with alcoholic liverdisease recovers from the acute phase, he or she is often very difficult to work with dueto altered mental status.

CASE STUDY

CW was a 53-year-old female admitted to the hospital with hepatic encephalopa-thy and a gastrointestinal bleed. Her history also revealed the following medical prob-lems: ARDS, COPD (steroid-dependent), sepsis syndrome, cholestasis, and a history ofalcohol abuse. She was 5’2" and weighed 140 lb and had a recent 10 lb weight loss. Heradmitting albumin was 2.5. Her needs were assessed to be 1300 to 1500 kcal/day and 60to 90 gm protein/day because of her level of encephalopathy, which had been refractoryto intervention. Her elevated ammonia level (100) fell to 63 after administration ofLactulose®.

Enteral feedings were initially attempted but were poorly tolerated as the patienthad high residuals and diarrhea. She was intubated and an open lung biopsy wasperformed. She had developed a decubitus ulcer on her sacral area. Portal hypertensionwas diagnosed. Enteral feedings were again attempted with a hepatic formula, in thethought that the higher branched-chain amino acid level would aid in reducing herlevel of encephalopathy. Her albumin level remained stable but she was poorly respon-sive. High residuals from the enteral feedings continued so TPN was initiated with finalconcentrations of D18 and a hepatic amino acid source at 4 percent with lipid 20 percent500 ml three times per week. This provided an average of 1818 kcal and 72 gm protein.Her calorie requirements were met and we were able to give her higher levels of proteinbecause of the utilization of a branched-chain amino acid formula.

CW’s BUN and Cr began to rise and her hemoglobin and hematocrit levels beganto fall. She was diagnosed with sepsis from Candida albicans and Aspergillus fumigatus(opportunistic infections are not uncommon as the liver fails); ARDS continued; andthrombocytopenia developed. Her condition continued to worsen and little hope wasoffered for her recovery. Her family elected to discontinue life support.

REVIEW QUESTIONS

1. What factors must be considered in the nutrition support of the patient with hepaticfailure?

2. An encephalopathic patient presents to the ICU. He is comatose. Height 5’1", weight132 lb. Determine his nutrient needs.


REFERENCES

Cerra FB, et al.: Disease-specific amino acid infusion (FO80) in hepatic encephalopathy: a prospective,randomized, double-blind, controlled trial. JPEN 9:288-295, 1985.

Fell J, Reynolds A, Meadows N, et al.: Manganese toxicity in children receiving long-term parenteralnutrition. Lancet 347(9010):1218-1221, 1996.

Flores DA, Aranda-Michel J: Nutritional management of acute and chronic liver disease. SeminGastrointest Dis 13: 169-178, 2002.

Fox SI: The digestive system. Human Physiology, 2nd ed., Wm. C. Brown Publ., Dubuque, IA, 1987.Guenter P and Slocum B: Hepatic disease: nutritional implications. Nurs Clin NA 18:1:71-80, 1983.Hiyama DT and Fischer JE: Nutritional support in hepatic failure. Nutr Clin Prac 3:3:96-105, 1988.Horst D, Grace ND, Conn HO, et al.: Comparison of dietary protein with an oral, branched chain-enriched

amino acid supplement in chronic portal-systemic encephalopathy: a randomized controlled trial.Hepatology 4: 279-287, 1984.

Kondrup J and Muller MJ: Energy and protein requirements of patients with chronic liver disease. JHepatology 27:239, 1997.

Marchesini G, Bianchi G, Merli M, et al.: Nutritional supplementation with branched-chain amino acids inadvanced cirrhosis: a double-blind, randomized trial. Gastroenterology 124: 1792-1801, 2003.

McCollough AJ, et al.: Am J Gastroenterol 92, 1997.McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition


Muto Y, Sato S, Watanabe A, et al.: Effects of oral branched-chain amino acid granules on event-freesurvival in patients with liver cirrhosis. Clin Gastroenterol Hepatol 3: 705-713, 2005.

O’Keefe SJ, Ogden J and Dicker J: Enteral and parenteral branched chain amino acid-supplementednutritional support in patients with encephalopathy due to alcoholic liver disease. JPEN 11:5:447-253, 1987.

Plauth M, Cabre E, Riggio O, et al.: ESPEN guidelines on enteral nutrition: liver disease. Clin Nutr 25: 285-294, 2006.

Shronts EP and Fish JA: Hepatic failure. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, MatareseLE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.

Shronts EP: Nutritional assessment of adults with end-stage hepatic failure. Nutr Clin Prac 3:3:113-119, 1988.Shronts EP and Fish JA: Nutrition support in hepatic failure. In: Nutrition Support Dietetics. Shronts EP, Ed.

A.S.P.E.N., Silver Spring, MD, 1989.Sokol RJ: Nutritional support in chronic liver disease. Address at 5th Annual Advances and Controversies

in Clinical Nutrition. Scottsdale, AZ, 1995.Wong K, Klein BJV, and Fish JA: Nutrition management of the adult with liver disease. In Dietitian’s

Handbook of Enteral and Parenteral Nutrition. 2nd ed. Skipper A, Ed. A.S.P.E.N. Publishers, Inc.Gaithersburg, MD, 1998.

Yoshida T, Muto Y, Moriwaki H, Yamato M. Effect of long-term oral supplementation with branched-chain amino acid granules on the prognosis of liver cirrhosis. Gastroloenterol Jpn 24: 692-698, 1989.


Chapter Ten:Cancer Patients

Cancer patients can face a multitude of nutrition-related problems, both fromcancer itself and from therapy. Incidence of malnutrition in the cancer populationranges from 30 to 87 percent (Heber and Tchekmedyian, 1992; Heber, 1995).

Surgery, radiation therapy, and chemotherapy all profoundly affect a patient’sability to ingest adequate nutrients. These effects will be discussed briefly. This chapterwill focus primarily on the appropriateness of extensive nutrition support and recom-mendations for patients with various complications related to the cancer or therapy.

Maldigestion and malabsorption occur in cancer patients and can be related to thetumor itself or to the changes in distribution of nutrients that occurs with cancer. Muscleand fat reserves appear to be redistributed to the liver and bone marrow and proteinconservation does not occur.

SURGERY

Depending on the type of cancer, a patient’s ability to chew or swallow may beimpaired. “If the gut works, use it,” but these patients may be best served with enteralnutrition support, with placement of a gastrostomy or jejunostomy tube during theprimary surgery. The incidence of malnutrition in patients with head and neck cancer isestimated at 25 to 74 percent (Lee, 1999; Mekhail, et al., 2001).

Complications that may occur after esophagectomy include reduced motility andgastric acid production, steatorrhea or fistulas related to the associated vagotomy, andstenosis of the esophagus (Kouba, 1988; Bloch, 1989).

Gastrectomy may cause the development of dumping syndrome (discussed inChapter Four) and hypoglycemia, and malabsorption, with the potential for relateddeficiencies of calcium, iron, B12 and fat-soluble vitamins. Post-gastrectomy patients


may be able to attain and maintain adequate intake with feedings through a jejunos-tomy tube until they can resume oral intake.

Resection of the small bowel may cause malabsorption, diarrhea and deficienciesof B12, fat-soluble vitamins, magnesium, calcium, and electrolytes. Adequate nutritiontherapy may be attainable with oral intake, enteral feedings utilizing elemental orpeptide formulas, or TPN, if the GI tract is not functional.

Pancreatectomy causes diabetes mellitus and malabsorption of carbohydrates, fats,proteins, fat-soluble vitamins and minerals. Total parenteral nutrition may be necessaryinitially, with transition to enteral feedings (utilizing elemental formulas) and, eventu-ally, oral feedings as tolerated by the patient.

RADIATION

Radiation therapy can have a vast effect on a patient’s ability to ingest and absorbnutrients. Taste and smell may be diminished, and difficulty in chewing and swallow-ing is a frequent side effect (this may be associated with stomatitis, mucositis anddecreased salivation) (Kouba, 1988; Bloch, 1989; Burgess, 1989). The formation of stric-tures and fistulas is possible, and malabsorption, diarrhea, nausea and vomiting areoften present.

Acute reactions occur within 10 to 17 days of radiation therapy. These reactionsinclude: mucositis, xerostomia, esophagitis, dysphagia, otitis media, fungal, bacterial,and viral infections (Hunter, 1996). Delayed reactions can include necrosis of the man-dible, ulceration of the mucosa, dental caries, endocrine dysfunction, and laryngealedema (Hunter, 1996).

These complications can preclude adequate intake and necessitate enteral support,when possible, or parenteral support as necessary. Enteral support is indicated if thepatient exhibits progressive weight loss with oral intake alone, has received radiationtherapy of the mouth or throat, has received extensive radiation therapy or is beingtreated with adjunctive chemotherapy or surgery.

Isotonic enteral or nutrient-dense formulas are often well tolerated in the patientwith head, neck or esophageal cancer; more elemental formulas may be required forpatients receiving radiation therapy to the stomach or small bowel. TPN may be theonly means available to provide adequate nutrition support and may help the patientwithstand the rigors of radiation therapy (Souba and Copeland, 1988).

CHEMOTHERAPY

Chemotherapy often provokes complications of nausea, vomiting and anorexia.Mucositis is another common side effect, and may alter a patient’s ability to maintainadequate nutrition intake. Other common complications are constipation and diarrhea.

Treatment with some chemotherapeutic agents can cause deficiencies of folate,calcium and magnesium (Bloch, 1989). Enteral nutrition support or TPN should beconsidered if all other methods of nutrition support fail. Many chemotherapeutic agentscan cause metabolic changes as well. (See chart on the following page).


NUTRIENT NEEDS

Cancer cachexia is a well described phenomenon. Weight loss may occur in up to40 percent of patients, while as many as 80 percent of patients with endstage diseasewill develop cancer cachexia syndrome (DeWys, 1979, 1980; Barber, 2002). The cachexiaappears to be caused by decreased intake of nutrients along with increased nutrientlosses and increased or inefficient energy metabolism (Hunter, 1996). The patient withcachexia generally has a further decline in nutritional status because of associatedanorexia and early satiety which then causes weight loss, immunosuppression, andother associated metabolic changes (Hunter, 1996).

