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Nutrition Support

Nutrition Support
Enteral & Parenteral Nutrition
7th edition Revised August 2009
by Martha G. Acevedo, ms, rd

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Nutrition Support:

Enteral & Parenteral Nutrition


7th Edition Revised August 2009
by 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 pa- tients 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 dieti- tians 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).

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 CPEU
CDM............12 Clock Hours
DTR........................ 12 CPEU

Edited by: Dale Ames Kline, MS, RD, CNSC


Copyediting/proofreading: Rich Kline, Gwen Hulbert Design: Knotwork
Graphic Design & Typesetting
1989-2009 Nutrition Dimension/Gannett Education, Inc.
No part of this course may be reproduced, duplicated or copied in any way without the written permission of the copyright holder.

Nutrition Support

ii

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Nutrition Support

Chapter Topic

iii

Contents

Page

Nutrition Assessment
Anthropometrics Biochemical Review Energy Requirements Protein Requirements
Subjective Global Assessment

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

15

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

31

Gastrointestinal Disorders
GI Tract Problems Malabsorption Short Bowel Syndrome Pancreas

45

Stress and Sepsis


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

59

Obesity and Diabetes Mellitus


Determining Nutrient Needs Nutritional Assessment Long-term Care Diabetes

73

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

Renal Disease
Nutritional Assessment Chronic Renal Failure Enteral Feedings TPN
Acute Renal Failure Protein

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

89

101

10 Cancer Patients

Surgery, Radiation, Chemotherapy Nutrient Needs

109

11 AIDS and HIV-Positive Patients



Effects of AIDS on Immune System Nutrition Assessment Nutrition Support

117

12 Transition to Home Care



Guidelines for Home Nutrition Support Complications of Long-term TPN

125

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

Nutrition Support

iv

Learning Objectives
After completing this course, the student will be able to:
1. Describe the pros and cons of using anthropometric measurements for the nutrition assessment of the critically ill patient.
2. Analyze the usefulness of serum albumin, prealbumin and transferrin in assessing the nutritional 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 re- moved,
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, carbohydrate, electrolytes and vitamins and minerals.

Nutrition Support

Introduction

utrition 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 disease
states that affect their nutritional status and/or ability to utilize particular nutrients. It
has evolved from simple tube feedings into a highly complex system which meets the
nutrition needs of patients who would not otherwise have survived medical crises.
Nutrition support patients can vary from an elderly patient with dementia who
requires enteral (gastric or duodenal tube) feedings, to a patient who has had significant
gastrointestinal surgery and requires parenteral (intravenous) feedings, to a patient who
has acute renal failure and septic shock and cannot digest and utilize nutrients except
through intravenous feedings.
Nutrition support is, therefore, a varied and highly specialized field, requiring an
increased level of knowledge by the nutrition care practitioner. This knowledge base
can only come with experience and the continual study of appropriate literature, as new
ideas and research are promulgated and new feeding formulas developed. No doubt the
field 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 excellent resource for the person interested or involved in nutrition support. ASPEN produces a bimonthly journal, Journal of Parenteral and Enteral Nutrition (JPEN), that provides state-of-the-art information on research and trends in nutrition care, and has
devised standards of care for various areas of nutrition support and standards of practice for the different disciplines providing care. Also published by ASPEN is a bimonthly publication Nutrition in Clinical Practice, a more hands-on resource which can
be invaluable in your practice and several excellent reference books.
ASPEN has a certification process for its members. Currently, nutrition support
certification is attainable for qualified dietitians, nurses, physicians, and pharmacists;
the designation is CNSC (Certified Nutrition Support Clinician).

Nutrition Support

Dietitians in Nutrition Support, a practice group of the American Dietetic Association, is also an excellent resource for dietitians, dietetic technicians and students interested in nutrition support. This practice group publishes an informative bimonthly
newsletter, Support Line, and conducts workshops across the country.
This course will provide practical guidelines and references for the nutrition care
practitioner, focusing on the clinical practitioners role. Methods of nutrition assessment, an overview of enteral and parenteral regimens, and guidelines for the nutrition
support of patients with specific diseases and conditions are included. As in all areas of
nutrition, research has changed accepted clinical practice and calculations. This course
reflects the latest thinking in clinical practice, and will be updated periodically throughout its publication period as information emerges.
Throughout the course, I refer to specific brand-name feeding formulas. I wish to
emphasize that these are included because they are in general use in hospitals everywhere. No mention of a brand name should be construed as an endorsement, except
where I have pointed out that one product meets specific criteria. There are no commercial objectives to any such mention, and neither I nor Nutrition Dimension, Inc., has
received any incentives or consideration for mentioning a specific brand name or company. Rather, I have attempted to use my own experience and that of the sources cited
in this course in the most practical way: by making specific points in terms the average
practitioner 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 postexamination 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 student
attempt 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 textual
material and facilitate completion of the post-exam. The case studies Ive designed
simulate typical problems and situations that occur in hospital care many of them, in
fact, are drawn from actual cases. Since nothing is ever totally by the book, these will
help the student see how a case can change, and how seemingly minor variations in lab
values 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, numerous
dietitians have responded with cogent observations and thoughtful advice for making it
better. Throughout the period, these recommendations have enabled me to make minor
corrections and clarifications in the text, which the publisher was able to incorporate in
subsequent printings. It is impossible to name all the dietitians who took the time to
write or call with advice, but their input and concern is greatly appreciated, as is that of
the reviewers for certification, who also made many excellent suggestions.

Nutrition Support

Chapter One:
Nutrition Assessment

utrition assessment is a valuable tool in the early identification of malnutrition


and/or undernutrition. Malnutrition and/or undernutrition has been estimated to
occur in at least one in five hospitalized patients. The incidence increases to almost 50
percent in patients with a longer length of stay (Hill, 1992). Often a patients nutritional
status will deteriorate during a hospital stay. Reasons for this decline in nutritional
status may include anorexia with resultant decreased intake, surgery, infection, medication interactions, chemotherapy and radiation therapy.
Malnutrition may increase the incidence of sepsis, cause poor wound healing and
poor respiratory effort, and decrease absorption of nutrients (Cerra, 1984). The patient
with malnutrition is at increased risk for infection because of compromised lymphocyte
function and growth. Antibodies, phagocytes and macrophages all have diminished
function and/or effectiveness (Kline, 1999). Morbidity associated with malnutrition has
been estimated at 25 percent, while mortality due to malnutrition alone occurs in about
5 percent of cases. Protein stores are depleted by as much as 75 gm/day during the
initial stages of malnutrition (Cahill, 1988). Early nutrition therapy may decrease a
patients propensity to develop malnutrition and delay or prevent the onset of these
complications.
The first step in providing appropriate nutrition therapy is nutrition assessment. In
performing a nutrition assessment, the practitioner must review all aspects of the
patients history, appropriate current factors, and clinical and biochemical parameters.
Initially, something as simple as a nutrition screening should be carried out (see chart
on the following page). The information obtained in the screening can be used as a
reference point for comparison later in the hospital course and can assist in identifying
the patient at increased risk for nutrition problems during the hospital stay.

Nutrition Support

Nutritional Screening
Height and weight
Diet history
Weight change history
Appetite

Chewing/swallowing problems
Diagnosis & chewing
Laboratory data
Bowel habits

After the initial screening has identified a patient as high risk, further evaluation
should include examination for any overt clinical signs of malnutrition. Obvious calorie/protein malnutrition may be manifested by muscle wasting, edema or ascites, and
changes in hair and skin condition. Symptoms of vitamin and mineral deficiencies may
include changes in the condition of the skin, eyes, mouth and gums. Neurological
changes such as ataxia, convulsions and encephalopathy may occur with malnutrition.
A more complete listing of physical changes associated with malnutrition can be found
in Appendix #1. Another course in this series, Nutrition Assessment: Tools and Techniques
also outlines the complexities of assessment in more detail.
Clearly, one of the most important components of assessment is height and
weight. These give an indication of current nutritional status, as well as of chronic
changes 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 percent
Females: 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 of
underweight or obesity, as shown on the next page. Factors such as edema, ascites, and
fluid overload should be taken into account in the assessment of weight for height data.

Ideal Body Weight Comparison


> 200 percent = Morbidly obese
> 150 percent = Obese
> 120 percent = Overweight
80 to 90 percent = Mild caloric depletion
70 to 80 percent = Moderate caloric depletion
< 69 percent = Severe caloric depletion
Hopkins B: Assessment of nutritional status. In Nutrition Support Dietetics. ed. by Shronts
EP, ASPEN, Silver Spring MD, pp 15-60, 1989.

Nutrition Support

Another comparison actual weight to usual weight can be made to determine


the relevance of changes in body weight. This comparison may be more important than
other assessments in the clinical setting as an indicator of malnutrition. An unintentional and/ or unexplained weight loss or gain of more than 10 percent of body weight
within 6 months or 7.5 percent within 3 months has been associated with increased
surgical mortality, and should alert the clinical practitioner to the possibility of complications affecting nutritional status.
Body mass index (BMI) compares weight to height and is sometimes utilized to
determine the incidence of obesity and/or malnutrition.

BMI
BMI =
19-25
21-27
>27.5
27.5-30
30-40
>40

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

appropriate weight (19-34 yr)


appropriate weight (>35 yr)
obesity
mild obesity
moderate obesity
severe or morbid obesity

17-18.5 mild malnutrition


16-17 moderate malnutrition
<16 severe malnutrition

ANTHROPOMETRICS
The use of anthropometrics, including measurements of skinfolds, mid-arm circumference, mid-arm muscle circumference, and arm muscle area, is of limited value in
care of the critically ill patient. Since anthropometric measurements represent chronic
changes, they are of more use in the assessment of the long-term outpatient and the
population as a whole. Anthropometrics, other than height and weight, are not often
utilized. They are more useful in tracking long-term patients to assess changes in nutritional status.
Nonetheless, the nutrition care practitioner should be familiar with the processes of
obtaining these measurements and of their utilization in assessing the patient. Measurements of skinfolds, including triceps skinfolds (TSF), involve the use of skinfold calipers. Interpretation of the results can be found in Appendix #3.
The technique is refined with practice, but different measurements may occur with
different practitioners or with the same practitioner at different times. The accuracy of
this 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 a
preestablished standard value, developed from data derived from the National Health
and Nutrition Examination Survey (NHANES II), as shown in Appendix #3.

Nutrition 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 to
identify the level of caloric depletion, as shown below:
Percent of Standard =

patient value
standard value

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 determining
the status of somatic protein stores. The chart on the following page shows the formulas
used to determine MAMC and AMA and the standards to which these values can be
compared.
Another means by which nutritional status can be determined, especially in the
elderly, is body mass index, or BMI. BMI is determined by dividing the patients weight
by 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 to
29, with evidence of nutritional depletion with a level less than 24 and possible obesity
with a level greater than 29 (Burns, 1992).

Arm Measurement Standards


(all measurements in centimeters)
MAMC = MAC (3.14 x TSF)
AMA = [MAC (3.14 x TSF)]2
4

Male
Female

TSF
Standards

MAC
Standards

AMA
Standards

12.5
16.5

29.3
28.5

25.3
23.2

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 is
a good indicator of creatine levels in the body, and can be used to estimate lean body
mass (Waiser, 1987).
Urine collected during a 24-hour period is analyzed for creatinine content. This
level is then compared to pre-established standards, shown below. Appendix #2 lists
expected creatinine height index values.

Nutrition Support

Creatinine Height Index (CHI)


% Cr Excretion =
Averages
Females:
Males:
Interpretation:

actual 24 hour Cr excretion


X 100
expected 24 hour Cr excretion

18 mg Cr/kg IBW (range 16-22 mg)


23 Crkg IBW (range 20-26 mg)
>80% = mild depletion
60 80% = moderate depletion
<60% = severe depletion

Measurement of creatinine excretion has limitations, and is subject to certain


variables. Dietary intake of creatinine, creatine and protein can affect the level of creatinine excreted and, therefore, the CHI.
Since creatinine excretion, as well as lean body mass, decreases with age, CHI may
not 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 is
limited or absent in these patients. Also, expected values may change with body frame
size. Because of these variables, CHI is not often used as a nutrition parameter. I do not
use 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 use
primarily in assessing visceral protein status, the status of hepatic protein synthesis and
micronutrient status (vitamins, minerals and electrolytes).
A simple method to determine if intake is adequate during illness is through
nitrogen balance studies. Since approximately 80 to 90 percent of all urinary nitrogen is
comprised of urinary urea nitrogen (UUN), nitrogen balance is determined by the
measurement of UUN in a 24-hour urine collection. Increasing UUN by 20 percent will
account for the non-urea urinary nitrogen losses. This value is then utilized in the
formula below.
Nitrogen balance =

24 hour protein intake (gm)


6.25

[(UUN x 1.2) + (2 to 4)]

A nitrogen balance of less than minus 2 suggests catabolism; a balance of more


than plus 4 indicates anabolism. Nitrogen balance studies tend to overestimate the
nitrogen actually lost and are dependent on the accuracy of urine collection and the
recording of protein intake. For the patient on total parenteral nutrition (TPN), the
amount of nitrogen per gram of protein will vary with the amino acid formula utilized.
(I generally use the figure 6.06.)

Nutrition Support

Nitrogen balance studies are difficult to complete in patients with hepatic or renal
failure and may be inaccurate in those patients with protein-losing enteropathies,
malabsorption, abscesses, and fistulas. It was determined that a twelve hour urine
collection for UUN can give a satisfactory estimate of a 24-hour UUN if the figure is
doubled (Candio, et al., 1991). This process works most effectively with those patients
on parenteral nutrition support; 24-hour urine collections are necessary for the patient
on enteral or oral feedings.
Urea kinetic modeling and urinary nitrogen appearance (UNA) can be used in the
patient with acute or chronic renal failure. While urea kinetic modeling is more accurate
than 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 interdialytic
intervals (Hopkins, 1993; Tayek, 1988). The following formula is then utilized to determine urinary nitrogen appearance (UNA):
(BUNf - BUNi) x 0.6BW + (BWf - BWi) x BUNf
where i = initial, f = final, BUN = blood urea nitrogen (gm/liter), and BW = body weight (kg)
Tests to determine a patients level of immunocompetence may be an effective
indicator of nutritional status. A malnourished patient is at increased risk for opportunistic infections. Total lymphocyte count (TLC) is recognized as a measure of immune
function and has also been used in determining nutritional status, as shown on the
following page, using the white blood count and the percentage of lymphocytes from
the blood count differential.
However, TLC is depressed by factors other than nutritional status. These factors
include infection, steroid or immunosuppressive therapy, cancer and its conjunctive
therapies, surgery, and certain inherited and acquired immune deficiency states
(Hopkins, 1989; Lang, 1989; Glassman, 1986).