Nutrition needs of cancer patients are similar to those of other stressed patients.Alterations in metabolism occur, but these are not uniform or very predictable. Forinstance, some patients exhibit an increase in resting energy expenditure, but othersshow a decrease in energy requirements (Hearne and Daly, 1986). The resting energyexpenditure is suggested to be abnormal in as many as 60 per cent of cancer patients(Tayek, 1992). Patients with cachexia do not utilize nutrients well; this is related to thealtered metabolism associated with solid tumors. Lean body mass is depleted, primarilyfrom skeletal muscle.

For patients who are hypermetabolic, who would benefit from weight gain, or whoundergo catabolism after surgery, radiation therapy or chemotherapy, a general rule ofthumb is the provision of 25 to 30 kcal/kg/day. At least 35 kcal/kg/day should beprovided for severely stressed or hypermetabolic patients (Bloch, 1993).

Protein needs may vary from 1.0 to 2.0 gm/kg/day, depending upon the needs ofthe patient. Supplementation with vitamins and minerals should be considered for thepatient with inadequate intake or one who has undergone surgery or therapy that may

Effects of Chemotherapy Drugs

Drug Metabolic change

Asparaginase hyperglycemia, pancreatitisChlorotrianisene hypercalcemiaCisplatin hyperuricemia, hypomagnesemiaDiethylstilbestrol hypercalcemiaMethotrexate deficiency of folate and calciumMithramycin hypocalcemia, hypokalemiaStreptozocin hypoglycemiaTamoxifen hypercalcemiaTaxol nausea, emesis, mucositisTretinoin hypertriglyceridemia, elevated LFTVincristine SIADH, hyponatremia

Bloch AS, 1998


cause deficiencies. Folate levels may fall in acute leukemia, lymphoma, and metastaticcarcinoma. Vitamin B6 levels drop in Hodgkin’s disease and zinc levels decrease withdiarrhea, small bowel drainage and cisplatin and diuretic treatment (Bloch, 1993).

Some controversy exists over the use of nutrition support for the cancer patient.Certainly, the patient who is terminal and not undergoing other therapy should prob-ably not be considered as a nutrition support candidate. But nutrition support mayenhance therapy by improving nutritional status, and the prevention of malnutritionmay reduce other complications. Most importantly, the quality of life can be vastlyimproved through the proper use of nutrition support. In the terminal patient, however,some studies suggest that quality of life is diminished with the addition of nutritionsupport (McCann, et al., 1994; Hill, 1998).

A.S.P.E.N. guidelines suggest that one to two weeks of preoperative nutritionsupport may be of benefit in moderately to severely malnourished patients and inmalnourished patients undergoing anticancer therapy if they are unable to adequatelyconsume or absorb nutrients.

Provision of nutrition support to the patient whose life would be prolonged butnot enhanced should be carefully considered, weighing both benefits and burdens forthe patient and his care. Nutrition support may be highly beneficial to the patient withgastrointestinal cancer or problems related to the GI tract that have occurred afterradiation, surgical, or chemotherapeutic intervention.

Typically, what works for other, non-cancer, patients in assessing needs works forcancer patients as well, as long as circumstances (such as surgery) are similar. Becausecancer patients undergoing radiation or chemotherapy are often unable to eat due tonausea and vomiting, oral supplementation is difficult. However, these patients areoften more highly motivated, making them more receptive to oral supplementation.

Relaxed, frequent small meals are often best tolerated. Between-meal supplementsor nourishments of high calorie, high protein foods are suggested. Modification inconsistency of foods is often helpful, depending upon the problem.

Since nausea and emesis are a frequent complication to the therapies for varioustypes of cancer, antiemetics are often utilized with some success. Chronic nausea, whichcan occur with advanced cancers, is more difficult to treat, but metoclopramide is usedinitially (Hardin, 1994). Megestrol acetate has been utilized to stimulate appetite for anumber of years and, in several studies, has been suggested to increase weight andimprove nutritional status in those patients treated (Feliu, et al., 1992; Tchekmedian, etal., 1992; Loprinzi, et al., 1990).

Enteral and parenteral nutrition support is sometimes of benefit, but should not beconsidered a therapy.

CASE STUDY #1JG was a 66-year-old male diagnosed with gastric cancer. His physician felt that the

cancer was inoperable, and the patient and his physician elected to treat the tumor withchemotherapy. After starting chemotherapy, JG was beginning to develop anorexia andhad experienced some weight loss when he was referred to a home care agency for homeTPN to supplement his oral intake. He had refused invasive jejunal tube placement forenteral feedings. Home TPN was initiated, to be given over 10 to 12 hours each night.


His physician had given JG approximately 6 weeks to live as a prognosis. JG’sweight was within normal limits for his height of 6’1"; he weighed 178 lb upon initiationof TPN.

He received adequate protein and caloric intake to meet his needs and his weightand labs were monitored on a weekly basis. We consulted with him and his familyregarding his oral intake. JG was still able to consume approximately 1200 kcal and 40to 60 gm protein each day, thus we adjusted his TPN accordingly. He complained ofexcessive weight gain and desired a reduction in his TPN to 5 days/week; this wasallowed since he was, at that time, able to maintain adequate fluid intake and caloric/protein intake through a combination of oral and parenteral intake. His lab valuesremained within normal limits.

Six weeks passed and JG was able to reach his goal of spending the Christmasholidays with his family. He then set his next goal of attending his daughter’s weddingin June. During the next 6 months, he vacationed, always assuring that he would havehis TPN available. He continued to eat fairly well, although he noticed more anorexiaand complained of early satiety. He was reminded to take his meals in small frequentfeedings and was encouraged to try any of a variety of supplements. He continued todo well, with the only changes in his weight occurring after chemotherapy. He proudlywalked his daughter down the aisle at her June wedding. He promptly set another goalof attending another family wedding in October.

JG’s nutritional status remained stable until he had another course of chemo-therapy. At that time, he experienced nausea, vomiting, and diarrhea to a greater de-gree. He was unable to take as much food in orally but he continued to tolerate his TPN.His albumin started a slow decline and his LFTs became elevated. He was able to travelto the wedding in October, but returned quite fatigued. His nutritional status remainedabout the same, but his general health continued to decline.

JG’s battle with cancer ended in November, 13 months after he was first diagnosedand given a prognosis of 6 weeks to live. Clearly, nutrition support played a significantrole in not only extending his life, but also improving his quality of life.

CASE STUDY #2PT was a 71-year-old male with lower esophageal cancer (at the gastroesophageal

juncture). He appeared to have no metastases. His history included a smoking history,chronic obstructive airways disease, a 50 lb weight loss over the previous seven months,and difficulty with swallowing. His admitting height and weight were 5’7" and 155 lb;his albumin was 3.0 gm/dl.

He was admitted prior to surgery and started on TPN of D18, lipid 2 percent andamino acid 5 percent at 60 ml/hr along with a regular diet. The TPN was then increasedto 90 ml/hr (2186 kcal and 108 gm protein). His needs had been assessed at 1800 to 2100kcal/day and 85 to 120 gm protein/day. On hospital day #3, he underwent anesophagogastrectomy. Two thirds of the proximal stomach and one third of the distalesophagus were removed. He also had a pyloroplasty and a jejunostomy tube wasplaced. TPN continued until post op day 3 when a fiber-containing enteral formula wasstarted at 20 ml/hr; TPN rate was decreased to 80 ml/hr.


The plan was for the enteral feeding to be gradually increased to 65 to 75 ml/hr tomeet his needs (formula was 1.2 kcal/ml and 53 gm protein/l). He started on clearliquids the following day. On post op day 5, the enteral feeding was at 70 ml/hr and theTPN was reduced to 30 ml/hr. He tolerated the j-tube feeding well.

PT’s course did not remain so smooth, however. His diet was advanced to soft; hedid not tolerate the diet and was placed back on enteral feedings with supplementalTPN. Over the course of the next week, he was gradually weaned onto a pureed diet;enteral feedings were decreased and TPN was discontinued. Oral calorie counts re-vealed near adequate intake as his appetite and intake continued to improve with thepureed diet and supplements. He was discharged home on a soft diet with supplementswith a reasonable quality of life.

REVIEW QUESTIONS

1. Evaluate the calorie/protein needs for a 25-year-old female with leukemia. Height,5’5", weight 110 lb.

2. Describe the nutrition problems that might be associated with radiation therapy ofthe head and neck area.

REFERENCES

Barber M: The pathophysiology and treatment of cancer cachexia. Nutr Clin Prac, 17: 203-209, 2002.Bloch AS: Cancer. In: Matarese LE, Gottschlich MM (eds.) Contemporary Nutrition Support Practice: A

Clinical Guide. Philadelphia: WB Saunders; 475-495, 1998.Bloch A: Cancer. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese LL, Shronts EP, Eds.

A.S.P.E.N., Silver Spring, MD, 1993.Bloch A: Nutrition support in cancer. In: Nutrition Support Dietetics. Shronts EP, Ed. A.S.P.E.N., Silver

Spring, MD, 1989.Burgess J: Cancer Therapy. In: Nutrition Support Dietetics. Skipper A, Ed. A.S.P.E.N. Publ, Rockville, MD,

1989.DeWys WD: Anorexia as a general effect of cancer. Cancer 43: 2013-2019, 1979.DeWys WD, Begg C, Lavin PT, et al.: Prognostic effect of weight loss prior to chemotherapy in cancer

patients. Eastern Cooperative Oncology Group. Am J Med, 69: 491-497, 1980.Feliu J, Gonzales-Baron M, Berrocal A, et al.: Usefulness of megestrol acetate in cancer cachexia and

anorexia. Am J Clin Oncol 15:436-440, 1992.Hardin TC: Pharmacologic management of anorexia in cancer. Support Line XVI:4:11-14, 1994.Hearne BE and Daly JM: Nutrition management of patients with head and neck cancer during radiation

therapy. Top Clin Nutr 1:4:80-88, Oct. 1986.Heber D and Tchekmedyian NS: Nutritional assessment of the cancer patient in the office. Oncology

7:11S:71-76, 1992.Heber D: Pathophysiology and treatment of malnutrition in cancer and HIV infection. Address at 5th

Annual Advances and Controversies in Clinical Nutrition, Scottsdale, AZ, 1995.Hill T: Ethical issues in the use of fluids and nutrition: when can they be withdrawn? In Health Care Ethics.

Monagle J and Thomasma D, Eds. A.S.P.E.N. Publishers, Gaithersburg, MD, 1998.Hunter AMB: Nutrition management of patients with neoplastic disease of the head and neck treated

with radiation therapy. Nutr Clin Prac 11:157-169, 1996.