Total Lymphocyte Count


% lymphocytes
100
1500 to 1800 = mild depletion
900 to 1500 = moderate depletion
< 900 severe depletion

TLC = white blood count X

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

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

Nutrition Support

A positive response, swelling around the injection site, indicates adequate immunocompetence and nutritional status. If the area of swelling is less than 5 mm in diameter, the patient has altered or poor immunocompetence and may also be malnourished.
Non-nutritional factors can affect immunocompetence, so delayed hypersensitivity skin
testing is not commonly utilized. Total lymphocyte count and delayed hypersensitivity
testing are rarely utilized at present for nutrition assessment.
Hepatic protein production can be studied by utilizing biochemistry values, such
as 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 20
days, 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 or
substance. In assessing a patient, and especially in addressing the adequacy of
renourishing a patient, always keep the half-life in mind. ) Decreased albumin levels are
associated with poor outcome, increased length of stay, increased incidence of complications, and death (Shronts, Fish, Hammond, 1998).
Appendix #4 shows non-nutritional factors affecting serum albumin levels, and the
chart at the top of the next page outlines the level of protein depletion associated with
various albumin, transferrin, and prealbumin levels.

Protein Depletion
Mild:
Moderate:
Severe:

Albumin

Transferrin

Prealbumin

2.8 to 3.5 gm/dl


2.1 to 2.7 gm/dl
2.1 gm/dl

150 to 200 mg/dl


100 to 150 gm/dl
< 100 mg/dl

10 to 15 mg/dl
5 to 10 mg/dl
<5 mg/dl

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

Calculating Transferrin Levels


Blackburn: Transferrin (mg/dl) = 0.8 TIBC (mg/dl) 43
Heymsfield: Transferrin (mg/dl) = 0.9 TIBC (mg/dl) 4.5
Grant: Transferrin (mg/dl) = 0.87 TIBC (mg/dl) + 10

Nutrition Support

10

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. Its
levels are also affected by the same factors as albumin and transferrin. Retinol-binding
proteins half-life of only 12 hours makes it highly sensitive to acute changes. Its levels
are 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 bodys response to an acute illness or injury, especially in
those patients in a critical care setting. While levels may be considered, measurement of
these 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 of
serum levels does not reflect actual body stores of all micronutrients. Assessment of intake
can be determined from diet history and clinical examination to detect specific deficiency
symptoms. 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 practitioner. If metabolic carts are available, indirect calorimetry can be used to determine
requirements through the measurements of oxygen consumption, carbon dioxide
production, and minute ventilation. The Weir equation, calculating resting energy
expenditure (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 REE
For maintenance: 1.3 x REE
Adjustment of REE is done to account for activity since REE is measured at a
steady state. Requirements for basal energy expenditure (BEE) can also be estimated
using 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 stress
states. Another method for calculating energy needs, utilizing caloric needs per kilogram of body weight, is utilizing a factor of 25 to 30 kcal/kg and/or less in the obese
patient where permissive underfeeding is recommended (see chapter on
obesity)(McClave, et al., 2009). Youll note that caloric requirements are lower than what
we once thought.
Carol Ireton-Jones has adapted the Harris-Benedict equation to account for the
presence of trauma, burns, and/or intubation (Ireton-Jones, 1989; Hopkins, 1993),
shown on the following page.

Nutrition Support

11

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

PROTEIN REQUIREMENTS
Protein requirements, determined from nitrogen balance studies described earlier,
can also be calculated from ideal body weight and by utilizing predetermined caloric
needs and specified calorie/nitrogen ratios. The RDA for protein is 0.8 gm/kg of body
weight. This factor changes with various disease states and will be discussed in later
chapters. Calorie/nitrogen ratio is based on the patients clinical condition. A level of
150 to 1 is generally accepted as reasonable, but this recommendation changes with
stress, renal disease, liver disease, etc.
Another method of calculating protein needs is based on the patients weight and
disease 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 patients
with impaired kidneys or liver function, protein needs may need to be lower. In the
following chapters the protein needs of various disease states will be discussed.
Nutrition assessment is only the first step in providing nutrition care and support
to our patients. With experience, the ability to make accurate assessments will improve.
The practitioner should continue to remain aware of changes in the patients medical
status as well as of changes in the methods of nutrition assessment.

SUBJECTIVE GLOBAL ASSESSMENT


Once you have completed a review of the patients medical and dietary history and
assessed nutrition status by examining the patients physical condition, you can adapt
this data for use in completing a subjective global assessment (SGA).
As described by Detsky, et al., specifically, five criteria obtained in the history and

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physical are utilized in the SGA. These include weight change history, dietary intake
change, gastrointestinal symptoms, the patients ability to function and the disease
process and its relation to nutritional needs. Physical assessment of loss of subcutaneous fat, muscle wasting, ankle edema, sacral edema and ascites is also considered in the
rating of the patient based on SGA.
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 of
greater than 10 percent is definitely significant.
Changes in dietary intake are described as normal or abnormal; the length and
degree of abnormal intake are also considered. Any gastrointestinal symptom (nausea,
vomiting, diarrhea and anorexia) lasting longer than two weeks is also noted. Functional ability is the patients energy level (i.e. bedridden, housebound, working). The
metabolic demand placed on the body by the illness is characterized as no stress, low
stress, moderate stress and high stress (Detsky, et al., 1987).

Criteria for History and Physical


*Weight change history: <5% weight loss over 6 mo. = minor depletion
5-10% weight loss over 6 mo. = potentially significant depletion
>10% weight loss over 6 mo. = significant depletion
*Change in dietary intake: Normal vs. Abnormal
Length of change ____________ Degree of change ______
Gastrointestinal symptoms: (i.e. nausea, vomiting, diarrhea, anorexia) >2 wks
Functional ability of patient:
Metabolic demand:

bedridden house bound

no stress
moderate stress

working

low stress
high stress

Physical Assessment related to loss of subcutaneous fat*, muscle wasting*,


ankle and sacral edema, and ascites:
0 = normal
1+ = mild depletion
2+ = moderate depletion
3+ = severe depletion
SGA rating (subjective): Category A = well nourished
Category B = moderate or suspected malnutrition
Category C = severe malnutrition
*primary importance

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Physical assessment is characterized as: 0 = normal; 1+ = mild; 2+ = moderate; and


3+ = severe, as used to assess degree of loss of subcutaneous fat, muscle wasting, ankle
and sacral edema and ascites (Lang and Cashman, 1989).
The SGA rating is then determined, utilizing subjective indices. Category A is
well-nourished; category B is moderate or suspected malnutrition; and category C
is severe malnutrition (Detsky, et al., 1987).
The most emphasis is placed on weight changes, poor dietary intake, loss of subcutaneous tissue and muscle wasting. In fact, weight loss and the pattern of weight loss
appears to be the most important component of SGA. Disadvantages to using the SGA
techniques in assessing your patient might include the difference in one persons assessment as compared to the next persons assessment, because of the subjectivity.
In beginning to use SGA, Jeejeebhoy suggests that we begin by performing assessments together as a group so as to attain a consensus and more consistency from practitioner to practitioner.
I feel that many of us use subjective global assessment without even knowing that
is what we are doing. This type of assessment comes more easily with experience and
exposure to a variety of patients, diseases and illnesses. For a more detailed discussion
on SGA, refer to Detsky, et al., 1987.

REVIEW QUESTIONS
Note: These review questions are an important part of the course. Please take the
time to complete them in writing, and compare your answers with those given at the
end of the coursebook. Completing the review questions in each chapter will also help
you with the post-examination.
1. Why are anthropometrics of limited use in the nutrition assessment of the critically ill
patient?
2. What are the best parameters for use in assessing protein status in critically ill patients?
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, 58" 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, 57" 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.

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Detsky AS, Baker JP, ORourke K, et al.: Predicting nutritional associated complications for patients
undergoing gastrointestinal surgery. JPEN 11:440-446, 1987.
Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D and fluoride. National Academy 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: Dietitians 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: Dietitians 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) and
American 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 of
intensive 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 Parenteral
and 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 11:5:73S77S, 1987.

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Chapter Two:
Enteral Nutrition

f the gut works, use it! This rule of thumb for clinical dietitians has been
reinforced by research showing the importance of maintaining healthy gut mucosa in
the 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 take
nutrients through the oral route either totally or in part. (JPEN, 2009).

NORMAL DIGESTION
The gastrointestinal tract acts to break down, metabolize and transport foods so
nutrients can be utilized by the body. Chewing initiates the breakdown of foodstuffs in
the 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 with
hydrochloric acid and pepsin. Except for the presence of intrinsic factor (necessary for
the absorption of vitamin B12), the stomach is not as vital to the digestive process as the
lower portions of the digestive tract. Digestion of protein begins in the stomach; digestion of carbohydrate and fat takes place in the duodenum.
The food (now called chyme) passes through the pyloric sphincter into the duodenum, which is approximately 25 cm long. The release of chyme into the duodenum
causes the release of enzymes by the pancreas and the gastrointestinal tract, as well as
the release of hormones into the bloodstream.

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Digestion of starch occurs primarily here, by means of pancreatic amylase. Intestinal brush border enzymes further hydrolyze the oligosaccharides so that they can later
be absorbed across the microvilli in the small intestine.
Normally, 90 to 95 percent of digestion occurs in the jejunum and ileum. The
combined length of these two organs is about 260 cm. Protein digestion, which began in
the duodenum, continues here with the help of trypsin, chymotrypsin, and elastase. The
free amino acids, dipeptides, and tripeptides are released and then absorbed across the
intestinal mucosa via carrier-mediated mechanisms, also known as pumps.
Bile, made by the liver and released by the gall bladder, is important in the digestion of fat by acting as an emulsifier, allowing lipases to break down triglycerides to
monoglycerides, lysolecithin and free fatty acids. Micelles complexes of approximately 20 fatty acids, monoglycerides, lysolecithin and bile are absorbed via the
brush border into the lymph system before entering the bloodstream. The fatty acids
end up in the liver where they are further metabolized.

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

Cells comprising the brush border villi are replaced every 3 to 5 days; their replacement is affected by nutritional status and the availability of various vitamins and minerals. Nutrient deficiencies affecting the regeneration of the villi can compromise digestion 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, and
various other minerals and electrolytes. Normal digestion can be altered by surgery,
sepsis, trauma, malnutrition and illness. Physiologically, the body may be better served

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by the continued use of the digestive tract, as much as tolerable, during these times. A
good knowledge of normal digestion and absorption can assist in adapting nutrition
support 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 transport
systems for amino acids and glucose (Martindale, 1996). Motility of the bowel can be
profoundly affected by medications such as anesthetics. Other drugs that can impact the
motility 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 provided
through 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 nutrients by mouth and a gastrointestinal tract that can be used safely and effectively. The
chart 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 enteral
feedings should be initiated in critically ill patients who are ..unable to maintain
volitional intake. (McClave, et al., 2009)
Enteral feedings should be initiated early, especially in those patients who are
critically ill. Artinian, et al., (2006) found that initiation of enteral feeding within 48
hours of admission in critically ill patients resulted in a 20 percent decrease in ICU
mortality and a 25 percent decrease in hospital mortality, with the greatest influence
seen in the sickest patients.
Enteral nutrition may be of use in the patient with major trauma and major surgery, with head injuries, in acute pancreatitis, in conjunction with radiation and chemotherapy, and in liver and renal failure. Feeding through the GI tract may be of limited
use during intensive chemotherapy and in the immediate postoperative or post-stress
period, even in a well-nourished patient who will likely resume oral intake within 5 to 7
days.
Enteral feedings are contraindicated for the patient with bowel obstruction, intractable vomiting, severe diarrhea, some forms of GI bleeding, persistent aspiration, and
problems with access that cannot be overcome, as shown on the following page
(A.S.P.E.N., 2002; Kudsk, 1996).

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Enteral Nutrition Criteria


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

Acute enteritis and removal of more than 90 percent of the small bowel may be
contraindications for the use of enteral nutrition support. The chart on the following
page 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 is
resumed within 12 to 24 hours of surgery. Ileus in the colon can last as long as five days
but enteral feedings can still be accomplished (Mueller, 1996).

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
Patients or guardians wish to forgo enteral support
Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN
26(suppl):2002; Guidelines for the provision and assessment of nutrition support therapy in the
adult critically ill patient, JPEN 33:3, 2009.