Kouba J: Nutritional care of the individual with cancer. Nutr Clin Prac 3:175-182, 1988.Lees J. Incidence of weight loss in head and neck cancer patients on commencing radiotherapy treatment

at a regional oncology centre. Eur J Cancer Care 8: 133-136, 1999.Loprinzi CL, Ellison NM, Schaid DJ, et al.: Controlled trial of megestrol acetate for the treatment of cancer

anorexia and cachexia. J Natl Cancer Inst 69:1268-1274, 1990.McCann R, Hall W, Groth-Juncker A: Comfort care for terminally ill patients: the appropriate use of

nutrition and hydration. JAMA 272:1263-1266, 1994.Mekhail TM, Adelstein DJ, Rybicki LA, et al.: Enteral nutrition during the treatment of head and neck

carcinoma. Cancer 91: 1785-1790, 2001.Souba WW and Copeland EM: Parenteral nutrition and metabolic observations in cancer. Nutr Clin Prac

3:183-190, 1988.Tayek J: A review of cancer cachexia and abnormal glucose metabolism in humans with cancer. Journal of

the American College of Nutrition 11(4):445-456, 1992.Tchekmedian NS, Hickman M, Siau, et al: Megestrol acetate in cancer anorexia and weight loss. Cancer

69:1268-1274, 1992.


Notes


Chapter Eleven:AIDS and

HIV-Positive Patients

As we are all well aware, the incidence of AIDS and HIV infection continuesto increase; now AIDS and HIV infection are perceived as chronic and long-termdiseases. This population of patients will continue to be at risk for malnutritionand, thus, may benefit from our early intervention and assistance. What causes themalnutrition seen with the AIDS and ARC (AIDS-related complex) patient? Thesepatients appear to have increased nutrient demands but have decreased intake andalterations in digestion, absorption, utilization and metabolism of the foods theydo ingest.

HIV, a retrovirus, acts by making its own DNA by utilizing genetic materialfrom the host cell. Once the virus penetrates into the cell, it eventually replicatesand destroys the functioning ability of the host cell. The virus also alters the cellmembrane and causes it to fuse to other cells, passing the virus from healthy cell tohealthy cell.

HIV affects cells that contain the glycoprotein receptor, CD4; these cells include Thelper cells, macrophages, monocytes, some B cells, and cells found in the centralnervous system. Obviously, the immune system is profoundly affected by HIV. Someeffects are shown in the chart on the following page.

Once the immune function of the patient has been impacted, the patient is atincreased risk for opportunistic infections such as protozoa, fungi, bacteria, and viruses.Some of these opportunistic infectious agents are listed on the next page.


BacteriaMycobacterium:

avium-intracellulare,tuberculosis, kansasii

LegionellaSalmonellaListeriaShigellaCampylobacterPneumococcus

FungiCandidaCryptococcus neoformansAspergillus speciesCoccidioides immitisHistoplasma capsulatum

VirusesCytomegalovirus(CMV)Herpes simplexVaricella-zoster (VZV)Epstein-Barr (EBV)Hepatitis BPapillomavirusPolyomavirus

ProtozoaPneumocystis cariniiToxoplasma gondiCryptosporidium speciesIsospora belli

Infectious Agents Common in AIDS Patients

Abnormalities characteristic of AIDSDepletion of CD4 helper T cellsElevated, normal or decreased CD8 (suppressor) cellsDecreased proliferative responses to mitogens and antigens in vitroImpaired delayed-type hypersensitivity reactionsDecreased gamma-interferon production in response to antigensDecreased humoral response to immunization (mainly primary)Decreased helper function for B-cell immunoglobulin productionDecreased macrophage-dependent T cell proliferationDecreased virus-specific cytotoxic lymphocyte function in vitro

Commonly detected abnormalitiesLymphopeniaDecreased proliferative responses to T cell and B cell specific antigensDecreased IL-2 productionDecreased: cytotoxicity to virally infected cells; monocyte chemotaxis;

immune complex formation; natural killer cell activity with normalbinding to cell

Decreased MCH class II antigen expression on monocytes & macrophages

Immune System Abnormalities in AIDS


The patient also has increased susceptibility to neoplasms, such as Kaposi’s sar-coma, non-Hodgkin’s lymphoma, squamous cell carcinoma, and small-cell undifferenti-ated carcinoma. Finally, because of the CNS involvement, the patient may develop AIDSdementia complex.

The most common gastrointestinal fungal infection is candidiasis; it generallyoccurs in the mouth and throat. Cytomegalovirus and herpes simplex virus also occurin the mouth and throat. Cytomegalovirus can also cause inflammation of the entire GItract and exhibits itself with diarrhea, steatorrhea, etc. (Moorwessel, et al., 1993).

Protozoa, such as Cryptosporidium parvum, cause watery diarrhea and malabsorp-tion. Other protozoa cause similar symptoms of malabsorption and diarrhea. Thismalabsorption causes weight loss, tissue-wasting and decreased levels of nutritionindices (Kotler and Grunfeld, 1995). The prevalence of HIV-related diarrhea may rangefrom 30 to 60 percent (Wanke, 1994). In 15 to 30 percent of patients, no pathogenic causeis found.

Antiviral therapy has advanced tremendously with the discovery of proteaseinhibitors. The drugs previously used to treat HIV, known as nucleoside analogues,inhibit the reverse transcriptase enzyme, inhibiting HIV, reducing viral load, and in-creasing CD4 T cell counts in serum (Bartlett, 1996). The newer drugs, protease inhibi-tors, prevent the HIV virus from attaching the polyproteins into a functional virus, inessence creating an immature virus that is unable to infect new cells. In patients takingprotease inhibitors, viral loads drop to undetectable levels.

As the viral load drops, so do many problems associated with HIV: immune dys-function, opportunistic infections, diarrhea, weight loss, malnutrition and death. Only10 percent of HIV+/AIDS patients take the protease inhibitors. Some of those that dofind the virus mutates and the drugs may no longer work effectively or at all. Onceprotease inhibitors are stopped, viral load again increases and the disease progresses.


Various studies have reported weight loss of 10 percent or more of usual bodyweight in 62 to 92 percent of AIDS patients studied (O’Sullivan, et al., 1985; Chelluri andJestremski, 1989; Ysseldyke, 1991). The weight loss appears to not be acute; rather, itoccurs with the presence of secondary infection — averaging 5 percent of body weightin 28 days (Grunfeld, et al., 1992). This weight loss results not only from the malabsorp-tion mentioned above, but also from decreased intake caused by anorexia and increasedenergy demands related to the disease and the infection itself.

Assessment of nutrient requirements for the patient with HIV may be difficult.No specific requirements have been established for the HIV and/or AIDS patient.Reports have shown an increase over REE of anywhere from 0 to 60 percent, depend-ing on whether the patient is hypermetabolic or acutely ill (Grunfeld, et al., 1992;Kotler, et al., 1991).

BEE can be determined and an appropriate stress factor can be applied, dependingupon the patient’s individual needs (see Chapters Four and Five). Typically, stablepatients require 30 kcal/kg (Hellerstein, 1996). Protein needs vary from 0.8 to 1.25 g/kgfor stable patients and 1.5 to 2 gm/kg for symptomatic patients (Gerrior, et al., 1997).


Define goals: To achieve repletion? Or maintain visceral and somatic protein stores?Remember, refeeding can lead to increased fat mass with minimal changes in LBM.

The patient with AIDS and ARC may be treated with a variety of medications and/or chemotherapy. Zidovudine (AZT) is a commonly utilized drug in the treatment ofAIDS but may alter the patient’s sense of taste and cause nausea and/or vomiting.

Many of the antibiotics utilized to treat the opportunistic infections (i.e. sulfadiaz-ine, pyrimethamine, ampicillin, chloramphenicol, amphotericin B, nystatin, ganciclovir,acyclovir, etc.) can cause anorexia, nausea, vomiting, and diarrhea. Chemotherapeuticagents utilized to treat the various malignancies that may occur can all have effects onthe GI tract and may affect intake.

NUTRITION SUPPORT

Optimally, the patient should be encouraged to increase intake via the oral route.You might advise him/her to try small frequent meals, utilizing calorically dense foods.Consistency of foods may require altering if the patient has difficulty chewing or swal-lowing due to an infection in the mouth or esophagus or because of medication whichcauses stomatitis.

Dietary treatment of diarrhea depends upon the cause of the diarrhea. Supplemen-tation with MCT may be of benefit, as may use of noncellulose fibers (pectin, guar gum,soy polysaccharide). At least 50 per cent of AIDS patients have gastrointestinal tractproblems at some point; malabsorption occurs in 30 to 60 per cent of these patients(Craig, et al., 1997).

Anorexia that frequently occurs with AIDS may occur with the use of AZT, at leastinitially. Other more experimental drugs that have been used for the treatment of anor-exia, both in this population and in patients with cancer, include dronabinol andMegace™. Dronabinol naturally occurs in marijuana and has been given in a dose of 2.5mg before lunch and dinner (VonRoenn, 1993). However, no significant weight gain hasbeen associated with treatment with dronabinol. Megace™ appears to stimulate appe-tite, significantly increase food intake and cause weight gain in about one-third oftreated patients (Gregory, et al., 1985; Kotler, 1997). However, the weight gain appears tobe in fat rather than in lean body mass (Kotler, 1997).

Because the AIDS patient is at risk for opportunistic infections, he or she is atincreased risk for food-borne illnesses. Care should be taken in food preparation toassure that the patient is not exposed to food-borne illnesses.

If the patient is unable to adequately consume enough nutrients orally, enteralfeedings may be of benefit. Only commercially prepared sterile products should beutilized. The patient may well tolerate intact nutrient formulas, but may require peptideor elemental formulas. High fiber formulas may be helpful.

Several formulas that appear to be well tolerated and may enhance immune func-tion are available. [Impact™ (Sandoz Nutrition), Advera™ (Ross Labs), and Immun-Aid(Clintec)]. While Advera™ has been studied specifically on AIDS patients, Impact™ hasnot. Take care to assure that the formula does not become contaminated (closed tubefeeding systems may be beneficial).


Parenteral nutrition support may be utilized to supplement oral or enteral intakeor provided instead of oral or enteral intake if the gastrointestinal tract is not functionalor the individual does not tolerate enteral nutrition support.

AIDS is known to affect metabolism as well, as indicated in the chart below

Guidelines suggested for other disease states apply here in that adequate, but notexcessive, calories from dextrose and fat are given and that adequate protein intake isprovided. Requirements for calories are 25 to 35 kcal/kg in the acutely ill patient; with40 kcal/kg in the chronic patient to promote weight gain. Protein intake should be 1 to1.5 gm/kg/d (Bell, et al., 1998). Multivitamins and trace elements should be added aswell. The diarrhea and steatorrhea associated with AIDS may cause increased losses ofB6, B12, folate, selenium, zinc, calcium, and magnesium (Bell, et al., 1998). TPN is givenand monitored in much the same way as with other illnesses.

Pharmacological intervention may stimulate protein anabolism or reverse meta-bolic abnormalities (Hellerstein, 1996). Growth hormone (GH) supplementation re-sulted in positive nitrogen balance and increased fat oxidation with a resultant increasein lean body mass and body weight. Side effects include diabetes, hyperlipidemia,carpal tunnel syndrome, and acromegaly.

The patient with HIV or AIDS is often highly motivated and actively involved inhis or her medical care. They often do well with home nutrition support and tend to bevery compliant with whatever is suggested and works. Nutrition assessment andsupport of the HIV and AIDS patient is often very beneficial to the patient and reward-ing to the nutrition care practitioner.

CASE STUDY

SF was a 32-year-old male admitted with the diagnosis of AIDS, brain abscess(Aspergillus), and right hemiplegia. He was first diagnosed with AIDS in June of 1993when he presented with Pneumocystis carinii pneumonia.

Organ FailureLateEarly

+++±

++++++

++++

++++

Hyper-metabolism

StarvationAdaptedEarly

++++

++

++++

+++

++++

++++

REEGlucose useFat useAmino acid useWeight loss

+ = mild ++ = moderate +++ = severe Adapted from Cerra, 1987

Metabolic Abnormalities in AIDS


Upon this admission, he related a three-week history of anorexia, nausea, vomit-ing, and headache; he had chronic diarrhea. He had lost 10 lb over the previous monthand was 68 kg on a 6’1" frame (83 percent of IBW). His protein stores appeared intact,with a serum albumin of 4.8. His needs were assessed to be 2500 to 2800 kcal/day and80 to 160 gm protein/day. He was placed on a diet as tolerated and supplemental TPN(1214 kcal, 60 gm protein).

Further work-up revealed the presence of two additional opportunistic infections:molluscum contagiosum and Pseudomonas. He was placed on amphotericin B andrifampin and was given Pneumocystitis carinii pneumonia prophylaxis medications.His PO intake was poor; TPN was increased to 60 ml/hr (1457 kcal 72 gm protein). Hisneurological status began to deteriorate and he developed intractable hiccups. Hisalbumin dropped to 3.4.

TPN was increased to 75 ml/hr (1822 kcal, 90 gm protein) with a goal rate of 100ml/hr (2428 kcal, 120 gm protein) to accompany his limited PO intake. His headachecontinued, causing worsening of his symptoms of nausea and vomiting.

He then became confused and dysarthric and was consuming only liquids. Hisalbumin dropped to 2.5. He developed chills and fever, along with projectile vomitingand ileus. TPN continued, with a goal of 100 to 115 ml/hr.

Comfort care was recommended when evidence of progressive invasion of theAspergillus in his brain appeared and he suffered a pontine infarct. TPN and the antibi-otics were discontinued and a morphine drip was initiated. Cheyne-Stokes respirationsbecame evident and the patient further deteriorated until he expired.

REVIEW QUESTIONS

1. What diseases appear to opportunistically impact the GI tract in the AIDS patient?2. What drugs are used to increase appetite in HIV patients?

REFERENCES

Bartlett JG: Protease inhibitors for HIV infection. Annals of Intern Med, 124(12):1086-1088, 1996.Bell SJ, Gramlich LM, Wanke C, et al.: HIV and AIDS. In: Dietitian’s Handbook of Enteral and Parenteral

Nutrition, 2nd ed. Skipper A, Ed. Gaithersburg, MD. A.S.P.E.N. Publishers, Inc., 1998.Chelluri L, Jestremski MS: Incidence of malnutrition in patients with acquired immunodeficiency syn-

drome. Nutr Clin Prac 4:16-18,1989.Craig C, Darnell B, Weinsier R, et al.: Decreased fat and nitrogen losses in patients with AIDS receiving

medium chain triglyceride-enriched formula vs. those receiving long chain triglyceride-containingformula. JADA 97:605-611, 1997.

Fields-Gardner C: A review of mechanisms of wasting in HIV disease. Nutr Clin Prac 10:167-176, 1995.Gerrior JL, Bell SJ, Wanke CA. Oral nutrition for the patient with HIV infection. Nurs Clin North Am

32(4):813-830, 1997.Gregory EJ, Cohen SC, Oives DW, et al.: Megestrol acetate therapy for advanced breast cancer. J Clin Oncol

3:155-160, 1985.Grunfeld C, Pand M, Shimuzu L, et al.: Resting energy expenditure, caloric intake, and short-term weight

change in human immunodeficiency virus infection and the acquired immunodeficiency syndrome.Am J Clin Nutr 55:455-460, 1992.


Hellerstein M: The spectrum of nutrition support for AIDS. Address at 5th Annual Nutrition SupportUpdate, San Diego, 1996.

Kotler DP, Tierney AR, Ferraro R, et al.: Enteral alimentation and repletion of body cell mass in malnour-ished patients with acquired immunodeficiency syndrome. Am J Clin Nutr 53:149-154, 1991.

Kotler DP: Lecture at A.S.P.E.N. 21st Clinical congress, Jan 1997.Moorwessel M, Hopkins B, Buzby KM: Human immunodeficiency virus infection. Nutrition Support

Dietetics, 2nd ed. Gottschlich MM, Matarese LE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD,1993.

O’Sullivan P, Linke RA, Dalton S: Evaluation of body weight and nutritional status among AIDS patients.JADA 85:1483-1484, 1985.

Von Roenn JH: Pharmacologic interventions for HIV-related anorexia and cachexia. Oncology 7:11S:95-99,1993.

Wanke C: Diarrhea and malnutrition in AIDS patients: incidence, etiology, and pathophysiology. CurrentNutritional Consultations. Mead Johnson & Company, Evansville, IN, 1994.

Ysseldyke LL: Nutritional complications and incidence of malnutrition among AIDS patients. JADA91(2):217-218, 1991.


Notes


Chapter Twelve:Transition to Home Care

Once your patient is no longer in crisis, the road to complete recovery is justbeginning. While most patients are able to resume oral intake and eventually return to asomewhat normal lifestyle, some patients will require long-term enteral or parenteralnutrition support at home.

There are many resources available to the patient going home on nutrition support.Your hospital social workers, case managers, and discharge planners are excellentresources for determining the best possible choices for the patient going home withnutrition support.

Home care providers are widespread, but vary in the type and quality of careprovided. Both the hospital resource people (discharge planners and social workers)and these home care agencies should be familiar with what is required by the HealthCare Financing Administration (HCFA) for determining eligibility for home care.

HCFA has also developed guidelines for reimbursement for home nutrition sup-port, which should be monitored when considering a patient for home nutrition sup-port. Home nutrition support can be very expensive and care should be taken to assurethat the patient has adequate insurance coverage or other resources to be able to affordthe home nutrition support regimen.

A.S.P.E.N. has developed Standards for Home Nutrition Support (Standards forHome Nutrition Support, 1988). The standards cover guidelines for provision of homenutrition support, patient selection, care plans, implementation, monitoring and guide-lines for termination of therapy.

The Dietitians in Nutrition Support practice group of ADA has developed a starterkit for dietitians involved with home care — this packet is very helpful and can beordered through the American Dietetic Association. Nutrition in home care and homenutrition support are also covered in other Nutrition Dimension home study courses.


GUIDELINES FOR HOME NUTRITION SUPPORT

Patients unable to meet their nutrient requirements with oral intake are candidatesfor enteral nutrition support. Those unable to meet nutrition needs with enteral nutri-tion because of inadequate gut function are candidates for parenteral nutrition support.

The patient’s home environment must be safe and stable and the patient’s medicalcondition must be stable enough to allow for discharge. The formula and the mode ofnutrition support utilized for home care must be appropriate for the medical conditionof the patient and should be as safe and as cost-effective as possible.

The patient going home on either enteral or parenteral nutrition support should betolerating the chosen method of support at adequate levels to meet his or her nutritionneeds before discharge. Changes should be made while the patient is in the hospital. Forexample, if a patient is to receive all of his enteral feedings while he sleeps, a morenutrient-dense formula might be in order (to insure that adequate nutrients are pro-vided during a shorter time span). This change in formula should be accomplishedwhile the patient is still hospitalized so that problems and any necessary alterations canbe identified. TPN/enteral feedings can be initiated at home with appropriate educationand follow-up, if necessary.

Patient education is important. A.S.P.E.N. has identified these key areas: Thepatient must know the type and amount of formula he is to receive, should understandthe method of infusion and should be taught proper technique for administration offeedings or TPN.

He should be taught that enteral feedings should not hang for longer than 8 to 12hours (or 24 hours if a closed feeding system is utilized) or that parenteral formulas shouldnot be left at room temperature for longer than 24 hours. He must be shown how to in-spect parenteral admixtures visually for integrity and abnormalities (Standards, 1988).

The patient receiving enteral nutrition support should be taught clean techniques,how to maintain the access site, and how to flush the tube, usually with water, afterfeeding to maintain patency.

Instruction on care of the TPN access route should be emphasized. Dietitians andnurses can teach the patient receiving parenteral nutrition aseptic technique for dressings,connection and disconnection of the IV tubing and flushing of the tubing after infusion.

The patient and caretaker should be made aware of any potential problems withcare of the equipment or complications associated with the provision of nutrition sup-port. He should have a contact to call with problems or questions and a health careprovider on 24-hour availability.

Routine monitoring systems should be set up for the patient. Monitoring caninclude home visits, telephone calls, return visits to the hospital or physician’s office,etc. Monitoring should include adequacy of nutrient intake, investigation for possibilityfor drug-nutrient interactions, weight changes, biochemical and other assessment datato determine tolerance to therapy, and physical examination (Standards, 1988).

Ideally, the patient will be followed by a home nutrition support team, comprisedof a physician, registered nurse, registered dietitian, and registered pharmacist. Nutri-tion care plans should be routinely reviewed and revised to best and most appropriatelymeet the patient’s nutritional requirements.