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BENEFITS OF ENTERAL FEEDINGS


Feeding through the gastrointestinal tract is more physiologically sound than
feeding with total parenteral nutrition. Enterally supplied nutrients first pass through
the liver on their way to becoming completely metabolized. The liver helps to metabolize nutrients so that they can be used most effectively by other organs and cells. TPNprovided nutrients are exposed to other organs as well as the liver after being introduced to the bloodstream.
The presence of nutrients and growth factors inside the gastrointestinal tract is
necessary to effectively preserve gut villi and gut integrity. The villi is preserved
through a maintenance of blood flow to the mucosa (Kudsk, 1996). The gastrointestinal
villi 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 villi
via feeding increases the availability of glutamine for the gut.
When enteral nutrition is not utilized, immune response lessens (decreased IgA
secretion) , with a resultant increase in bacterial growth and possible gut bacterial
translocation (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 bacterial
translocation and increased risk for systemic infection, as well as an increased risk for
multi-organ dysfunction syndrome (Jabbar, et al., 2003; Kudsk, 2002). Glutamine, available in enteral feedings and supplemented in elemental feedings, appears to be preferentially 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 in
preventing 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 difficult
as one might think. Nasogastric tubes can be utilized in patients with an intact gag
reflex. However, these tubes may increase the risk of aspiration. Ideally, nasoenteric
tubes should be passed into the duodenum or jejunum, as the critically ill patient may
benefit because of delayed gastric emptying and increased risk for aspiration with
nasogastric tubes.
Placement of tubes into the duodenum requires more skill and may require fluoroscopy or endoscopy. Number 8 or #10 French tubes are usually well tolerated by most
patients and can be used for most types of feedings. Smaller tubes are utilized for

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nasojejunal (NGJ) feedings. However, larger-bore tubes (#12 to #14 French) may be
necessary when more viscous feedings are utilized (Krey, 1989).
Enterostomies are necessary when longer-term enteral nutrition support is indicated. A gastrostomy tube can be placed into the stomach either percutaneously via
endoscopy (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 sphincters
and are able to absorb and metabolize most nutrients, but who are unable to take
enough 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 is
given to patients with a gastrostomy while only 55 percent of prescribed feeding is
provided 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 significant
gastrectomy, severe gastroparesis, or atrophic gastritis), a needle catheter or larger-bore
jejunostomy may be utilized (Kirkland, 1989). Jejunostomy feedings can be initiated
within 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; two
sphincters (esophageal and duodenal) and the ligament of Treitz separate the esophagus
from the feeding site. Since aspiration occurs anywhere up to 89 percent of patients
receiving enteral feedings, jejunostomy feedings may be beneficial in that the aspiration
risk falls to 0.67 to 1.37 percent (Kearns, 1996). However, the incidence of Clostridium
difficile (C. diff) associated diarrhea is significantly higher in patients with post pyloric
feedings (JPEN, 2009).

FORMULAS
Enteral formulas can generally be classified into four categories: intact nutrients,
predigested or elemental, disease-specific, and modular, with subcategories, shown in
the 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 and
catabolic. They can also be used in patients who experience dysphagia or other swallowing disorders, or who are otherwise unable to ingest oral nutrition.
Standard intact nutrient formulas are usually lactose-free and generally are isotonic. Usually inexpensive, they are composed of approximately 55 percent calories
from carbohydrate, 10 to 15 percent from protein and 30 percent from fat. Some of the
intact formulas are more nutrient-dense than the conventional feedings (1.2 kcal/mL as
opposed to 1.0 kcal/mL) and contain canola oil rather than more saturated fats.

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Enteral Formulas
Intact nutrient formulas standard or calorically dense, including
fiber containing formulas
Predigested or elemental formulas peptide formulas
Disease-specific formulas
Modular formulas
Immune-modulating formulas

Calorically-dense intact nutrient formulas can be used in those patients requiring


fluid restriction, cyclic feedings or bolus feedings. These feedings contain 1.5 to 2.0
kcal/mL and are usually higher in nitrogen as well. Tolerance to these formulas is not as
good, since the increased fat used to make them calorically dense is cleared more slowly
from the stomach.
Fiber-enriched intact nutrient formulas are usually isotonic and can be used in
those patients with either diarrhea or constipation. Patients with impaired gastric
emptying should not be given a fiber rich formula (Charney, 2001). Many facilities
utilize fiber enriched formulas as their house formula. Fiber content of enteral formulas ranges from 5 to 14 gm/l.
Predigested or elemental feedings require minimal digestion and can be utilized in
the patient with a partially or minimally functional gastrointestinal tract. Elemental and
peptide feedings can be used in patients with decreased absorptive capacity, such as
those with Crohns disease, gastrointestinal fistulas and malabsorption. They may also
be 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 vegetable
oils and MCT oils).
Peptide formulas have an osmolality of about 450 mOsm/kg, while elemental
feedings are even more hypertonic (500 to 800 mOsm/kg). The hypertonicity is caused
by the presence of amino acids, di- and tripeptides, and simple carbohydrates.
Hypotonic or hypertonic feedings may delay gastric emptying and can cause
diarrhea. Because the gut needs to maintain isotonicity in relation to the bloodstream, a
hypertonic solution will be made more isotonic by the gut taking up fluid, thereby
increasing the potential for diarrhea.
Peptide formulas may improve anabolism and nitrogen balance better than elemental formulas. Some peptide formulas may also stimulate protein absorption and
reduce diarrhea in hypoalbuminemic patients (Brinson and Koltz, 1988; Skipper, 1989).
Peptide formulas will be discussed further in a later chapter.

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Disease-specific formulas have been developed for liver disease, renal failure,
pulmonary disease, stress and sepsis, diabetes and AIDS. All are lactose-free and may
be hypertonic. Disease-specific formulas are generally more expensive and usually
require some digestion and absorption. Most formulas contain adequate vitamin/
mineral supplementation once calorie/protein requirements are met. These formulas
will be discussed at greater length in later discussions of specific diseases.
Modular formulas are utilized in those patients where the above formulas are not
satisfactory because of specific nutrient needs of a patient. Modules are available for the
addition of carbohydrate, fat, protein, vitamins and minerals. Generally, commercially
prepared formulas meet patients needs. Modular formulas are more difficult to use and
monitor and require a highly trained staff to insure that they are mixed properly, therefore are more likely to be used in a teaching hospital.
Immune-modulating formulas are supplemented with arginine, glutamine, nucleic
acid, omega-3 fatty acids, and antioxidants. A.S.P.E.N. and SCCM guidelines suggest
that these formulas should be utilized for patients with the following conditions: major
elective surgery, trauma, burns, head and neck cancer, and in critically ill patients on
mechanical ventilation. These formulas should only be utilized with caution in patients
with severe sepsis (McClave, et al., 2009).
The literature suggests that arginine deficiency occurs in these conditions. The
addition of RNA and eicosapentaenoic acid (EPA) and docosohexaenoic acid (DHA)
enhance the immune response. The omega-3 fatty acids also appear to aid in decreasing
the incidence of cardiac arrhythmias, the incidence of acute respiratory distress syndrome (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 reduced
duration of mechanical ventilation, morbidity related to infection, and reduced length
of stay (McClave, et al., 2009). However, in patients with severe sepsis, the supplementation 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, incidence
of organ failure and incidence of mortality (Gadek, et al., 1999; Singer, et al., 2006; Pontes-Aruda, et al., 2006).

METHODS OF FEEDING
Once the type of feeding has been determined and access to the GI tract has been
attained, the method of feeding should be decided upon. A patient can be fed with
bolus feedings, intermittent feedings, or continuous feedings.
In a critically ill patient, or a patient just beginning enteral feedings, continuous
feedings are generally utilized. Continuous feedings require the use of a feeding pump
or gravity drip and usually run over a 12- to 24-hour period. Continuous feedings are

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always recommended for feedings that run into the small intestine (although gravity and
bolus feedings can be administered into the small intestine) and may also be used for
feeding into the stomach. Continuous feedings may allow for attainment of calorie and
protein needs more quickly, in fact, within 24 to 48 hours (JPEN, 2009), and may reduce
the risk for aspiration associated with high residuals and gastroesophageal reflux.
Continuous feedings of isotonic formula are usually implemented with fullstrength feedings at a rate of 10 to 40 mL/hour. Full strength isotonic feedings are
utilized because hypo- and hypertonic feedings are associated with delayed gastric
emptying. The feeding rate is then increased gradually by 10 to 20 mL/hr every 8 to 12
hours until adequate to meet the patients nutrition needs, within 96 hours for the
critically ill patient.
Intermittent feedings usually do not require the use of a feeding pump, but use a
gravity-drip system. Feedings are given in a volume of 250 to 400 mL over 30 minutes
or more, every three to six hours. The feedings are spaced throughout the day and given
to patient tolerance, but based on nutrition needs. Patients may be fed in this manner as
often as six to eight times per day. Intermittent feedings are used only for feedings into
the stomach and are only recommended for the patient who is stable and not critically
ill. Residual in the stomach should be checked before each feeding.
Bolus feedings are generally not recommended in the critically ill patient because
of the increased risk for aspiration and other complications, such as vomiting and
diarrhea. Bolus feedings are similar to intermittent feedings, in that a large volume is
administered. However, bolus feedings are given over a very short period of time (as
little 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, nausea
and/or vomiting should be checked as needed.
Diarrhea may necessitate a change in the method of feeding, the type of feeding or
the strength of feeding. Gastric residuals of up to 250 to 500 mL (McClave, et al., 2009
and 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. abdominal
distention, nausea, and vomiting) and adjust or hold the feeding accordingly. If the
gastric residual is greater than 250 mL after a second check, consideration should be
given to usage of a gastric motility agent. Increases in abdominal girth of greater than 8
to 10 cm necessitate temporary holding of the enteral feeding (Ideno, 1993). Feedings
should be held with gastric residuals of greater than 500 mL (JPEN, 2009).
Diarrhea is invariably blamed on the tube feeding. However, diarrhea may also be
caused by medications, including sorbitol-based medications, antibiotics and certain

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antacids. Sorbitol is often found as a component of liquid-based medications and may


be in foods, such as pear nectar. Doses of sorbitol at levels greater than 10 gm can cause
an osmotic diarrhea (Johnston, et al., 1994). Medications containing magnesium (like
antacids), potassium, or phosphorus should also be ruled out as the cause of any diarrhea (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 may
occur. Other causes of diarrhea include malabsorption with short bowel syndrome,
Crohns disease, ulcerative colitis, AIDS, pellagra and antibiotic-associated enterocolitis.
The patient with poorly controlled diabetes mellitus may also be at a higher risk for
diarrhea (Eisenberg, 1993).
Diarrhea may occur from contamination, a problem which should decrease with
the use of closed systems (a method for enteral feedings in which the formula is provided in a sealed container or bottle which is spiked and hung for feeding without
being opened). The advantages of closed feeding systems include reduced risk of
contamination and/or spoilage and increased hang time by the bed. Closed feeding
bags and sets are safe for 24 to 48 hours (Vanek, 2000; Wagner, 1994).
C. diff colitis and antibiotic associated colitis. Clostridium difficile is an anaerobic
spore-forming rod that is increasingly found in both infants and adults, especially in
adults who have been hospitalized or in a nursing facility and/or have been given
antibiotics. Antibiotic therapy alters the gastrointestinal flora; C. diff colonizes in the
bowel and releases toxins; these toxins result in diarrhea and colitis (Yimam, 2007). The
onset of diarrhea occurs within days or months of antibiotic therapy. The antibiotics and
antimicrobials that are most often associated with C. diff diarrhea are ampicillin,
amoxicillin, cephalosporins, and clindamycin (Yimam, 2007). Most cases resolve with
treatment i.e. Metronidazole (Flaggyl) or oral Vancomycin. Relapse or recurrence
occurs in 8 to 50 percent of cases; risks for recurrence include age, an ICU stay, new
delivery of antibiotics, hypoalbuminemia, and an extended hospital stay (Aslam, 2006;
Bartlett, 2006). C. diff infections, however, can worsen and evolve into pseudomembranous colitis, with symptoms of profuse diarrhea, leukocytosis, and marked abdominal
tenderness and distension.
The occurrence of C. diff colitis and antibiotic-associated colitis does not preclude
continued enteral feedings. In fact, the presence of enteral feeding may aid in decreasing 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 antibiotic
associated diarrhea (Jenkins, et al., 2005) and may be useful for both the prevention and
treatment of C. diff colitis (Dendukuri, et al., 2005). However, one should exercise caution with the introduction of probiotics (live bacterial cultures) in a critically ill or
immunocompromised patient. In patients with recurrent C. diff infections, some studies
suggest that the use of the probiotics S. boulardii (Florastar) and L. rhamnosus GG
(Culturelle) may be of benefit (McFarland, 2006). Also, fiber-containing enteral formulas may reduce diarrhea in some patients.

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Isotonic formulas should be utilized as often as possible. Diarrhea can also be


controlled with banana flakes and soluble fiber as well as with medications such as
paregoric, Lomotil, Lactobacillus acidophilus (lactinex), or antidiarrheals only after C.
difficile has been ruled out. Changes in the formula to an elemental or peptide formula
may be necessary, especially in the patient with malabsorption or intestinal atrophy.
However, some studies suggest that there is no difference in the incidence of diarrhea
when 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) that
worsens with enteral feedings and improves when feedings are held may benefit from
bowel rest and TPN (Delegge, 2006).

ASPIRATION PNEUMONIA
Aspiration pneumonia is also a risk for the enterally fed patient, especially if the
tube 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 reported
at an incidence of 0.8 to 95 percent in enterally fed patients; however, the rate of aspiration 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 cough
or gag reflex, mechanical ventilation, and/or delayed gastric emptying are at increased
risk for aspiration (Hamaoui and Kodsi, 1997; JPEN, 2009). Tests to determine whether
aspiration has occurred include utilizing glucose oxidase reagent strips to test for
glucose (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 of
the patients 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 an
increased incidence of toxicity from the addition of blue dye to formulas. This toxicity
resulted in systemic sepsis and death in some cases. Blue dye appears to be absorbed in
some cases, especially in the critically ill. The composition of blue dye is similar to that
of ADP; the blue dye replaces the ADP in cellular respiration, thus stopping it, resulting
in 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 the
head of the bed elevated at a 30 to 45-degree angle; monitor gastric residuals; strive for
postpyloric 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 for
assessment of tolerance. These levels should also be closely monitored for evidence of
dehydration in the patient with diarrhea as well as those with infection and sepsis.