HCFA has established these guidelines for reimbursement eligibility:• The patient is receiving feeding via a feeding tube and has a limitation with

ingestion, digestion, or absorption (Medicare guidelines, 1996).• The formula comprises the patient’s entire nutrition intake.• Expected length of nutrition therapy is longer than 3 months.• Documentation for the necessity of a feeding pump is available (i.e. aspiration,

chronic diarrhea).• Enteral intake is between 20 to 35 kcal/kg, unless further documentation is

provided to support a greater kcal intake (Cappoza, 1996).• Premixed parenteral solutions have necessity documented and the simplest

infusion pump is utilized (Weckworth, 1993).• The patient must have access to proper tube placement.

• Contraindications to home enteral feedings include:- a temporary impairment of the gastrointestinal tract (less than 90 days).- severe malabsorption preventing absorption of nutrients- enteral feeding is required because of anorexia- enteral feeding is utilized only as a supplement (Medicare)

• Requirements for total parenteral nutrition include:- a severe pathology of the GI tract which “prevents adequate absorption of sufficient nutrients to maintain weight and strength commensurate with the patient’s general condition” (Medicare)- TPN is required for longer than 3 months- adequate nutrition is not possible via oral or enteral routes- TPN provides intake of 20 to 35 kcal/kg; anything other than this requires

special documentation- Protein intake is from 1.0 to 1.5 gm/kg/day; any other intake requires special

documentation- Pt must have central venous access- Evidence must exist that enteral or pharmacological interventions have been

attempted without success

• Contraindications to home TPN include:- Ability to safely and effectively utilize GI tract- GI impairment is temporary- Patient is metabolically unstable- TPN is supplemental to oral or enteral intake


In 1995, the Joint Commission on Accreditation of Healthcare Organizations(JCAHO) released nutrition care standards for home care. The standards include:

• Interdisciplinary nutrition care planning is performed, as appropriate, as part ofthe patient’s care. The patient’s nutritional status must be assessed. (This can becompleted by a “qualified health care provider”, i.e. a nurse, dietitian, physician,or pharmacist.)

• Authorized individuals (i.e. physician) prescribe or order food and nutritiontherapies.

• Responsibility for the preparation, storage, distribution, and administration oforal, enteral, and parenteral nutrition is defined and assigned.

• Food and nutrition therapies are prepared and stored under proper conditions ofsanitation, temperature, light, moisture, ventilation, safety, and security toprevent bacterial growth and contamination.

• Food and nutrition therapies are distributed and administered in a safe, accurate,and a timely manner to the patient for whom they have been prescribed orordered.

• The organization has a process for providing food or nutrition therapy when dietor diet schedules are altered, i.e. transitional feedings.

• Each patient is monitored on an ongoing basis for the effectiveness and appropri-ateness of nutrition therapies (JCAHO, 1997).

• Each home care company or provider must interpret these guidelines and definehow each standard will be met. Potentially, the nutrition screening initiativecould be utilized to determine those patients at risk. The Level I screen is a basicscreen that can be utilized by nursing on their initial visit to identify patients atnutrition risk. The Level II screen can then be utilized to identify specific riskfactors for moderate to high risk patients (NSI, 1992).

COMPLICATIONS OF LONG-TERM TPNComplications of long-term TPN include metabolic bone disease, cholestasis,

chronic liver disease, carnitine and taurine deficiency, and changes in vitamin and traceelement nutriture. We should be aware of the possibility of these complications andmonitor for changes accordingly with laboratory testing, as shown on the followingpage.

Metabolic bone disease is difficult to treat. Liver complications can be reduced byavoiding overfeeding, and scheduling cycled feedings, oral or enteral feedings to pre-vent cholestasis, and discontuining TPN. Supplementation of necessary carnitine,taurine, vitamins and trace elements can prevent deficiencies (McCrae, 1989).


Home nutrition support is growing by leaps and bounds. More and more of ourpatients will require and receive home nutrition support in the future. Our job is toinsure that this therapy is of benefit to them, is safe, and provides adequate nutrients tothem to sustain their lives.

REFERENCES

Accreditation Manual for Home Care, 1997-87. Joint Commission on Accreditation of Health CareOrganizations, Oakbrook Terrace, IL. 1997.

Cappoza C: Reimbursement and Medicare Standards. Support Line XVIII:6:6-8, 1996.DMERC Region D Supplier Manual: US Dept. of Health and Human Services, 1996.McCrae JD: Home parenteral nutrition. Dietitian’s Handbook of Enteral and Parenteral Nutrition. Skipper A,

Ed. A.S.P.E.N. Publ., Rockville, MD, 1989.Nelson JK and O’Shea R: Home nutrition support: enteral and parenteral. Nutrition Support Dietetics.

Shronts EP, Ed. A.S.P.E.N., Silver Spring, MD, 1989.The Nutrition Screening Initiative: Washington, DC: pub. A5944, March, 1992.Standards for Home Nutrition Support: Nutr Clin Prac 3 (5) 202-205, 1988.Weckwerth J, Nelson JK, and O’Shea R: HCFA guidelines: Home nutrition support. In: Nutrition Support

Dietetics, 2nd ed. Gottschlich MM, Matarese LE, Shronts EP, Eds. A.S.P.E.N., Silver Spring, MD, 1993.

Lab Monitoring for Long-term TPN

Metabolic bone diseaseTest for vitamin D nutriture, calcitonin & parathyroid hormoneIonized calcium, biochem panelUrinary calcium, phosphorus, ureaUrinary sodium and creatinine

Liver complicationsLiver function testsBiopsy

Carnitine deficiencyPlasma carnitine

Taurine deficiencyPlasma taurine

Vitamins and trace elementsPlasma levels


Notes

131©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

CHAPTER ONE: NUTRITION ASSESSMENT

1. Anthropometrics typically measure chronic, not acute, changes in nutritional status.

2. The best measures of protein production in the critically ill patient are transferrin,thyroxine-binding prealbumin, and retinol-binding protein.

3. Factors affecting parameters of protein status include liver disease, infection, post-operative status, stress, fluid imbalance, renal disease and dialysis.

4. Utilizing actual weight (within range for IBW) of 59 kg x 25 kcal/kg = approximately1500 kcal/day. Protein needs are based upon 150:1 Kcal/N ratio; therefore are1500/150 = 10 x 6.25 = 62.5 gm protein. However, in trauma patients, protein needsare usually estimated at 1.5 to 2.0 gm protein/kg, thus 90 to 120 gm protein/d.

5. Utilizing Ireton-Jones equation for ventilated patient: 1784 -11(75) +5(93 kg) +244 (1)+ 239 (0)+804 (0) = 1668 kcal. Protein needs are determined by cal:N ratio of 150:1 =69.5 gm protein.

Notes:

CHAPTER TWO: ENTERAL NUTRITION

1. A duodenal or jejunostomy tube could be effectively used post-gastrectomy.

2. For a CVA patient, an isotonic intact nutrient formula via a gastrostomy tube or anasogastric tube into the duodenum would likely be well tolerated.

3. A nutrient-dense formula should be used to assure adequate provision of nutrientswith additional water as needed.

4. Review medications and antibiotics that may precipitate diarrhea, including sorbitol,potassium elixirs, lactulose, and hypertonic solutions. The patient may benefit fromthe addition of fiber to the diet, either by utilizing a fiber-rich formula or by addingfiber to the existing formula. Make sure that the feeding is at isotonicity. Stools couldbe tested for growth of pathogenic bacteria. Recommendations for anti-diarrhealmedications could be made, as well.

5. For the critically ill patient, feedings should be given continuously into the duode-num or jejunum (distal to the ligament of Treitz).

Review Question Answers

132©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.


6. With high gastric residuals, the feeding may be held. You should assure that thefeeding is isotonic. You could recommend that feedings should be into the smallbowel since obstruction in the stomach does not necessarily mean there is also anileus in the small bowel.

7. A patient in a long-term care facility may best tolerate intermittent feedings, utilizinga closed system of enteral formulas via gastrostomy or jejunostomy.

Notes:

CHAPTER THREE: PARENTERAL NUTRITION

1. TPN may be implemented since ileus is likely in the stomach and small bowel, andsince the patient had been receiving nothing by mouth for five days The patient isalready underweight and would benefit from TPN until enteral feedings can beimplemented. Transition to enteral feedings should be made as early as possible.

2. Recommend that central venous access be attained or recommend that a formulawith a final dextrose concentration of less than D10 be utilized. A formula with afinal dextrose concentration of more than 10 percent will not be tolerated in a pe-ripheral vein. The final concentration of the TPN formula ordered is greater than10%.

3. First check for signs of infection (reddening, puffiness) around IV site and changesite, as necessary, culturing for growth of bacteria. Since the patient is not toleratingfat, you could recommend removal of lipid from TPN regimen. Suggest insulincoverage for increased glucose levels and monitor BUN and creatinine levels forfurther alteration in renal function, because current levels are acceptable and mayreturn to normal as renal function improves (but no change in formula is indicatedfor now).

4. Attempt enteral or oral feedings as soon as possible. Make sure that the patient is notbeing overfed or is not receiving excess calories from dextrose via his TPN.

5. Suggest increased calories from fat be provided (up to a level of 40 - 50% caloriesfrom fat), with calories from dextrose decreased. Increased calories from fat are oftenbeneficial in efforts to decrease carbon dioxide production, improve respiratoryquotient and improve the patient’s chances of weaning from the ventilator. Assurethat patient’s nutrient requirements are met, but that patient is not overfed. If youhave a metabolic cart, measure CO2 production and O2 consumption to determinethe appropriate mix of nutrients. If CO2 production is greater than it should be, youmay be overfeeding the patient in total calories and/or carbohydrate calories.

133©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

6. 80 ml/hour x 24 hours = 1920 ml or 1.92 liters400 ml dextrose x 0.5 (% dex) = 200 gm dextrose x 3.4 kcal = 680 kcal x 1.92 liter =1306 kcal (dextrose)400 ml aa x .12 (% aa) = 48 gm x 1.92 liter = 92 gm protein x 4 kcal/gm = 369 kcal

(protein)200 ml lipid x 2 (kcal/ml) = 400 kcal x 1.92 liter = 768 kcal (fat)

Total kcal: 2443Nonprotein kcal: 2075Protein: 92 gm

7. 50 ml /hour x 24 hours = 1200 ml or 1.2 liters1200 ml total = 600 ml each of dextrose and amino acid600 ml x 0.5 (% dex) = 300 gm x 3.4 kcal = 1020 kcal from dextrose600 ml x 0.10 (% amino acid) = 60 gm protein x 4 kcal = 240 kcal from protein500 ml x 2.0 (kcal/ml in 20% lipid) = 1000 kcal from lipid

Total calories: 2260 kcalNonprotein kcal: 2020 kcalProtein: 60 gm

Notes:

CHAPTER FOUR: GASTROINTESTINAL DISORDERS

1. Start enteral feedings soon after post-op, via J-tube or into stomach or duodenum,with isotonic intact protein formula. Taper enteral feeding slowly as patient’s oralintake increases through intake of antidumping diet and/or small frequent feedings.

2. Dumping syndrome may occur with decreased tolerance to concentrated sweets andsugars and the need to limit fluid intake with meals. Slow feedings and/or smallfrequent meals will be necessary initially, advancing later to a less restrictive regi-men.

3. TPN may be required initially after surgery. Taper TPN as other modes of feeding aretolerated. Closely work with patient to provide well-tolerated formulas or foods.Initially, patient may require lactose-free and low-fat formulas (and, in some cases,an elemental or peptide formula). Feedings should be given in a small volume with acontinuous feeding. Patient can later be transitioned to oral intake, slowly with a low-residue, lactose-free diet in frequent small feedings. Consider supplementation with amultivitamin/mineral.


768 kcal from fat ÷ 2443 kcal = 31% kcal from fat92 gm protein ÷ 6.25 = 14.7 gm nitrogenCalorie:nitrogen ration 141:1

1000 kcal from fat ÷ 2260 kcal = 40% kcal from fat60 gm pro ÷ 6.25 = 9.6 gm nitrogen2020 nonprotein kcal ÷ 9.6 = 210Calorie: nitrogen ration 210:1

134©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.


4. Recommend TPN, including lipid if no evidence of fat intolerance is noted.Notes:

CHAPTER FIVE: STRESS AND SEPSIS

1. Changes with stress include: increased catecholamine production with decreasedinsulin and increased glucagon; increased secretion of ACTH; increased glucocorti-coids and mineralocorticoids (which later return to normal); increased synthesis (butdecreased utilization) of glucose; increased use of amino acids for energy; and ketosis.

2. A mix of CHO and fat calories with fewer than 30 - 40% calories from fat should beused. Optimally, fat should be provided with a mix of Ω-3 and Ω-6 fatty acids. IfCHO-intolerant, limit dextrose infusion to less than 5 mg/kg/minute.

3. 108 to 144 gm protein per day, utilizing a factor of 1.5 to 2.0 gm pro/kg/day becauseof the increased level of stress.

Notes:

CHAPTER SIX: OBESITY AND DIABETES MELLITUS

1. First, determine the adjusted ideal body weight:Actual weight: 100 kg; IBW: 50 kg

100 kg - 50 kg = 50 kg x .2 = 10 kg + 50 kg = 60 kg (adjusted ideal body weight)Using 60 kg and a factor of 25 - 30 kcal/kg (factors for moderate to severe stress,page 71), determine estimated caloric needs: 1500 - 1800 kcal/day. Use the idealbody weight to determine protein requirements: 75 - 100 gm pro/day (using factorsof 1.5 - 2 gm pro/kg/day.)

2. Patient is at his Ideal Body Weight.. Needs are estimated at 2250 kcal/day, basedupon 25 kcal/kg and considering that we do not want to overfeed this patient whois facing a difficult wean from the ventilator. Protein needs are estimated at 90-135gm protein/day (using a factor of 1.0 – 1.5 gm protein/kg/day with acute renalfailure). Enteral feedings should be attempted with the usual isotonic formula – nota renal formula, unless electrolyte disturbances are noted.

Notes:

135©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.


CHAPTER SEVEN: RESPIRATORY FAILURE

1. Enteral feedings for the intubated patient are not only possible, but also optimal.Feeding tubes should be placed in the duodenum and the patient’s head shouldremain at a 45-degree angle to his body to decrease aspiration.

2. For the CO2 retainer who is being weaned from the ventilator, a mix of calories withabout 60% calories from fat would be used. Care should be taken not to overfeed thepatient either calories or protein.

3. Caloric requirements for this 45 kg female would be about 1100 - 1300 kcal (25-30kcal/kg), with reduced calories given if respiratory distress increases (increaseddyspnea, decreased pO2, increased pCO2, etc). Protein requirements would be 68 - 90gm/day. Recommend enteral feedings if possible with an isotonic, intact proteinformula through the duodenum or jejunum.

Notes:

CHAPTER EIGHT: RENAL DISEASE

1. Nutritional parameters of use in assessing the renal failure patient would includeheight and weight, weight changes, transferrin levels and physical exam.

2. All water soluble vitamins should be supplemented in renal failure, with increasedamounts of B6 (10 mg), C (100 mg) and folate (1mg) over the RDA.

3. Caloric requirements are 2000 - 23300 kcal/day; protein requirements are 75 - 90 gm/day. Recommend TPN since bowel is not functioning; utilize usual amino acidformula or solution. A possible formula might be: : 400ml D18, 400ml amino acids5%, 200 ml 20% intralipid @ 85ml/hr. This would provide about 2600 nonproteincalories, 77 gm of protein, and 2900 total calories. Supplement with water solublevitamins, and monitor trace elements if on TPN for an extended period. Limit addi-tion of phosphorus and potassium. Begin low rate enteral feedings with isotonicconventional formula as soon as possible. Transition off TPN and enteral feedings asable to tolerate normal renal diet.

4. Caloric requirements: Adjusted body weight 62 kg x 25 = 1550 kcal. Protein needsare 59kg (based on IBW) x 1.2 = 71 gm protein. If the patient is able to tolerate en-teral feedings, recommend conventional formula, adjusting to a renal formula ifelectrolyte disturbances persist.

Notes:

136©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.


CHAPTER NINE: LIVER DISEASE

1. You must consider changes in CHO metabolism and the possibility of hypo- or hy-perglycemia, changes in fat metabolism and development of fatty liver, increasedprotein needs but decreased ability to utilize protein, and alterations in storage,synthesis and transport of vitamins and minerals.

2. Use IBW of 57 kg since pt may have ascites, resulting in calorie needs of 1400 to 1700kcal/d (25 to 30 kcal/d) and 57 to 85 gm protein/day (1 to 1.5 gm protein/d).

Notes:

CHAPTER TEN: CANCER PATIENTS

1. 1300 - 1500 kcal/day, 50 - 125 gm pro/day. Based on a factor of 25 - 30 kcal/kg/dayand 1.0 - 2.2 gm pro/kg/day as indicated by increased stress level. Additionalcalories can be added to allow for weight gain.

2. Alterations in taste and smell; difficulty in swallowing; decreased secretions leadingto dry mouth.

Notes:

CHAPTER ELEVEN: AIDS & HIV-POSITIVE PATIENTS

1. The following diseases appear to opportunistically impact the GI tract in the AIDSpatient: candidiasis, cytomegalovirus, herpes simplex and various protozoa.

2. The drugs used to increase appetite are Dronabinol and Megace (megastrol acetate).Notes:

137©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Physical Changes with Malnutrition

Condition Deficiency

Hair easily pluckable, dyspigmented Protein-calorie 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

Tongue magenta Riboflavin glossitis Niacin, folate, iron, B6, B12

Skin xerosis Vitamin A, essential fatty acids follicular hyperkeratosis Vitamin A, essential fatty acids petechiae, ecchymoses Vitamin C, Vitamin K

Nails koilonychia Iron

Muscle wasting Protein-calorie malnutrition

Beading of ribs Vitamin D and calcium

Appendix #1

138©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

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 TablesMen (age 25-59) Women (age 25-59)

Ideal Creatinine Height Weight Excretion Creatinine (inches) (lb) (mg/24 hrs) Height Index

8.178.288.368.408.518.628.768.868.989.119.249.389.499.619.80

128813251359138614261467151815551596164216911739178518311891

585960616263646566676869707172

102-111103-113104-115106-118108-121111-124114-127117-130120-133123-136126-139129-142132-145135-148138-151

Men are wearing 5 lb of clothing, and shoes with 1-inch heels Women are wearing 3 lb of clothing and 2-inch heelsSource: Metropolitan Life Insurance Company, 1983.

124127130133137141145149153158162167171176181

585960616263646566676869707172

101104107110113116119123128132136139143147151

Ideal Creatinine Height Weight Excretion Creatinine (inches) (lb) (mg/24 hrs) Height Index

83085187590092594997710061044107611091141117412061240

Creatinine Height Index

626364656667686970717273747576

5.635.685.745.815.875.936.016.096.236.326.426.516.606.696.78

Appendix #2

Men Women

139©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

5

226

238

243

247

239

236

223

10

237

245

250

255

249

245

235

25

252

257

264

269

265

260

251

18

19

25

35

45

55

65

%

Male Female

AGE

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

90

237

236

246

257

260

266

264

95

245

249

264

272

274

280

279

Anthropometric Measurement Standards

Source: Frisancho, A.R..American Journal of Clinical Nutrition, 1981, 34:2540-2545

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

AGE

Triceps Skinfold Percentiles (mm)

Arm Muscle Circumference (mm)

Appendix #3

140©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Nutrient Absorption

Stomach Intrinsic factor secretion

Duodenum Vitamin A, B1, iron, calcium, glycerol and fatty acids, monoglycerides,

amino acids, mono- and disaccharides

JejunumEntire: Glucose, galactose, ascorbic acid, amino acids, glycerol and fatty acids,

monoglycerides, folic acid, biotin, copper, zinc, potassium,vitamins D, E, B

1, B

2, B

3, B

6, iodine, magnesium, calcium, phosphorus

Proximal: Vitamin A, folic acid, iron, disaccharidesDistal: Disaccharides, dipeptides

IleumEntire: Sodium chloride, vitamins D, E, B

1, B

2, B

3, B

6, iodine, magnesium,

calcium, phosphorusProximal: Disaccharides, potassiumDistal: B

12 and intrinsic factor

ColonEntire: Water, Vitamin KTransverse: Water, biotin

Appendix #5

Appendix #4

Non-nutritional Factors Affecting Serum Proteins

Albumin Transferrin Prealbuminhydration status iron deficiency renal diseasenephrotic syndrome pregnancy liver diseaseburns chronic illness stressliver disease blood loss surgeryacute stress infection infectioneclampsia liver disease dialysisinfection uremia chronic illnesstrauma nephrotic syndrome hydration statussurgery increased iron storeschronic illness hydration status

surgery

141©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Name_______________________________ Rm#____________________________Doctor______________________________ Diagnosis_______________________Formula_____________________________ IV Rate____________ ml/hr____________________________________ Calorie/Nitrogen ratio__________________________________________________ Height ________Patient Needs: Calories/day_____________ Protein gm/day____________