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26

Glucose levels may increase with refeeding, but may also be associated with stress,
steroid administration and diabetes mellitus. The management of glucose should
include 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 with
gastrointestinal 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 should
be supplemented in patients with serum levels less than 2 mg/dl (Skipper, 1989). Some
tube-fed patients become hyperphosphatemic with nutrition support and may require
the 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 not
only 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 other
nutrients into the cells.
This occurrence, along with the depletion of phosphorus that occurs during starvation, can result in a severe depletion of phosphorus in the extracellular space. Refeeding
syndrome 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 (Solomon
and Kirby, 1990). Low phosphorus levels can cause serious complications, including
cardiac 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 serum
potassium 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 products
utilize short-chain peptides for more efficient absorption. (Peptide transport across the
intestinal wall does not require the use of the sodium pump.) Use is often restricted to
hypoalbuminemic and critically ill patients.
Short-chain fatty acids (SCFA) acetate, propionate, and butyrate form in the
gastrointestinal tract as a by-product of the digestion and fermentation of enterally
provided fiber. SCFA are further metabolized to ketones and glutamine.
SCFA are the primary fuel preferred by the mucosa of the colon (Palacio, 1990); up
to 540 kcal/day from SCFA can be absorbed. The colon obtains 60 to 70 percent of its
energy requirements from SCFA (Cummings and MacFarlane, 1997). These fatty acids
are also important in preventing gut atrophy, both in the colon and in the small intestine

Nutrition Support

27

(although to a lesser extent). Fiber (or SCFA, if a patient is unable to tolerate dietary
fiber) increases blood flow to the colon, stimulates enzyme secretion by the pancreas,
and promotes mucosal cell growth in the intestine (Rombeau and Kriple, 1990). These
effects may help to decrease the incidence of bacterial translocation. Gut atrophy appears 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 of
SCFA to both enteral formulas and TPN.
Enteral nutrition support appears to be the best means of support for nearly all
patients, including the critically ill. Used correctly in conjunction with oral feedings
and/or total parenteral nutrition, enteral nutrition should enable the nutritional repletion necessary for wound healing and recovery from acute or chronic illnesses. The
efficacy of the use of immune enhancing formulas is not entirely clear; therefore, I can
not 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?

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Drakulovic MB, et al.: Supine body position as a risk factor for nosocomial pneumonia in mechanically
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Jabbar A, Chang WK, Dryden GW, McClave SA: Gut immunology and the differential response to feeding
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Jenkins B, Holsten S, Bengmark S, Martindale R. Probiotics: a practical review of their role in specific
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Kearns PJ: Gastric vs. Small-bowel feeding. Current Issues in Enteral Nutrition Support, Report of the
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Kirkland ML: Enteral and parenteral access. Dietitians Handbook of Enteral and Parenteral Nutrition. Skipper,
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Klein S, Kinney J, Jeejeebhoy K, et al.: Nutrition support in clinical practice: Review of published data and
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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 moratorium. 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
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McClave SA, Martindale RRG, Vanek VW, McCarthy M, et al.: Guidelines for the provision and assessment
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Metheny N, Smith L, Wehrle M, et al.: pH, color, and feeding tubes. RN p.25, January 1998.
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Mueller CM: Enteral nutrition management: gastroparesis, ileus, pseudo-obstruction, diarrhea. Current
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Chapter Three:
Parenteral Nutrition

Parenteral nutrition provides nutrients to a patient via vascular access. Parenteral

nutrition can provide most necessary nutrients to patients unable to utilize their gastrointestinal tracts effectively. In patients with non-functioning GI tracts, parenteral
nutrition may make the difference between life and death. Because parenteral nutrition
is much more complex and expensive than enteral nutrition therapies, its use must be
closely monitored. It should only be utilized in those patients who meet strict preestablished criteria.

CRITERIA FOR USE


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

Criteria for Total Parenteral Nutrition


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 days
of hospitalization and only when enteral nutrition is available
In patients with protein-calorie malnutrition and no feasibility of enteral
nutrition, TPN should be initiated as soon as possible

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Patients who are unable to absorb nutrients through the gastrointestinal tract
because of massive small bowel resection, certain diseases of the small intestine, severe
diarrhea, and intractable vomiting should have total parenteral nutrition as part of their
nutrition therapy. The parenteral route should also be considered in patients with acute
pancreatitis.
Patients who are unable to utilize their gastrointestinal tracts over 5 to 7 days and
who are also severely malnourished or catabolic should also be treated with parenteral
nutrition. The use of parenteral nutrition in these patients can help to alleviate nutrition
depletion and to aid in their recovery (Skipper, 1989). A VA study of 1250 patients
showed a decrease in postoperative complications of 10 percent when severely malnourished patients were given TPN for 7 to 10 days prior to surgery (Buzby, 1991).

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

Total parenteral nutrition (TPN) should be considered in patients who have had
major surgery, who exhibit moderate stress caused by illness or injury and who cannot
be fed through the GI tract for 7 to 10 days. Patients with enterocutaneous fistulas that
preclude enteral feeding may be considered candidates for bowel rest and parenteral
nutrition. Other patients who might benefit include those with hyperemesis
gravidarum, 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 would
benefit from it. Those well-nourished patients with minimal injury or stress, or those in
the immediate postoperative period, are seldom benefited by TPN. A functional gastrointestinal tract is a contraindication, and TPN should not be used when it is not
desired by the patient or when the patient has a very poor prognosis.

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

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Central venous access can be attained via the subclavian, internal jugular and
femoral veins. Long-term TPN patients may require indwelling catheters placed under
the skin for a distance before the line enters the cephalic, external jugular, internal
jugular 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 are
more readily placed than the more invasive indwelling catheters. PICC lines are often
used for the patient who is receiving TPN or intravenous antibiotics at home and, more
and more, while hospitalized. PICC lines are inserted in the arm and the catheter is fed
into smaller peripheral veins to the superior vena cava or right atrium so that central
line concentrations can be used. PICC lines can be inserted by radiologists or trained
nurses 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 of
dextrose, amino acids and electrolytes must be reduced so that the final osmolality of
the solution is low enough to prevent thrombophlebitis.
Because solutions with osmolality greater than 900 mOsm/dl require administration through a central line, the amount of nutrients provided in a peripheral vein is
limited, unless the patient can tolerate large volumes of fluid. TPN administered
through a central vessel (subclavian, internal or external jugular veins) is usually more
concentrated 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 or
central veins.
Total nutrient admixtures (TNA) are now utilized more frequently in the clinical
and home setting. TNA is a combination of all three nutrient (carbohydrate, protein, and
fat) sources in contrast to the more traditional admixture of carbohydrate and protein
with a piggybacking of the fat source.
TNAs add convenience, reduce contamination and precipitation, and are easily
administered. An added benefit to the patient is that continuous lipid infusion appears
to be better tolerated and may be less immunosuppressive.
Improper mixing of the additives in the solution can cause precipitation. It is
important 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 concentration of amino acid and/or dextrose can be more stabilizing to the emulsion. On
the other hand, a higher concentration of lipid can be less stabilizing. Increased concentration 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 a
pharmacist, utilizing a laminar flow hood. Many pharmacies utilize computerized mix
machines, which may reduce the incidence of precipitation. The 1.2 micron filters
prevent precipitates and emboli from being transmitted to patients (Driscoll, et al., 1996).

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TPN bags usually can hang for 24 hours without danger of precipitation or spoilage. Any solution remaining after 24 hours should be discarded. Mixed bags can be
stored safely, under refrigeration, for up to seven days. Lines for administration of TPN
should 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 sheltered
from light. At least 50 percent of vitamin A and 30 percent of vitamin E may be lost due
to 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 energy
sources for TPN. Crystalline L-amino acid formulas supply the protein and an energy
source, while electrolytes, minerals, vitamins and trace elements are added to complete
the formula.
Dextrose can be compounded from base concentrations from 5 to 70 percent (with
a final concentration of <35 percent), depending on the patients needs and ability to
tolerate the dextrose and osmotic load.
When peripheral parenteral nutrition is utilized, the final concentration of dextrose
in solution must be kept at 5 to 10 percent. Since the hydrated form of dextrose is utilized, its caloric value is only 3.4 kcal/gm. Recommendations for carbohydrate administration 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 precipitate
cholestasis, hyperglycemia, increased liver function tests, synthesis and storage of fat
and increased carbon dioxide production.
Lipid emulsions are available in three forms. They provide 1.1 kcal/ml, 2.0 kcal/ml
and 3.0 kcal/ml. Lipid emulsions can be utilized as both a provider of essential fatty
acids and as a calorie source. The 3.0 kcal/ml lipid emulsions are utilized only for
compounding.
Historically, lipid emulsions have been primarily utilized to prevent essential fatty
acid deficiency, with the infusion of 500 ml of 10 percent lipid (1.1 kcal/ml) three times
per week. However, the use of lipid as a significant energy source has become more
prevalent. In stressed patients, lipid calories may be utilized as well as or better than
dextrose 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. Administration
of 20 to 40 percent of calories from fat appears to improve nitrogen sparing and may be
of use in the patient who has become glucose intolerant (Grant, 1985).
While lipid emulsions are an excellent way to provide increased calories to a
patient, one must consider the possible deleterious effects to the immune system of
increased amounts of linoleic acid. Linoleic acid is converted to arachidonic acid, an
omega-6 fatty acid (-6), in the liver and absorbed by the cells as such. They can act as a
precursor to eicosanoids, which stimulate the production of prostaglandins, one of
which PGE2 can be immunosuppressive.

35

Nutrition Support

The literature suggests that the use of linoleic acid as a fat source should be
limited in patients with a depressed immune system or those who have been
stressed by trauma, surgery or illness (Grant, 1985). Because of this, we have recently changed our standard TPN formulas to be lower in fat, attempting to provide
approximately 30 percent calories from fat in the central formula and a lower percentage from fat in the peripheral formula. (For a more detailed discussion of fats
and immunity, see Nutrition Dimension courses Nutrition & Immunity, Part I and/or
Nutrition & Immunity Part II).
Since omega-6 fatty acids appear to negatively affect immunocompetence, possibly
due 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 the
omega-6 fatty acids may be of benefit in enhancing immunocompetence.
While two to three fatty acid sources are available in most enteral formulas, the
only available parenteral lipid in the United States contains linoleic acid. Alternative
sources, such as medium-chain triglycerides (MCT), or structured lipids (mixtures of
MCT and long-chain triglycerides [LCT]) are being studied and are available outside
the 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 lipid
sources. MCT are more readily available for energy than LCT since they are rapidly
cleared and are less carnitine dependent. However, MCT do not contain essential fatty
acids and cannot be utilized as a sole fat source (Jensen, 1994). Currently the use of MCT
in parenteral lipid emulsions has been approved in Europe.
Structured lipids can provide essential fatty acids and provide protection from
immunosuppression which can occur with the exclusive use of LCT. Structured lipids
behave like lipoproteins and are readily available for fuel (Jensen, 1994).

Structured Lipids
MCT
C10
C10
C10

+
C18
C18
C18

LCT

Structured Lipid*
C10
C18
C18

C10
C10
C18

C18
C10
C18

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

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

Nutrition Support

36

nitrogen balance and decreased weight gain. Supplementation may help (Helms, et
al., 1990). Because the metabolism of LCT is dependent upon carnitine, lipid clearance and associated high triglyceride levels may improve with carnitine supplementation in depleted patients. However, carnitine is not currently available for use
with TPN in the clinical setting and appropriate levels of supplementation have not
been determined.

PROTEIN
Protein can be supplied with crystalline L-amino acid preparations. These formulas
are generally comprised of 40 to 50 percent essential amino acids and 50 to 60 percent
nonessential amino acids.
Concentrations of amino acid formulas range from 3.5 percent to 15 percent for use
in 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 acceptable to allow for adequate calories to spare protein. Critically ill patients require 100 to
150 kcal/gm of nitrogen to assure that the protein provided is utilized for protein
synthesis and not for energy.
For the patient who has no difficulty tolerating protein, protein requirements are
0.8 gm/kg/day for the non-stressed patient with an increased requirement to 1.2 to 2.5
gm/kg/day for the critically ill patient.
Disease-specific amino acid formulas have been developed for those patients with
renal and liver disease. High branched-chain amino acid formulas have also been
developed that, theoretically, aid in the treatment of the highly stressed patient. These
specific 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 deficiencies and to prevent their development. Because the absorption and utilization of
vitamins is altered when they are given parenterally, (Skipper, 1989) the recommended
dosages are greater than RDA levels.
The chart on the following page lists the American Medical Associations recommended dosages for parenteral administration of vitamins. Vitamin K (12 to 14 mg/
week) should be administered to patients on TPN, especially those without a functional GI tract.
Critical illness does not change the basic requirements for the electrolytes sodium,
calcium and chloride, but the requirements for potassium, phosphorus and magnesium
change dramatically during periods of stress and refeeding.
Existing deficiencies of these nutrients may become evident as the patients
refeeding begins. Electrolyte administration must be individualized for each patient,
and serum levels should be monitored closely throughout the course of parenteral
nutrition administration.

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37

Parenteral Vitamin Dosages


Vitamin A
Vitamin D
Vitamin E
Ascorbic Acid
Folacin
Niacin
Riboflavin
Thiamine
Pyroxidine
B12
Pantothenic Acid
Biotin

3300 IU
200 IU
10 IU
100 mg
400 mcg
40 mg
3.6 mg
3 mg
4 mg
5 mcg
15 mg
60 mcg

Zinc, copper, chromium, and manganese are routinely added to parenteral formulas. Essential trace elements which may be added in long-term parenteral nutrition
include selenium, iodine, molybdenum, fluorine and cobalt. Other trace elements, such
as vanadium, nickel, tin, silicon and arsenic, have not been shown to become deficient
in those patients receiving long-term TPN, (Russell, et al., 1985) and so are not added to
TPN formulas.
The chart below shows recommended dosages of trace elements.

Parenteral Trace Element Dosages


Copper
Zinc
Manganese
Chromium
Selenium
Iodine
Molybdenum

0.3 mg
3 mg*
0.7 mg
20 mcg
120 mcg
120 mcg
20 mcg
* higher in patients with diarrhea and higher GI losses

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38

FORMULAS
As mentioned above, peripheral formulas are less nutrient-dense than central
formulas. A final dextrose concentration of 10 percent or less is required, and the addition 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 admixture, which includes the lipid emulsion as well as dextrose and amino acids, may be
beneficial to the patient who requires feeding through a peripheral line. Total nutrient
admixtures have been shown to remain stable in solution and are generally fairly well
tolerated through a peripheral line (Hoheim, et al., 1990).
A sample of a typical peripheral parenteral total nutrient admixture can be found
in 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 decreased
fat intolerance. Disadvantages may include increased risk for bacterial growth because
of the limited use of in-line filters (larger and more porous filters have been developed
and are being used). Very fine in-line filters remove microorganisms and other matter
that may contaminate the admixture. However, the larger filter is required in a TNA, to
allow lipid particles to pass through. Also, the presence of fat creates an improved
medium for bacterial growth.
Monitoring the formula for breakdown and other problems (i.e. calcium phosphate
precipitation) may also be difficult because the emulsion is more opaque. A sample of a
typical central TPN total nutrient admixture is provided in Appendix #9.

Total Nutrient Admixture


Advantages
Decreased cost
Decreased fat intolerance
Ease of administration
Disadvantages
Increased risk for bacterial growth
Difficult to monitor

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

39

Nutrition Support

MONITORING THE TPN PATIENT


The status of the patient receiving parenteral nutrition support should be monitored carefully. Initial determination of weight, and serum values of electrolytes, glucose, BUN and creatinine should be made. Baseline serum magnesium, calcium, phosphorus, cholesterol, triglycerides, albumin or transferrin and liver function tests should
also be determined (Lenssen, 1989). A summary of monitoring is shown below.

TPN Monitoring
Values

Initial

2X Daily

Daily

2X Weekly

Weekly

weight
electrolytes
glucose

X
X
X

X
X

X
X

BUN
creatinine
magnesium

X
X
X

calcium
phosphorus
cholesterol

X
X
X

X
X

X
X
X

X
X
X

X
X
X

triglycerides
albumin
(or transferrin)

X
X

X
X

liver functions
fluid balance
access site

X
X
X

X
X

NOTE: When marks appear in two or more columns, values should be


monitored more frequently at first, then less frequently as patient stabilizes.

Electrolyte levels should be initially monitored twice a week and then weekly
throughout the course of TPN therapy. Electrolytes and glucose should be monitored
daily initially, and every other day as the patient stabilizes. Monitoring of nitrogen
balance may help determine the adequacy of protein intake and demonstrate degree of
metabolic stress and recovering.
Fluid balance should be monitored daily to determine if any weight gain is from
fluid overload or actual increase in body mass. A weight gain of more than 0.5 kg/day
may indicate fluid overload.

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40

Inspection of the patients intravenous access site for signs of infection and other
complications noted in the next section should be made every day.

COMPLICATIONS
Complications of parenteral nutrition include phlebitis at the access site, pneumothorax during the insertion of the central line, thrombosis of the vein and infection of
the venous access line. Treatment of occlusions includes urokinase for catheter thrombosis; hydrochloric acid for occlusions caused by mineral precipitate; and ethanol for
occlusions related to lipids (Werlin, et al., 1995).
Metabolic complications are summarized in Appendix #10.
A frequent complication of parenteral nutrition therapy associated with the critically ill patient is an alteration in glucose metabolism. Because of his illness, the patient
may be insulin-resistant or glucose-intolerant, and the introduction of a large dextrose
load via TPN can exacerbate this problem. Hyperglycemia can be caused by overfeeding (excessive dextrose infusion) and is more likely to occur with diabetes, organ failure
and stress.
To prevent the onset of a hyperglycemic, hyperosmolar, non-ketotic coma, glucose
levels should be monitored every 4 to 6 hours initially. Once insulin dosages have been
determined and implemented and the hyperglycemia is under control, glucose levels
should continue to be monitored closely and adjustments made as necessitated by the
patients condition.
Hypoglycemia may occur if TPN is discontinued too quickly; therefore, it should
be tapered off gradually over a 24-hour period (or by decreasing to 40 ml/hr for one
hour, then discontinuing), with monitoring of glucose levels.
Hyperlipidemia may occur when lipid emulsions are given to a patient with
existing familial hyperlipidemia. A sedative called Diprivan (Propofol) maybe utilized
in ventilator-dependent patients. This medication is lipid based and must be considered
as a calorie and fat source. In patients receiving TPN with lipid and concurrent Propofol
infusions, serum triglyceride levels should be routinely monitored and adjustments
should be made to the amount of lipid in the TPN if serum levels are greater than 400
mg/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 for
measurement of serum lipids. If the lipids are piggybacked, then blood should be
drawn prior to infusion or 6 hours post-infusion. If the lipids are part of a three-in-one
mixture, it does not matter when the blood is drawn. If serum lipid levels are consistently high, over 400 mg, lipid emulsions may need to be limited to every other day or
once weekly, depending on the patients caloric needs and serum triglycerides level
(Banks, 1997).
Electrolyte imbalances may occur during TPN. Hyperkalemia may occur with
renal insufficiency, while hypokalemia can occur due to protein anabolism and insufficient potassium administration. The uptake of glucose into the cell occurs with the
uptake of potassium into the cell, which may result in hypokalemia, common during

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41

refeeding and insulin therapy. Increased potassium losses may occur because of diarrhea, vomiting and/or fistulas, and as side effects of such drugs as steroids, potassiumwasting diuretics and certain antibiotics. Adequate potassium levels can be maintained
through supplementation.
Malnourished patients frequently are at risk for the development of hypophosphatemia. This occurs during refeeding due to inadequate phosphorus administration
(because of the role phosphorus plays in glycolysis and synthesis of new cells). Other
causes are alkalosis, antacid use, hypomagnesemia and hypokalemia, and metabolic
acidosis. Phosphorus can be given as needed.
Hyperphosphatemia, as well as hypermagnesemia, is typically seen only in patients with renal insufficiency or failure. Decreased magnesium levels may come from
increased losses and impaired absorption in the GI tract, as well as with aminoglycoside
therapy and chemotherapy (Skipper, 1989).
Phosphorus levels must be monitored and intake of phosphorus must be individualized to a patients requirements. Often, no phosphorus is given to these patients. If
magnesium levels are low, supplement to return levels to normal. Care should be taken
not to oversupplement.
Elevation of liver function tests may occur with some patients on TPN after one to
two 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. The
etiology of TPN-related cholestasis is unknown. Treatment includes cyclic TPN, initiation of low rate enteral feedings, avoidance of overfeeding, and the elimination of
copper 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 either
carbohydrate calories or total calories. This may make ventilator weaning more difficult
and could compromise patients with existing pulmonary disease. Care should be taken
that patients do not receive excessive calories and that a mix of calories from both
carbohydrate and fat sources is provided.
A number of the following questions require computation of TPN solutions. The
values to be used are shown in Appendix #10.

REVIEW QUESTIONS
1. Your patient is 52" and weighs 99 lb (45 kg). She had a small bowel resection 5 days
ago 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 of
400 ml dextrose 40 percent , 400 ml amino acid 10 percent, and 200 ml lipid 20
percent was ordered (along with standard electrolytes, vitamins and minerals). He
has no central venous access. What do you do?
3. Your 80-year-old female patient is intubated in the ICU. She has been diagnosed with
sepsis based upon a fever of 101F, an elevated WBC count, and a positive DISIDA

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42

scan (a nuclear medicine study to detect inflammation/possible infection). She has


been on TPN for 4 days. Her triglyceride level is 342, blood glucose is 240, and
BUN is 40 with a creatinine of 2.0. What, if any, adjustments would you recommend for her TPN solution?
4. Your postoperative patient (10 days) on TPN has elevated liver function tests, which
were not shown prior to the operation. There is no history of cirrhosis or other liver
disease. What do you do?
5. The pulmonologist has requested a consult from you to adjust the TPN on his intubated patient who has difficulty weaning from a ventilator. What do you suggest?
6. Figure the caloric content, nonprotein calorie content, protein content, percent calories
from fat, and calorie: nitrogen ratio of the following TPN formula: 400 ml dextrose
50 percent ; 400 ml amino acid 12 percent; 200 ml lipid 20 percent per liter. Total
Nutrient Admixture at 80 ml/hr for 24 hours.
7. Figure the caloric content, nonprotein calorie content, protein content, percent calories
from fat, and calorie: nitrogen ratio of the following TPN formula: 500 ml dextrose
50 percent; 500 ml amino acid 10 percent at 50 ml/hr for 24 hours; 500 ml lipid 20
percent 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 Dietitians 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 11:1:8085, 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, OCallaghan TA, Joswiak BJ, et al.: Clinical experience with three-in-one admixtures administered 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.

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43

Jensen GL, Blackburn GL, Bistrian BR, et al.: Parenteral infusion of long- and medium-chain triglycerides
and 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 Dietitians 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
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.
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 & Rehab
12:2:198-202, 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 of
total 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. In
Hyperalimentation: 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:223S225S, 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 Crohns
disease 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.

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Notes

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45

Chapter Four:
Gastrointestinal Disorders

Gastrointestinal disease and its associated treatment, including surgery, can have

a profound impact upon digestion, absorption and, eventually, nutritional status.


Appropriate nutrition support should be implemented as quickly as feasible to lessen
the severity of nutritional depletion and enhance potential for recovery.

MOUTH
The mouth plays a small role in digestion, breaking down food through mastication so that it can pass into the esophagus. Some initial digestion takes place here, with
the breakdown of carbohydrate by salivary amylase. Nutrition problems may result
from decreased intake caused by poor dentition, stomatitis and dysphagia. A solution to
these problems may be as simple as altering food consistency so that the food can be
ingested more readily. Foods of liquid consistency may be well tolerated and oral
supplements should be offered.
If stomatitis is so severe that no food can be ingested, a short period of enteral
feeding via a nasogastric tube may be indicated. Generally, any isotonic intact protein
formula is well tolerated in this case. Since stomatitis is related to chemotherapy or
radiation therapy and is often short-lived, patients suffering from it should be able to
resume oral intake once the therapy has ended.
Dysphagia (difficulty in swallowing) may be of longer duration and may never
resolve depending upon the severity and cause of the dysfunction. The assistance of
a speech pathologist is important in the treatment of patients with dysphagia, to help
determine whether it is caused by a neurological or muscular disease or related to a
surgical procedure and in which phase of the swallow the problem lies oral, pharyngeal or esophageal.

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46

A modified barium swallow is valuable in determining the extent of a patients


swallowing disorder and can be useful in determining prognosis. Diet may be modified
to include very soft or pureed foods, and to restrict thin liquids. (Thick liquids, such as
milkshakes, puddings and custards, are more easily swallowed than thin liquids.)

Mouth Problems Affecting Nutrition


Poor dentition
Stomatitis
Dysphagia
Swallowing disorders
Surgical procedures
glossectomy
surgical resection
jaw wiring
corrective surgery
Guidelines for the use of enteral nutrition in the adult patient. JPEN 11:5,1993.

If a patient is unable to protect his airway or cannot manage to swallow effectively


enough for adequate nutrition intake, he may be a candidate for short- or long-term
enteral 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 formations of the teeth or jaw.
Depending upon the ability of a patient to maintain oral intake, enteral feedings
may be indicated until he can adapt to changes that have occurred. Normal mastication
and swallowing is usually affected to the extent that semisolids or liquids are best
tolerated. When a route for provision of adequate nutrition is found, patients with oral
surgery 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 be
diagnosed as having esophageal strictures, which can narrow the esophagus so severely
that no food can pass through to the stomach.
Dietary modifications for this condition could include a trial period of a lowcarbohydrate, 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 strictures
will get worse, a regimen of liquid or pured foods or, perhaps, an enteral tube feeding

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47

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 occurrence of esophageal cancer. Replacement of the esophagus may be performed during
the same surgery. This replacement may be accomplished by using a portion of the
intestine or colon to take the place of the removed esophagus, or the esophagus may be
left drastically shortened. Other surgical interventions may include pulling the stomach
to the remaining portion of the esophagus.
Obviously, either of these types of surgeries can cause significant problems with
adequate intake of nutrition. These patients may have early satiety, symptoms of dumping (premature emptying of the stomach contents into the duodenum, which can cause
such symptoms as sweating, shakiness, and diarrhea), or difficulty in swallowing. Since
the transition to oral intake may be a slow one, these patients should have enteral
nutrition support via a jejunostomy tube or with low-volume feedings into the stomach
during the immediate postoperative period. TPN may be used in conjunction with the
enteral feedings to provide adequate nutrition intake.
Isotonic feedings are generally well tolerated. Enteral feedings should continue as
patients relearn how to eat, and be tapered off and discontinued only when adequate
oral intake can be maintained. An antidumping diet and small, frequent feedings may
be best tolerated during this relearning period.

STOMACH
Surgical resection, gastrectomy, gastroparesis and gastric outlet obstruction all
impact feeding.
Ingested food is further broken down in the stomach, where hydrochloric acid and
enzymes such as pepsin and trypsin begin to act upon protein molecules in the foodstuffs. Intrinsic factor is made in the stomach and is necessary for the later absorption of
vitamin B12 in the ileum. Conditions affecting nutritional status include resection of the
stomach, gastrectomy, gastroparesis, and gastric outlet obstruction.
The body can usually adapt to resection of the stomach, but the transitional period
may be long and difficult. Resection necessitates B12 injections, since intrinsic factor will
no 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 of
adequate gastric acids. This population is also at risk for iron deficiency anemia because
of the hypochlorhydria. These patients may require supplemental B12 and iron, or even
intramuscular injections of B12 and iron, if these levels are depleted.
One of the primary symptoms of gastrectomy is late dumping syndrome, which
occurs because of the loss of the pyloric sphincter, resulting in quick release of carbohydrate from the stomach to the small intestine, causing an increase in insulin release.
These symptoms generally occur two to four hours after meals.

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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 by
adding 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 carbohydrate, high in protein and moderate in fat. Patients who cannot tolerate adequate oral
intake may be supplemented with duodenal feedings, utilizing an isotonic formula at
an appropriate volume to allow for tolerance. Tolerance may be assessed symptomatically: little or no residual, minimal diarrhea, minimal or no abdominal discomfort. The
amount that can best be tolerated will be different with individual patients. Gastroparesis (paralysis of the stomach) is discussed in the later chapter on diabetes.
Gastric outlet obstruction may occur for a number of reasons, including stenosis of
the pylorus and changes in gastric emptying time related to surgery. If it is severe
enough to prevent oral or enteral intake for more than 5 to 7 days, and/or presents a
potential long-term problem, patients with gastric outlet obstruction may require
enteral 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 gastric
outlet obstruction, because determination of when the obstruction will open (or if
surgery will be required) is difficult. Some resolve within a few days; others may require jejunal feedings for weeks or months.