TPN Monitoring Form

Appendix #6

Date

Weight

Intake Total

IV

PO

Other

Non-Pro kcal PO

IV

Pro Intake PO

IV

Total

BUN

Creatinine

Na

K

CL

CO2

Ca

PO4

Glucose

Total Protein

Albumin

HGB/HCT

GGT

Alk Phos

Amylase

Total Bilirubin

Magnesium

Transferrin

Cholesterol

Triglycerides

WBC

Total Lymphocytes

PT

UUN

Nitrogen Balance

Other

Charted

142©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Appendix #7

34

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

5*

5*

5*

5*

10*

15*

5*

5*

5*

5*

10*

15*

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

400i

400i

400i

400

400

1.8

2.4

2.4

2.4

2.4h

2.4h

1.8

2.4

2.4

2.4

2.4h

2.4h

MALES

FEMALES

Vitamins

Dietary Reference Intakes:Recommended Dietary Allowances & Adequate Intakes

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)e

Vita

min

B 12 (µ

g)

Fola

te (m

cg)f

Thia

min

(mg)

Vita

min

C (m

g)

Ribo

flavi

n (m

g)

Vita

min

E (m

g)d

Vita

min

D (m

cg)b

,c

Vita

min

K (m

cg)

Prot

ein

(gm

)

Age

Vita

min

A (m

cg)a

NOTE: This table (taken from the DRI reports, see www.nap.edu) presents Recommended Dietary Allowances (RDAs) in bold type andAdequate Intakes (AIs) in ordinary type followed by an asterisk (*). RDAs and AIs may both be used as goals for individual intake. RDAs areset to meet the needs of almost all (97-98%) individuals in a group. For healthy breastfed infants, the AI is the mean intake. The AI for otherlife stage and gender groups is believed to cover needs of all individuals in the group, but lack of data or uncertainty in the data prevent beingable to specify with confidence the percentage of individuals covered by this intake.

a As retinol activity equivalents (TAEs). 1 RAE=1 mcg retinol, 12 mcg β-carotene, 24 mcg α-carotene, or 24 β-cryptoxanthin. The RAE fordietary provitamin A carotenoids is twofold greater than retinol equivalents (RE), whereas the RAE for preformed vitamin A is the same as RE.

b As cholecalciferol 1 mcg cholecalciferol = 40 IU vitamin D.c In the absence of adequate exposure to sunlight.d As α-Tocopherol includes RRR-α-tocopherol, the only form of α-tocopherol that occurs naturally in foods, and the 2R-stereoisomeric

forms of α-tocopherol (RRR-, RSR-, and RSS-α-tocopherol) that occur in fortified foods and supplements. It does not include the 2S-stereoisomeric forms of tocopherol (SRR-, SSR-, SRS-, and SSS-α-tocopherol), also found in fortified foods and supplements.

143©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Appendix #7 cont.

1,300*

1,300*

1,000*

1,000*

1,200*

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*

30*

30*

21*

24*

25*

25*

20*

20*

Minerals

Copp

er (m

cg)

Man

gane

se (m

g)Fl

uorid

e (m

g)

Chol

ine

(mg)

g

Chro

miu

m (m

cg)

Pant

othe

nic A

cid

(mcg

)Bi

otin

(mcg

)

Phos

phor

us (m

g)

Calc

ium

(mg)

Iron

(mg)

Mag

nesi

um (m

cg)

Iodi

ne (m

cg)

Zinc

(mg)

Sele

nium

(mg)

Mol

ybde

num

(mcg

)

34

43

45

45

45

45

34

43

45

45

45

45

e As niacin equivalents (NE). 1 mg of niacin = 60 mg of tryptophan; 0-6 months = preformed niacin (not NE).f As dietary folate equivalents DFE). 1 DFE = 1 mcg food folate = 0.6 mcg of folic acid from fortified food or as a supplement consumed

with food = 0.5 mcg of a supplement taken on an empty stomach.g Although AIs have been set for choline, there are few data to assess whether a dietary supply of choline is needed at all stages of the life

cycle, and it may be that the choline requirement can be met by endogenous synthesis at some of these stages.h Because 10-30% of older people may malabsorb food-bound B12, it is advisable for those older than 50 years to meet their RDA mainly by

consuming foods fortified with B12 or a supplement containing B12.i In view of evidence linking folate intake with neural tube defects in the fetus, it is recommended that all women capable of becoming

pregnant consume 400 mcg from supplements or fortified foods in addition to intake of food folate from a varied diet.j It is assumed that women will continue consuming 400 mcg from supplements or fortified food until their pregnancy is confirmed and they

enter prenatal care, which ordinarily occurs after the end of the periconceptional period - the critical time for formation of the neural tube.Sources: National Academic Press. Washington DC. 2002-2005. These reports may be accessed via http://www.nap.edu

144©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Example of Standard TPN Admixtures

Standard Central TPN Formula

Nutrient Content of One Liter of TPN

Nutrient CompositionAmino Acids 50 gm (8 gm Nitrogen)Dextrose 180 gm (612 kcal)Lipid 20 gm (200 kcal)

Nonprotein calorie to nitrogen ratio: 100:1; 20% of total calories come from fat

Final concentrationsAmino Acids 5%Dextrose 18%Lipid 2%

Standard Peripheral TPN Formula

Nutrient Content of One Liter of TPN

Nutrient CompositionAmino Acids 40 gm (6.4 gm Nitrogen)Dextrose 80 gm (275 kcal)Lipid 30 gm (300 kcal)

Final concentrationsAmino Acids 4%Dextrose 8%Lipid 3%

Nonprotein to calorie ratio: 90:1; 40% of total calories come from fat

Electrolyte Concentration (each 20 ml contains):Na 35 mEqK 20 mEqMg 5 mEq

Cl 35 mEqCa 4.5 mEqAc 30 mEq

The following electrolytes will be present in solution:Na+ 55 mEq Cl- 61 mEqK+ 30 mEq Ac 64 mEq

Electrolyte Concentration (each 20 ml contains):Na 35 mEqK 20 mEqMg 5 mEq

Cl 35 mEqCa 4.5 mEqAc 30 mEq

The following electrolytes will be present in solution:Na+ 55 mEq Cl- 61 mEqK+ 30 mEq Ac 64 mEqMg++ 5 mEq PO4 12 mMolCa++ 4.5 mEq

Vitamins and MineralsMVI-12 10 ml/24 hoursTrace elements 3 ml/24 hours

Vitamins and MineralsMVI-12 10 ml/24 hoursTrace elements 3 ml/24 hours

Osmolality 980 mOsm/L with additives

Appendix #8

145©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Computation of Nutrition Content

TPN Solution #1: 400 ml D50, 500 ml a.a. 10%, 100 ml lipid 20% @ 100 ml/hr

100 ml/hr X 24 hrs = 2400 ml or 2.4 liters400 ml D50: 400 ml X 0.5 (% dex) = 200 gm (dex) X 3.4 kcal/gm = 680 kcal dex

680 kcal X 2.4 liters (100 ml/hr X 24 hours) = 1632 kcal500 ml aa 10% : 500 ml X 0.1(% a.a.) = 50 gm (pro) X 4 kcal/gm = 200 kcal pro

200 kcal X 2.4 liters = 480 kcal pro50 gm pro X 2.4 liters = 120 gm pro

100 ml lipid 20%: 100 ml X 2 kcal/ml = 200 kcal lipid200 kcal X 2.4 liters = 480 kcal lipid

Hydrated dextrose = 3.4 kcal/gm*20% lipid = 2 kcal/ml

10% lipid = 1.1 kcal/mlProtein = 4 kcal/gm**

Determining Nutritional Values from TPN

Appendix #9

*in concentrations of 5 to 70%, noted as “D5, D40 etc.”** in various concentrations, expressed as “a.a. 5%, 10% etc.” (a.a. = amino acids)

Total calories: 1632 (dex)+480(pro) + 480(lipid) = 2592 total kcalNonprotein calories: 1632 (dex) + 480 (lipid) = 2112 nonpro kcalGrams of nitrogen: 120 gm pro ÷ 6.25 = 19.2 gm NCalorie/Nitrogen ratio: 2112 (nonpro kcal) ÷ 19.2 (gm N) = 110:1 (kcal/N)Percent calories from fat: 480 (kcal lipid) ÷ 2112 (nonpro kcal) = 23% fat kcal

TPN Solution #2: 500 ml D50, 500 ml a.a. 10.0% @ 60 ml/hr, with 500 ml lipid 10% over 10 hr, once a day

60 ml/hr = 1440 ml/day = 720 ml dex + 720 ml a.a.720 ml X .5 (% dex) = 360 gm (dex) X 3.4 kcal/gm = 1224 kcal dex720 ml X .10 (% aa) = 72 gm pro X 4 kcal/gm = 288 kcal pro500 ml X 1.1 (lipid) = 550 kcal lipid

Total calories: 1224 +288 + 550 = 2062 total kcalNonprotein calories: 1224 (dex) + 550 (lipid) = 1774 nonpro kcalGrams of nitrogen: 72 ÷ 6.25 = 11.5 gm NCalorie/Nitrogen ratio: 1774 nonpro kcal ÷ 11.5 gm N = 154:1 (kcal/N)Percent calories from fat: 550 (kcal lipid) ÷ 1774 (nonpro kcal) = 31% fat kcal

(per liter)

146©

199

1-20

09 N

utrit

ion

Dim

ensi

on, I

nc.

Metabolic Complications of TPN

Condition Treatment

Correct electrolytes in formula, slow downthe rate of feeding and monitor carefully

Monitor glucose 6x/day, adjust insulindose, increase lipid calories, decreaseCHO calories if possible

Immediate glucose infusion; monitorglucose; taper off TPN gradually

Limit lipid emulsions to every other day, iftolerated and meets caloric needs

Decrease potassium in formula

Increase potassium in TPN; determine ifthere are unrecognized losses

Increase PO4 supplementation (can be

done in the TPN). Monitor other minerals.

Decrease PO4 in TPN. Individualize. Often

no PO4 is given.