DUODENUM
Digestion continues in the duodenum, with further breakdown of protein to amino
acids, fats to glycerol and fatty acids, and carbohydrates to mono- and disaccharides.
Enzymes for this digestion are released from the intestinal mucosal cells and from
the pancreas. Hormones triggered by the presence of food in the stomach cause the
release of these enzymes, and alert the gall bladder to release bile for the absorption of
fat. Initial absorption of fatty acids, amino acids, and simple sugars begins in the duodenum. Vitamin A and thiamine are also absorbed through the duodenum.
If any portion of the duodenum is resected, the initial phases of digestion and the
readying of nutrients for absorption may be affected. However, as much as one-half of
the small bowel can be resected without long-term negative affects (Bernard and Shaw,
1993). The patient may have some problems, including symptoms of lactose intolerance
and/or dumping syndrome. Altered absorption of iron and calcium may also be
present. If iron deficiency anemia occurs, oral or intramuscular iron supplementation
may be necessary, and calcium supplementation may be beneficial as well.

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Consequences of Duodenal Resection


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

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 fatsoluble vitamins (A, D, E, and K), are all absorbed through the jejunum. Minerals, such
as 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 is
often selected for placement of feeding tubes. Either needle catheter jejunostomies or
regular jejunostomies can be placed in patients requiring short- or long-term enteral
feedings who cannot utilize gastric or duodenal feedings.
Jejunostomy feedings are beneficial because they utilize the digestive and absorptive capacities of the GI tract. Elemental, peptide, predigested or intact nutrient formulas 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 of
elemental or peptide products if intact formulas are not tolerated (as indicated by
increased diarrhea, cramping and/or abdominal discomfort.)
If the jejunum must be resected because of small bowel disease, cancer, trauma or
adhesions, the ileum is usually able to expand its role so that absorption is not affected
greatly. Initially, however, patients with a resected jejunum may experience malabsorption of lactose, fat, and protein. Decreased transit time through the gut may also precipitate symptoms similar to those experienced with dumping syndrome.
Because ileal adaptation may take some time, patients should be followed closely
and advised to choose a low-residue, lactose-free diet in small frequent feedings. Multivitamin/mineral supplementation should be considered. Eventually, a more normal
diet can be resumed, depending upon the patients tolerance (Beyer, 1989).
Should enteral feedings be necessary, care should be taken to assure continuous
feedings at a well-tolerated volume. Depending on the site of resection, elemental or
peptide formulas may be necessary, especially if the resection has involved a large
portion of the jejunum. Intact nutrient isotonic formulas may be well tolerated in those
patients with more distal resections.

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

ILEUM
The ileum is the only site of absorption of bile salts and vitamin B12. It is also the site
of absorption of chloride, sodium, potassium and disaccharides, as well as many nutrients 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 steatorrhea (passage of large amounts of fats in the feces). The maldigestion and malabsorption
of fat is caused by the inability to absorb bile salts. The unabsorbed bile salts cause the
colonic 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 can
occur. Because there is no barrier between the ileum and the colon, bacteria normally
found in the colon can migrate into the ileum. This overgrowth may precipitate diarrhea
or steatorrhea, and result in malabsorption of carbohydrate, protein, fat and fat-soluble
vitamins.
Loss of the ileocecal valve can also decrease transit time, with resulting malabsorption (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 adequate
nutritional status and allow time for the remaining intestine to adapt. Once a patient
can tolerate feedings into the gut, enteral or peptide-based formulas with medium-chain
triglycerides as a fat source are best tolerated, since medium chain triglycerides do not
require bile for absorption. These allow for healing and growth of villi. Once oral
feedings 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 of
the gut to absorb these nutrients. Lactose intolerance may occur; increased amounts of
high fiber foods may precipitate diarrhea or discomfort.
Oral intake should be introduced and advanced slowly to allow for adaptation and
better availability for absorption.
Massive small bowel resection may be necessary because of Crohns disease, small
bowel infarct or ischemia, trauma, etc. This terminology usually refers to resections of
more than two-thirds of the small bowel, with less than 100 cm of small bowel remaining. Malabsorption of nearly all nutrients occurs (depending upon which portions of the
small bowel have been resected).
Total parenteral nutrition is vital for patients who have undergone such a resection
and may be necessary for the rest of the patients life. If enteral nutrition is implemented, elemental low fat formulas should be given via a continuous drip system (to
enhance absorption of nutrients). If a patient is eventually able to tolerate oral feedings,
small, frequent feedings can be initiated and individualized to patient tolerance.

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Transition to enteral or oral feeding is often frustrating for the patient and the
dietitian. Ive had highly motivated patients who become extremely disheartened at
their inability to quickly resume eating whatever they want. One of the greatest services
we can provide these patients is counseling to help them understand their condition.
Exercise patience.

Nutrition Problems & GI Diseases


Protein deficiency
Fat malabsorption/deficiency
Anorexia
Vitamin C deficiency
Vitamin B12 deficiency
Zinc deficiency
Copper deficiency
Calcium deficiency

Carbohydrate deficiency
Weight loss
Diarrhea
Fat-soluble vitamin deficiency
Folate deficiency
Magnesium deficiency
Iron deficiency

COLON
The primary role of the colon is the reabsorption of water and electrolytes, and the
production of biotin and vitamin K. Diseases that may require a colon resection include
colon cancer, diverticulitis, ulcerative colitis and Crohns disease.
Total parenteral nutrition may be of use in patients with severe ulcerative colitis or
Crohns disease. Generally, Crohns disease patients respond better to TPN and bowel
rest than patients with ulcerative colitis (Beluzzi, et al., 1995). Parenteral steroid administration appear to be effective with Crohns patients, regardless of nutrition regimen
(Hanauer, 1997). Patients with significant colon resection may require supplementation
with biotin and vitamin K. Generally, however, patients can gradually tolerate a lowresidue or low-fiber, low-lactose diet and should eventually be able to resume a normal
diet after adapting to the surgical changes.

MALABSORPTION
Malabsorption of nutrients can also be related to diseases such as cancer, sprue,
Crohns disease, ulcerative colitis, AIDS and infectious diseases of the GI tract. Malnutrition 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 of
diminished nutrient intake, malabsorption from the small bowel because of resection or
disease, maldigestion of fat and fat-soluble vitamins after ileal resection, and drugnutrient interactions (Fleming, 1995).

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Commonly prescribed drugs for IBD include sulfasalazine, corticosteroids, and


cholestyramine. all of which can cause significant nutrient deficiencies (sulfasalazine
interferes with folate absorption; corticosteroids interfere with calcium absorption; and
cholestyramine interferes with fat and fat soluble vitamin absorption) (Fleming, 1995).
Fat malabsorption steatorrhea is commonly observed, and fat-soluble vitamins are affected. The primary symptom of malabsorption is diarrhea. Normal stool
color is present with malabsorption of carbohydrate, lactose, fluid and electrolytes. The
stool may become yellow or silver with fat malabsorption; its consistency may become
oily or floating and it may have an offensive odor. Lactose malabsorption often causes
watery diarrhea (Hermann-Zaidins, 1989). Diarrhea and fistula drainage cause losses of
electrolytes and trace elements.
Zinc deficiency is quite common in patients with IBD and other diarrhea related
illnesses. The deficiency of zinc appears to be related to decreased absorption rather than
to increased demand for the nutrient (Fleming, 1995). Other nutrients that may become
deficient include selenium, vitamin D, vitamin C, vitamin A, folate, and magnesium.
Debate continues over the optimal treatment for fat malabsorption. Typically, total
fat intake has been restricted and medium-chain triglycerides have been used to enhance absorption and reduce diarrhea. However, recent studies suggest that no benefit
is served by limiting the fat in the diet and that, in fact, the higher calorie intake from fat
is 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 intolerance). It may result in decreased transit time, diarrhea, abdominal discomfort, and
associated nutritional ramifications. The type of carbohydrate that is not absorbed
effectively should be identified and restricted in the diet. Protein malabsorption is
uncommon, but may require using elemental or peptide formulas or supplements.
Intact nutrient formulas may be more beneficial than defined-formula diets for patients
with Crohns disease, ulcerative colitis, and inflammatory bowel disease (Ginsberg and
Albert, 1989; Afdhal, et al., 1989). Others (OMorain, 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 the
increased glutamine content of elemental diets and/or the lower fat content of the
elemental diet (Fleming, 1995). Other studies suggest that patients with IBD have a
better 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 or
primary therapy. TPN and bowel rest appears to be more beneficial for the patient with
Crohns disease than for the patient with ulcerative colitis.
Nutrient requirements for patients with gastrointestinal disease and/or following
gastrointestinal surgery are generally increased. With significant malabsorption after
major GI surgery, enteral calorie needs are increased by 150 to 200 percent. Protein needs
are also increased by 150 to 200 percent. Generally, 30 to 35 kcal/kg/day and at least 1.5
gm protein/kg/day is required. Vitamin and mineral supplementation should be considered as well, based on each patients specific needs and the extent of the resection.

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SHORT BOWEL SYNDROME


Short bowel syndrome (SBS) occurs when greater than 50 percent of the small
bowel is resected or bypassed (Bernard and Shaw, 1993). Several factors are important
in determining how severe symptoms will likely be: the remaining length and site of the
small bowel; whether the stomach and/or colon has been resected; whether the ileocecal 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 is
characterized by significant malabsorption of fluid, electrolytes and other nutrients as a
result of chronic diarrhea, frequent dehydration and electrolyte disturbances. As a
result, 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 of
the small bowel removed: if the ileum is present; if the ileocecal valve is present; and if
the remaining colon is not diseased (Rombeau, 1995; Carbonnel, et al., 1996).
In order to determine the most effective method of nutritional treatment, we must
be aware of the portions of the small bowel that are remaining: whether the ileocecal
valve is present; the presence or absence of the colon; and the adaptive capacity of the
remaining gut (dependent upon the presence of disease, such as Crohns disease or
ulcerative colitis) (Espat, 1994).
Resection of the ileum of greater than 100 cm and/or the loss of the ileocecal valve
will cause significant steatorrhea and decreased B12 absorption; the absence of the
ileocecal 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 oxalate
urinary stones and decreases in water and electrolyte reabsorption (Wilmore, et al., 1994;
Stralovich, 1993; Simko, 1980). Because the duodenum, ileum, jejunum, and, to a lesser
extent, colon are where minerals, trace elements, and vitamins are absorbed, deficiencies of these nutrients may occur.
After extensive bowel resection, adaptation does occur, but this period of adaptation may take as long as one to two years. TPN is necessary during this period to provide adequate nutrient intake and, in essence, keep the patient alive. Early initiation of
enteral feedings into the remaining bowel or even oral intake can be of benefit because
of the advantages of enteral feedings in preventing mucosal atrophy, stimulating intestinal adaptation, and decreasing the risk of bacterial translocation (Byrne, et al., 1996).
Often, TPN and enteral/oral feedings must continue simultaneously for anywhere
from one month to several years. The type of enteral formula utilized is dependent on
the patients individual needs. Patients with less than 100 cm of bowel left will usually
require TPN on a long-term basis. If the patient has only 110 cm of bowel left with no
colon, defined-formula diets are of benefit; patients with more bowel remaining, especially with the presence of the colon, may well tolerate an intact nutrient formula (Bernard, et al., 1993). Intact nutrient formulas may be beneficial because of their isotonicity
and stimulation of the intestinal tract (Stralovich, 1993; Simko, 1980; Rombeau, 1995).
Oral intake, once initiated, should consist of small frequent feedings consisting of
high protein, complex carbohydrate, and low fat foods. Restriction of disaccharides
(lactose, maltose, and sucrose) is often necessary. Because calcium and magnesium may
have formed soaps with unabsorbed long chain fatty acids, oxalate absorption is altered

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54

and increased (normally the calcium and magnesium bind the oxalates) (Ladefoged, et
al., 1996). High oxalate foods may require restriction if the colon has been resected.
Supplemental vitamins and minerals are usually required (Bernard, et al., 1993). Zinc
may 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 with
specific nutrients that appear to stimulate the gut, glutamine, fiber, and short-chain fatty
acids, along with growth factor (Wilmore, et al., 1994). The addition of these nutrients to
an oral diet resulted in weaning of TPN in several long-term TPN patients with SBS.
Growth hormone appears to increase mucosal hyperplasia and colonic mass
following resection. It also increases water and sodium in the small bowel and colon
and may increase amino acid transport (Wilmore, et al., 1994; Byrne, et al., 1996).
Glutamine increases hyperplasia as well, while enhancing glucose and sodium absorption (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 into
the colon will be fermented to short-chain fatty acids, thereby enhancing sodium and
water absorption.

PANCREAS
The pancreas, though not part of the gastrointestinal tract, is important to digestion
and absorption. Hormones secreted by the pancreas include glucagon and insulin.
Pancreatic juice, containing enzymes such as amylase, trypsin and lipase, is secreted
into the duodenum when chyme is present. Pancreatic and duodenal enzymes are vital
for the adequate digestion and later absorption of nutrients. Pancreatic cancer, severe
acute pancreatitis and pancreatitis with associated abscess, fistula or pseudocyst have a
marked effect on nutritional status.
Acute pancreatitis is characterized by hypermetabolism and hypercatabolism
(Seidner and Fish, 1998). Negative nitrogen balance is common, as is alterations in
glucose metabolism (Shaw and Wolfe, 1986). As is the case in sepsis, elevations in
catecholamines, 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 from
parenteral nutrition. Absolute indications for TPN are acute necrotizing pancreatitis,
pancreatic fistulae, pancreatic pseudocyst, and pancreatic abscess. Gastrointestinal
feedings had been contraindicated because of the associated gastric atony, ileus, intestinal 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 patients
with pancreatitis, with no increase in serum triglyceride levels or worsening of the
pancreatitis as long as pancreatitis is not caused by hypertriglyderidemia (Kudsk, 1990).
However, Espat recommends that, in acute pancreatitis, IV fat should be limited to
the severely malnourished or those patients with severe glucose intolerance because of
the stimulation of the pancreas by the fat infusion. Patients with pancreatic disease

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receiving TPN typically require insulin supplementation but otherwise appear to tolerate support. However, the incidence of glucose intolerance may be lower in enterally
fed patients with severe acute pancreatitis (Kakfarentzos, et al., 1997).
Peptide or elemental feedings into the jejunum below the ligament of Treitz cause
some secretion of hormones and pancreatic activity; however, the enzymes released are
low in concentration. The feedings were safely tolerated in some studies of mild and
moderate pancreatitis and the expected problems of stimulation of the pancreas with
elevated serum amylase levels, ileus, and leakage around the jejunostomy tube did not
occur (Kudsk, 1990). It appears that the adynamic ileus that occurs with pancreatitis is
limited 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, et
al., 1984; Bouffard, et al., 1989).
The goal of nutrition support in pancreatic disease is to replete nutrition stores and
to maintain these stores throughout the course of the illness. Calorie needs in acute
pancreatitis are estimated at 1.3 to 1.5 times BEE. During chronic pancreatitis, the estimated needs are lowered to 1.0 to 1.3 times BEE. Suggested protein requirements are 1.0
to 1.3 gm protein/kg/day for chronic pancreatitis, with an increase to 1.5 to 2.0 gm
protein/kg/day for acute pancreatitis (Aalyson, 1989).

CASE STUDY #1: GASTROINTESTINAL DISEASE


Note: Nothing can replace experience in nutrition support. The judgment of the
dietitian, physician and pharmacist is of paramount importance. Accordingly, Ive
included case studies to illustrate how cases progress, what twists and turns occur and
how the nutrition support team must constantly make adjustments. It is hoped that
these studies will help the material come alive, and that the student taking the course
will give each one his or her close attention.
Case study #1: GB was a 32-year-old male who was admitted to the medical surgical floor with a diagnosis of inflammatory bowel disease that was thought to be ulcerative colitis. His symptoms of severe bloody diarrhea and an associated 25 lb weight
loss over three months resulted after he had consumed water from a trout stream. He
had been treated as an outpatient with prednisone and 5 aminosalycilate (an analgesic).
When this therapy became ineffective, his therapy changed to an increased dosage of
prednisone along with sulfasalazine and metronidazole (Flagyl). He was admitted to
the hospital after further weight loss and was started on TPN. His colonoscopy revealed
disease from the rectum to the left half of the transverse colon.
His TPN regimen was a peripheral formula of final concentration of dextrose 8
percent, amino acid 4 percent and lipid 3 percent at a volume of 2500 ml/day. The TPN
was administered through a PICC line and provided approximately 1830 kcal and 100
gm protein. He also continued to consume a full liquid diet. His anthropometrics included a height of 59 and a weight of 71.4 kg. His needs were assessed to be 1800 to
2100 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

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ulcerations. Surgery (colectomy) was considered vs treatment with continued TPN and
a change in drug regimen to methotrexate and cyclosporin. Two days later, his symptoms lessened and he was started on cyclosporin (an immunosuppressant thought to be
effective because of the autoimmune component of the disease). The TPN continued
and his diet was advanced to low residue bland. His symptoms continued to decrease
and he tolerated the diet and TPN well. His complaints changed from problems with his
GI tract to knee pain and other arthralgias (possibly associated with increased hydration). He continued to tolerate the TPN and diet and regained approximately ten
pounds. His TPN was tapered until it was discontinued and he continued on his PO
diet. A follow-up colonoscopy revealed marked improvement in his colon with few
ulcerations and reduced colitis.
The TPN and nutrition support provided to this patient enabled his nutritional
status and GI symptoms to improve. Surgery was avoided and he was discharged home
without 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 included 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?

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Silver Spring, MD, 1989.
Afdhal NH, Kelly J, McCormick PA, et al.: Remission induction in refractory Crohns disease with
nonelemental 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 and
pediatric 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 Crohns
disease: 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 Prac
8:153-162, Aug, 1993.
Beyer PL: Short-bowel syndrome. Dietitians 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. JPEN
13:1:26-27, 1989.
Byrne TA, Morissey TB, Nattakom TV, et al.: Growth hormone, glutamine, and a modified diet enhance
nutrient 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.
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Byrne TA, Browning B, Tu N, et al.: A new treatment option for patients with short bowel syndrome:
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Carbonnel F, et al.: The role of anatomic factors in nutritional autonomy after extensive small bowel
resection. 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 Crohns 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.
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Fleming CR: Nutritional considerations in inflammatory bowel disease. A.S.P.E.N. 5th Annual Advances
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Grant JP, James S, Grabowski V, and Trexler KM: Total parenteral nutrition in pancreatic disease. Ann Surg
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Hanauer S and Meyers S: Management of Crohns disease in adults. Am J Gastroenterol 92:559-566, 1997.
Hermann-Zaidins MG: Malabsorption. Dietitians Handbook of Enteral and Parenteral Nutrition. Skipper A,
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Howard L, Michalek AV, and Alger SA: Enteral nutrition and gastrointestinal, pancreatic, and liver
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Saunders, Philadelphia, 1990.
Kakfarentzos F, Kehagias J, Mead N, et al.: Enteral nutrition is superior to parenteral nutrition in severe
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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/
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Kudsk KA, Campbell SM, OBrien T, and Fuller R: Postoperative jejunal feedings following complicated
pancreatitis. Nutr Clin Prac 5:1:14-17, 1990.
Ladefoged K, Hessov I, Jarnum S: Nutrition in short-bowel syndrome. Scand J Gastroenterol. 31 Suppl
216:122-131, 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 formula
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McClave SA, Martindale RG, Vanek VW, et al.: Guidelines for the provision and assessment of nutrition
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Nightingale J, Lennard-Jones J, Walker E, et al.: Jejunal efflux in short bowel syndrome. Lancet 336:765-768,
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OMorain C, Segal AW, Levi AJ: Elemental diet as primary treatment of acute Crohns disease; a controlled
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Purdum P and Kirby D: Short-bowel syndrome: A review of the role of nutrition support. JPEN 5:93-101, 1991.
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Saverymuttu S, Hodgson JGF, Chadwick VS: Controlled trial comparing prednisolone with an elemental
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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 Surg
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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
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Wilmore DW, Ziegler TR, and Byrne TA: Is long-term TPN essential in the short bowel patient? A.S.P.E.N.
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Chapter Five:
Stress and Sepsis

his chapter will discuss sepsis and surgery, how the body reacts to these stressors, and the nutrition support requirements of patients subjected to such stress. (Another Nutrition Dimension course, Nutrition & Immunity, Part I, deals with the dietary
and nutritional effects of stress in greater detail.)
The stressed or septic patient is unique in that nearly all of his metabolic pathways
may be altered. Determining the optimal method and mode of feeding to meet his
individual requirements is quite a challenge. The additional factor of individual or
multiple organ failure must also be considered, and may prevent adequate provision of
calories and, especially, protein.
Sepsis is defined as a systemic inflammatory response to infection. Systemic Inflammatory Response Syndrome (SIRS) is much like sepsis but is an inflammatory
response to various types of insults, i.e. pancreatitis. Severe sepsis is defined as sepsis
accompanied by organ dysfunction, hypoperfusion, and/or hypotension. Septic shock
is sepsis with hypotension that is unresponsive to fluid resuscitation with resultant
perfusion abnormalities.
So what happens from a nutrition perspective when a patient is admitted with
sepsis? The patient is hypermetabolic; there is increased production of glucose with
increased uptake at the cellular level; and protein and fat are broken down at a faster
rate.

THE STRESS RESPONSE


The body reacts to stress (or threats), whether emotional or physical, with a message 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

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the same, whether the perceived threat is physical or emotional. Only the duration and
intensity varies.
During the stress response, stimulation of the autonomic nervous system causes an
increased production of catecholamines (epinephrine and norepinephrine). This decreases the release of insulin into the blood, and increases glucagon release to allow a
sudden burst of energy for action. These increased catecholamines, along with glucocorticoids, 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 stimulation
of the pituitary and adrenal glands.

The Stress Response


BRAIN/RAS (reticular activating system)

HYPOTHALAMUS
CRF (corticotropin-releasing
factor)

PITUITARY GLAND

Sympathetic Autonomic
Nervous System

Hormones
Adrenal
Medulla

Epinephrine
Norephinephrine

Pancreas

ACTH

TSH

Adrenal
Cortex

Thyroid
Gland

Growth hormone
Prolactin
Vasopressin

Insulin
Glucagon
Thyroxine
Glucocorticoids
Aldosterone
Mineralocorticoids

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Glucocorticoids (cortisol, cortisone, and deoxycorticosterone) and mineralocorticoids


(aldosterone and deoxycorticosterone) also increase, but typically return to their normal
levels rather quickly. Glucocorticoids act to increase the synthesis of glucose by the liver
through 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.

Effect of Hormones on Metabolism


Glucocorticoids
Increases:
protein breakdown
fat breakdown
glucose mobilization
Decreases:
insulin action

Catecholamines
Increases:
fat breakdown
protein synthesis
glucose synthesis

Aldosterone
Conserves:

Insulin
Decreases:

sodium
potassium

Growth hormone
Increases:
protein breakdown
fat breakdown

Glucagon
Increases:

protein synthesis
fat synthesis

protein synthesis
glucose synthesis

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

Protein Metabolism During Stress and Sepsis


Albumin

Tissue repair

AMINO ACID
POOL


Skin
(collagen)




LIVER
 Acute Phase
(Protein synthesis)
Proteins

Gut
Urea
Fibrinogen
Glucose
Muscles
(enzymes,
(Stress level Complement
secretory IgA)
indicator) Retinol-binding
protein
Prealbumin

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Nutrition Support

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

Alterations in Metabolism During Stress and Sepsis


STRESS


STRESS
HORMONES

Carbohydrate

Protein


GLUCOSE

 glycogen breakdown
 gluconeogenesis

 proteolysis
 protein synthesis
 protein for immune
organs & cells

 fat breakdown
 fatty liver / cirrhosis
 arterial plaque

Fat

Insulin
Blood Sugar

 blood sugar
 glycosuria
 sensitivity of tissues

 steroid hormones

Cholesterol

production

Ketosis may occur during stress and sepsis, possibly related to decreased insulin
availability and increase in fatty acid synthesis. This results in reduced nitrogen loss and
more efficient utilization of energy sources. However, this adaptation does not occur
readily 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, prolonged stress may precipitate multi-system organ failure, which can cause further
changes in carbohydrate, protein and fat metabolism.
These alterations, summarized above, may be recognized by increased serum
triglyceride levels (resulting from increased mobilization of fatty acids), increased blood
urea nitrogen levels (caused by decreased protein synthesis and reduced utilization of
aromatic amino acids) and progressive reduction in serum glucose levels (caused by the
reduced ability for gluconeogenesis) (Shronts and Fish, 1989). Adequate nutrition
support of the stressed or septic patient is critical to enhance the bodys ability to recover from the stressed state.

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NUTRITION REQUIREMENTS
Energy. During the acute phase of a septic episode, focus should be on metabolic
support or maintenance. Recommendations are to feed hypocalorically at a rate of 25
kcal/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/kg
with 1.5 to 2.0 gm protein/kg, taking care to avoid overfeeding.
When available, indirect calorimetry, utilizing a metabolic cart, should be used to
determine caloric requirements. Indirect calorimetry will be discussed further in Chapter Seven: Respiratory Failure. Calorie requirements can be provided with a mix of
carbohydrate and fat sources.

Caloric Requirements in Stress & Sepsis


Metabolic support
25 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.

Its important to avoid overfeeding, since hyperglycemia causes cellular disfunction, an increased risk of infection, and intracellular shifts of electrolytes. Overfeeding
can also result in increased CO2 production.
Fat. No more than 30 to 40 percent of calories, but at least 4 percent, should be
provided by fat to meet essential fatty acid needs. The type of fat is of importance in
stressed or septic patients, since certain fats are known to inhibit immune function.
Omega-6 (-6) fatty acids, including linoleic acid, are precursors to arachidonic
acid itself a precursor to types of prostaglandins, thromboxanes, prostacyclins, and
leukotrienes that can have a deleterious effect on immune functions, as shown below.
Omega-3 (-3) fatty acids, on the other hand, are metabolized to forms of prostaglandins, thromboxanes, prostacyclins and leukotrienes that have a lesser effect on the
immune system. Omega-3 fatty acids may mitigate the deleterious effects of -6 fatty
acids on the immune system, when given in adequate amounts. The chart on the following page outlines the effects of -3 and -6 fatty acids on immunity.
To increase the amount of -3 fatty acids available to the enterally fed patient,
formulas containing canola oil or fish oils (including eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA)), should be used. The lipid emulsions for TPN currently
available contain linoleic acid (so that essential fatty acids are available to the patient on
total parenteral nutrition).