Adjust formula

Increase Mg in formula

Reduce or discontinue TPN if severe

Reduce total calories or substitute fatcalories for some CHO calories

Reduce amino acids and nitrogen in TPN

Determine if there are increased losses;increase Na in TPN and/or reduce fluids

Probable Causes

Refeeding Syndrome

Hyperglycemia

Hypoglycemia

Hyperlipidemia

Hyperkalemia

Hypokalemia

Hypophosphatemia

Hyperphosphatemia

Hypermagnesemia

Hypomagnesemia

Elevated LFTs

Increased CO2

Pre-renal azotemiaIncreased BUN

Hyponatremia

Overfeeding patients who haven't eaten inover 2 days or are severely malnourished.Rapid drop in serum PO

4, Mg, K

Glucose intolerance, insulin-resistance,sepsis, diabetes

Too much insulin, too abrupt discontinuationof TPN

Severe sepsis, stress, familial condition

Renal insufficiency

Protein anabolism; insufficient K+ in TPNespecially during initial refeeding; diarrhea,vomiting, fistulas; side effects of drugs; lossesfrom gut or kidneys

Inadequate PO4 in TPN, especially during

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 GItract

Overfeeding or cholestasis from pancreatitis

Overfeeding with carbohydrate calories; lungdisease

Excess amino acids; renal insufficiency,dehydration

Overhydration from TPN and IV fluids;increased losses from urine or gut; inad-equate sodium in TPN

Appendix #10

147©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

1. Enteral Nutrition should be considered:a. when a patient has had inadequate intake for 1 to 2 daysb. in a patient with a complete small bowel obstructionc. when an advanced directive is present and specifies “no artificial nutrition support”d. in a patient with a small bowel resection along with TPNe. with severe diarrhea that is resistant to medication therapy

2. The serum levels of transferrin, albumin, and prealbumin are all affected by nutrition status, liver disease, surgery, hydration status, renal disease, and chronic illness.

a. True b. False

3. Determine the basal energy requirements for a 55-year-old female, 5’10", 190 lb, utilizing actual weight. a. 1000 kcal b. 1275 kcal c. 1550 kcal d. 1750 kcal e. 2000 kcal

4. Your patient is a 72-year-old male, 6', 180 lb. Maximum carbohydrate administration should be limited to:

a. 475 gm CHO/day b. 590 gm CHO/day c. 353 gm CHO/day d. 708 gm CHO/day e. 220 gm CHO/day

5. Linoleic acid in lipid emulsions causes no known ill effects to patients. a. True b. False

6. Standard trace elements added to TPN include: a. sodium, potassium, phosphorus, and chloride b. zinc, copper, chromium, and manganese c. vanadium, nickel, tin, and silicon d. zinc, copper, magnesium, and nickel e. trace elements are never added to TPN

7. The work of breathing in a COPD patient can increase energy expenditure by as much as 700 kcal/day. a. True b. False

Answer each question by checking the correct answer online or filling the circle corresponding to the cor-rect 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.

ExaminationSUP09

148©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

Exam (cont.)

8. Which are good measures of protein status in the chronic renal failure patient? a. albumin, transferrin, and prealbumin b. retinol-binding protein and prealbumin c. albumin and transferrin d. all of the above e. none of the above

9. 90 to 95 percent of digestion occurs in the: a. duodenum b. duodenum and jejunum c. jejunum and ileum d. duodenum and ileum e. mouth, esophagus and stomach

10. For a ventilator dependent outpatient on a G-tube feeding, the optimal form of delivery is with a bolus feeding every 4 hours.

a. True b. False

11. Diarrhea can be caused by: a. antibiotics b. hypoalbuminemia c. antacids d. niacin deficiency e. all of the above

12. The critically ill patient can best be managed nutritionally with: a. feeding through an enteral tube into the duodenum b. feeding through an enteral tube into the jejunum c. TPN and adjunctive low volume enteral feedings d. feeding through an enteral tube into the stomach e. all of the above

13. Resection of the ileocecal valve may lead to: a. malabsorption of nutrients b. steatorrhea c. bacterial overgrowth d. B12 deficiency e. a, b, and c

14. Patients with pancreatitis always require TPN through treatment of the acute stages. a. True b. False

SUP09

149©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

Exam (cont.)

15. Your patient is diagnosed with alcoholic liver disease and has an ammonia level of 110. He is 42 years old, 5’10", 150 lb. He does not appear confused, but has an albumin level of 2.0. His daily protein requirements are:

a. 102 gm b. 50 gm c. 35 gm d. 20 gm

16. Complications of appropriately provided long-term TPN can include: a. cholestasis b. metabolic bone disease c. renal failure d. chronic liver disease e. a, b and d

17. Which symptoms of alterations in carbohydrate metabolism can occur with stress and sepsis? a. increased glucose levels b. decreased glucose levels c. neither a or b d. both a and b

18. Adding fiber to enteral feedings increases formation of acetate, propionate, and butyrate. a. True b. False

19. Your patient is 62 years old, 5', 110 lb. She is hospitalized with severe sepsis after surgery for cholecys-titis. She is ventilator-dependent. Her needs are:

a. 1130 kcal b. 1300 kcal c. 2750 kcal d. 1500 kcal

20. Glutamine is: a. an essential amino acid b. an essential amino acid during stress c. a fuel source for the gut, kidney and lungs d. b and c e. a and c

21. Your patient has had a resection of the stomach and duodenum and a J-tube has been placed. What type of feeding is not a good choice?

a. elemental b. isotonic intact protein c. peptide d. blenderized e. b and d

SUP09

150©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

Exam (cont.)

22. Determine protein, nonprotein kcal, and total kcal from the following solution: 500 ml D50, 500 ml amino acids 8.5 percent at 50 ml/hr with 500 ml 10 percent lipid emulsion over 10 hours every day.

a. 1400 nonprotein kcal, 1570 total kcal, 43 gm protein b. 1570 nonprotein kcal, 1774 total kcal, 51 gm protein c. 2020 nonprotein kcal, 2224 total kcal, 51 gm protein d. 2235 nonprotein kcal, 2565 total kcal, 60 gm protein e. 800 nonprotein kcal, 1460 total kcal, 22 gm protein

23. A patient who has had a gastric resection may need supplemental: a. B12 b. iron c. B6 d. all of the above e. a and b

24. Your patient is a 62-year-old male, 5’10", 180 lb. He is ventilator-dependent after surgery. He shows no signs of sepsis. His BUN is 28 and Cr is 1.2. What are his daily protein requirements?

a. 40 gm b. 163 gm c. 82 gm d. 65 gm e. impossible to determine from data given

25. TPN with an osmolality of 1100 is usually well tolerated through a peripheral vein. a. True b. False

26. Determine the nonprotein and total kcal and protein in the following daily solution: 400 ml D70, 400 ml amino acids 10 percent, and 200 ml 20 percent lipid emulsion @ 75 ml/hour with MVI-12 and trace elements.

a. 1352 nonprotein kcal, 1512 total kcal, 40 gm protein b. 2434 nonprotein kcal, 2722 total kcal, 72 gm protein c. 2735 nonprotein kcal, 3024 total kcal, 72 gm protein d. 2845 nonprotein kcal, 3225 total kcal, 76 gm protein e. 2900 nonprotein kcal, 3450 total kcal, 82 gm protein

27. Determine nonprotein cal:N ratio and percent nonprotein kcal from fat from the formula in Question 26.

a. 211:1, 30 percent cal from fat b. 238:1, 26 percent cal from fat c. 169:1, 37 percent cal from fat d. 185:1, 42 percent cal from fat e. 190:1, 48 percent cal from fat

28. Fatty liver changes can occur in the following instances: a. liver failure b. overfeeding of kcal c. cholestasis d. a, b, and c e. a and c

SUP09

151©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

Exam (cont.)

29. A ventilator-dependent patient is optimally fed: a. via TPN b. via a G-tube feeding c. via a duodenal or jejunal feeding d. via a stomach feeding e. not fed unless on ventilator for more than 10 days

30. Supplemental __________ is required for the renal failure patient. a. vitamins B6, C and B12

b. vitamin C, folate, and iron c. vitamins A, D, and B6

d. vitamins B6 and C, folate e. potassium, vitamin D, folate

31. Acute liver failure may result in hypoglycemia. a. True b. False

32. Feeding with TPN but no enteral feedings can cause: a. cholestasis b. decreased immunocompetence c. decreased nitrogen balance d. increased immune response e. a, b, and c

33. Your 5’4", 90 lb, 65-year-old female patient is ventilator-dependent after being hospitalized for exacer-bation of COPD. Her caloric requirements are:

a. 1000 to 1200 kcal/day b. 1400 to 1800 kcal/day c. 2200 to 3000 kcal/day d. more than 3000 kcal/day e. cannot determine from data given

34. Your patient in Question 33 has protein requirements of: a. 49 to 78 gm protein/day b. 60 to 82 gm protein/day c. less than 49 gm protein/day d. more than 102 gm protein/day e. cannot determine from data given

SUP09

152©

199

1-20

09 N

utrit

ion

Dim

ensi

on/G

anne

tt E

duca

tion,

Inc.

Exam (cont.)

35. Your 22-year-old male patient with multiple trauma is 6’, 160 lb. His BUN is 28, Cr 1.6, glu 200 and he has a total protein of 3.5 with an albumin level of 1.9. He has diarrhea. His medications include gentamycin, lasix, sliding scale insulin, among others. He develops ARDS and is on a ventilator. You are comfortable in recommending which of the following: a. oral intake

b. full strength isotonic intact protein formula c. maintaining and NPO status d. half-strength diabetic formula e. any of the above 36. A solution of 400 ml D40, 400 ml amino acids 10 percent, and 200 ml 20 percent lipid emulsion is

appropriate for the patient with only a peripheral venous access. a. True b. False

37. Adequate magnesium is necessary for the pulmonary patient in order to allow adequate oxygen trans-port and maintain diaphragm strength.

a. True b. False

38. Total parenteral nutrition is considered the administration through an IV of: a. carbohydrate, protein, and fat b. vitamins, minerals, and electrolytes c. antibiotics and other medications d. all of the above e. a and b

39. The addition of blue food dye to enteral feedings is an effective means to detect aspiration. a. True b. False

40. Only formulas containing essential amino acids should be used for the renal failure patient. a. True b. False

SUP09

Nutrition Support Enteral & Parenteral Nutrition

Documents

Transcript of Nutrition Support Enteral & Parenteral Nutrition