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Fatty Acids and Immunity

-6

PGE2
TXA2
PGI2
LTB4

Potent inflammatory agent


Potent platelet aggregator and vasoconstrictor
Weak vasodilator
Powerful inducer of chemotaxis, adherence
of cells & inflammation

-3

PGE3
TXA3
PGI3
LTB5

Weak inflammatory agent


Weak platelet aggregator and vasoconstrictor
Active vasodilator & inhibitor of platelet aggregation
Weak inducer of chemotaxis, adherence of cells
& inflammation

The efficacy of adding -3 fatty acids to TPN lipid emulsions is currently being
studied, but no alternative is presently available. Perhaps in the immunocompromised
patient on TPN, care should be taken to limit the total calories from fat to less than 30
percent of total calories.
However, we must again weigh what is best for the individual patient. While
increased fat intake may alter immunocompetence, it may also enable the patient to be
weaned from the ventilator. We cant make a blanket statement about fat calories in
TPN. Once the composition of lipid emulsions can be altered to contain fewer -6 fatty
acids, this subject may not be as controversial.
Carbohydrate. Since hyperglycemia and insulin resistance are part of the stress
response, the provision of calories from carbohydrate may require limitation and close
monitoring for patient tolerance. In the glucose-intolerant patient, glucose should be
limited 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 as
1.5 to 2.0 gm protein/kg/day.
Renal and liver function should also be considered when assessing protein requirements. The immunocompromised, septic or stressed patient also may have renal insufficiency or acute renal failure. Care of acutely ill renal patients and patients with hepatic
insufficiency or failure is discussed in later chapters.
While arginine is not an essential amino acid in the healthy individual, it appears
to become essential during periods of stress and sepsis (Kirk and Barbul, 1990). Arginine increases secretion of growth hormone, prolactin, insulin, glucagon and insulin-like
growth factor 1 (IGF-1). Through the actions of these hormones, it appears that nitrogen
balance and wound healing are improved during periods of stress as these hormones
improve cellular growth. Arginine also appears to enhance the immune response by
improving T cell production (Kirk and Barbul, 1990). Peripheral lymphocytes are increased in number by arginine and the mitogenic response of immune cells to antigens
Con A and PHA is improved (Daly, et al., 1988).

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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 powerful stimulator of immunity and wound healing, while prolactin is a stimulator of anabolism or cellular growth. These factors result in decreased weight loss and increased
wound healing (Young, 1991; Kirk, 1990). Arginine also appears to play a role in increasing insulin release.
Arginine accelerates wound healing and improves immunity The mechanisms are
not clearly understood, but are believed to be related to arginines chemical makeup
and metabolism, as shown in the chart on the following page.
Arginine may be of benefit to the critically ill patient by improving or preserving
immune function (Daly, et al., 1988). Supplemental arginine has been added to some
enteral formulas; they contain approximately 5 percent (7 to 20 gm/1500 kcal) of total
protein as arginine. The addition of arginine via an enteral formula may be beneficial to
patients with blunt torso trauma and in malnourished patients who will undergo
elective gastrointestinal surgery. Arginine can be added to TPN at levels of 5 to 12.5 gm
arginine/100 gm amino acid (Fish, 1994). The addition of enteral arginine to formulas
for the septic patient is not effective and may be harmful (VanWay, 2007).
Pontes-Aruda has extensively studied the effects of enteral nutrition with
eicosapentanoic acid, glutamine and antioxidants when utilized during critical illness
and sepsis. His studies, published in Critical Care Medicine, suggest that using these
specialized formulas appear to reduce incidents of organ failure, ventilator days, ICU
days, and mortality (by 60 percent)(Pontes-Aruda, et al., 2006, 2007).

Arginine
Ornithine
NH3 + CO2 + 2 ATP

 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

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Glutamine, while generally described as a non-essential amino acid, becomes an


essential amino acid during periods of catabolism or extreme stress. Glutamine comprises
61 percent of the amino acid pool in skeletal muscle and, along with alanine, is the primary 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 a
greater rate, thereby depleting intracellular glutamine by more than 50 percent. During
stress, glutamine synthesis increases. The gut appears to play a role in the metabolism
of glutamine by converting skeletal muscle glutamine to nitrogen and alanine; these are
then 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 the
Krebs 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. Replicating 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 and
is important for gluconeogenesis in the liver (Long, et al., 1995). Glutamines other
functions include transport of ammonia between tissues; regulation of glycogen synthesis in the liver; and acting as a precursor in the formation of purine and pyrimidine
rings (Zaloga, unpublished; Smith and Wilmore, 1990).
Glutamine is stored in the muscles of the body and released when the demand
increases. Without an exogenous supply of glutamine during stress and sepsis, the
muscles shrink and glutamine can become depleted. When glutamine is not available or
the 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 (Lacey
and Wilmore, 1990).
During a catabolic or stressed state, levels of glutamine in the blood fall 20 to 30
percent, indicating that glutamine may be vital to the bodys response to stress. Reduced protein synthesis, atrophy of intestinal mucosa and impaired immune response
result (Lochs and Hubl, 1990).
In animal studies, stressed animals supplemented with glutamine showed improvement in the quality of the gut wall and reduced incidence of weight loss and
infection 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 translocation and may help to improve patient outcome (Jensen, et al., 1996).
Bacterial translocation is defined as the passage of viable indigenous bacteria
from the gastrointestinal lumen, through the epithelial mucosa to mesenteric lymph
nodes 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; bacterial
overgrowth; and endotoxemia) (Hermann, 1995) contribute to translocation. The incidence of bacterial translocation is lower when the gut is utilized for feeding (Moore and
Jones, 1986). Glutamine is metabolized in the gut and then serves as energy for the
enterocyte. During stress, glutamine uptake by the GI tract increases (Austgen, 1991).

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When glutamine is supplemented, plasma and muscle glutamine levels increase; intestinal cell integrity and villous height are better maintained; and mucosal DNA activity is
maintained.
Glutamine is available in all enteral formulas, primarily as glutamic acid, but must
be supplemented in free amino acid formulas.
Generally, glutamine content ranges from 5 to 8 gm per 16 gm of nitrogen. This
corresponds 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 may
require up to 40 gm of glutamine/day (Brantley, 2007). Glutamine is not typically stable
in 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 to
TPN, 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 at
levels 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) enteral
feedings can be started to stimulate the gut mucosa and prevent gut atrophy. Glutamine
can also be added to enteral formulas by mixing 10 gm glutamine with 30 ml water and
infusing 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 been
established, but we do know that the need for certain vitamins and minerals increases.
The chart below summarizes the vitamins and minerals required for each metabolic
process.

Nutrients Needed for Metabolic Processes


Carbohydrate metabolism
Thiamine, riboflavin, niacin, B6, B12, biotin, pantothenic acid, sulfur,
phosphorus, potassium, magnesium, manganese, copper, chromium
Protein metabolism
Niacin, B6, folic acid, biotin & pantothenic acid, phosphorus,
potassium, sulfur, magnesium, zinc & copper
Fat metabolism
Thiamine, riboflavin, niacin, panthothenic acid, biotin, phosphorus,
magnesium, iron, copper & sulfur
Steroid synthesis
Riboflavin, niacin, pantothenic acid & magnesium, cholesterol as
substrate
Catecholamine synthesis
B6, C, iron, magnesium & copper, tyrosine as substrate

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

NUTRITIONAL REPLETION
Nutritional repletion of the critically stressed or septic patient should begin when the
patient has been fluid resuscitated and is hemodynamically stable. If at all possible, early
enteral nutrition support should be initiated. Hypoperfusion to the gut can occur with a
mean arterial pressure below 60; enterally feeding a patient who is significantly hypotensive 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 nutrition
support. The gut appears to influence the production of cortisol, glucagon and norepinephrine (Alexander, 1988; Kudsk, 1988). When the GI tract is utilized, the gut wall
appears to be maintained and the levels of stress hormones appear to be decreased. A
decrease in septic complications in trauma patients has been shown to occur when these
patients are fed enterally (Minard and Kudsk, 1994).
When the GI tract is not utilized, the intestinal villi atrophy. This causes a breakdown in the intestinal wall mucosal integrity, which can allow translocation of gut
bacteria into the lymphatic and portal circulation. In an already immunocompromised,
critically ill patient, this can be a deciding factor in the patients outcome.
Enteral feedings should be initiated slowly into the small bowel if possible. While
an ileus may persist for several days in the colon, the small bowel does not develop an
ileus 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 hypermetabolic 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 patients nutrition needs is attained.
While enteral feedings are the nutrition support method of choice in the stressed or
septic patient, the use of total parenteral nutrition is warranted in some instances, as
discussed in Chapter Three. Adjunctive parenteral nutrition can be of use in patients
who cant meet their nutritional requirements with enteral feedings alone.
The stressed or septic patient is often the patient in the ICU who never seems to
improve, then suddenly everything kicks in and he recovers. There are times, too, when
nothing works for these patients, and they eventually die after long and expensive treatment. Nutrition support is important for these patients, but we must remember that it is
only one of many therapies theyre receiving. Sometimes it seems there is little we can do.

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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 respiratory
distress syndrome (ARDS). Her medical and surgical history was benign except for a 10year history of bulimia and anorexia. Upon admission, she was 54" 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. She
was 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 to
decrease caloric intake to prevent overfeeding and TPN was discontinued when the
enteral feeding was increased to 50 ml/hr (1440 kcal, 64 gm protein). She continued to
tolerate the feeding. Enteral feedings gradually increased to 65 ml/hr (1560 ml, 1872
kcal, 82 gm protein). Enteral feedings continued to be well tolerated and were further
increased 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 was
edematous.
She stabilized and came out of the acute septic stage but had suffered ischemia of
both lower extremities, all of her fingers and her nose because of the DIC. She faced
bilateral 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 had
improved: albumin 2.5; prealbumin showed mild depletion and transferrin showed
moderate depletion. Enteral feedings resumed at 60 ml/hr (1440 ml, 1728 kcal, 62 gm
protein) 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 were
tolerated 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 and
enteral feedings were changed to 11 hours at night at 100 ml/hr (1320 kcal/47 gm
protein). She was taking 60 to 75 percent of a regular diet, but continued to exhibit
symptoms of an eating disorder as she consistently avoided certain food groups and
concentrated only on increasing her intake of high protein foods. Enteral feedings were
changed to a more nutrient-dense formula at 50 ml/hour over 12 hours (900 kcal, 33 gm
protein). 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 occupational
therapies. Her oral intake improved and revealed adequate intake to allow discontinuing her enteral feedings. Albumin stabilized at 3.4 to 3.8. Multivitamins were given (she
had supplemental zinc, vitamin C, and vitamin A in her enteral feeding). Weight
dropped 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.
PKs devastating illness was likely related, in part, to her immunocompromised
state caused by a combination of her anorexia/bulimia and an acute illness. She became
very septic and developed DIC, an unusual coagulopathy that results in disturbed

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blood flow to extremities. As a result, she was lucky to survive, but will have to continue on with bilateral AKAs and reduced usage of her once dominant hand. PK has
returned to the hospital to visit on multiple occasions. While she is confined to a wheelchair because of bilateral AKAs, she has rehabilitated well and lives as normal a life as
possible. Luckily, PK had early nutritional support and was able to tolerate enteral
feedings from the beginning.

CASE STUDY #2
LG was a 50-year-old female admitted to the ICU after surgery to repair a dissecting ascending aorta that extended all the way to her renal arteries. Post-operatively she
developed respiratory failure and ARDS and acute renal failure. Other problems include
obesity (54, 94 kg) and anemia, as well as coronary artery disease (CAD).
LG was started on CRRT (continuous renal replacement therapy) post op day 2 and
was started on TPN the same day. Her TPN formula was: amino acid 5 percent, dextrose
18 percent, and lipid 2 percent at 70 ml/hr (1700 kcal and 84 gm protein). Her needs
were assessed to be 1700 to 1900 kcal per day and 65 to 100 gm protein per day. Her
BUN was 46, Cr 4.3, glu 364, and albumin 2.4. Insulin was given for the increased
glucose this may have been elevated because of the dextrose load of the TPN because
of the stress response, and/or because of a predisposition for glucose intolerance.
Four days later, LGs condition had not improved; she was now pharmacologically
paralyzed; her albumin was 1.5 (further evidence of a highly catabolic state), BUN was
36 and Cr 3.2 and glucose was 231. TPN increased to 80 ml/hr (1943 kcal and 96 gm
protein). Her course continued much the same with little improvement in lab values.
She had a tracheostomy and was converted to hemodialysis. Nutrition status remained
stable 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, 58, 160 lb
(72 kg).

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Brantley SL. Glutamine metabolism: nutritional and clinical significance. A.S.P.E.N. Clinical Nutrition
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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
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.

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Minard G and Kudsk K. Effect of route of feeding on the incidence of septic complications in critically ill
patients. Sem Resp Inf 9:228-231, 1994.
Moore EE and Jones TN: Benefits of immediate jejunostomy feeding after major abdominal trauma. J
Trauma 26:874-881, 1986.
Moore F, Moore E, Jones T, et al.: TEN vs. TPN following major abdominal trauma-reduced septic morbidity. 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 Med
34(9): 2006.
Pontes-Aruda A, DeMichele S, Seth A, et al.: The use of an enteral diet with EPA, GLA and antioxidants in
critical illness. Crit Care Med, 2007.
Shronts EP and Fish JA: Surgery, sepsis, and trauma. Dietitians 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:137S146S, 1990.

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Chapter Six:
Obesity and Diabetes Mellitus

he nutrition care of the diabetic or obese patient is really no different from the
care of any other critically ill patient. Care should be taken that the patient is not overfed; intentional underfeeding of the critically ill obese patient requires close monitoring
and remains controversial. The existence of additional illnesses, including renal, cardiac,
and/or respiratory disease should be evaluated and appropriate adjustments in the
nutrition support regimen should be made to optimize nutrition care and status.
The nutritional monitoring of the diabetic patient should include awareness of
changes in weight, laboratory data and clinical condition.

DETERMINING NUTRIENT NEEDS


Nutrition support of a critically ill obese patient is a challenge, partly because the
precise determination of caloric and protein needs is difficult. The percentage of lean
body mass in obese patients is difficult to determine. We know that as a person becomes
more obese, total lean body mass increases. But, due to excessive fat stores, the percent
of lean body mass in relation to total body weight decreases. In fact, because of this
decrease in percent of lean body mass, a very obese patient may have caloric expenditures as low as 16 to 18 kcal/kg of body weight.
Permissive underfeeding or hypocaloric feeding is recommended for critically ill
patients with a BMI greater than 30. This means that these patients should be fed at
levels 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)].

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

NUTRITION ASSESSMENT
Nutrition assessment of an obese patient is difficult because his fat stores make
determination of lean body mass by conventional methods nearly impossible. Therefore, we must consider laboratory data, including the parameters for evaluating protein
stores:
Serum albumin
Serum transferrin
Serum prealbumin
Serum retinol-binding protein
Total lymphocyte count
Important factors to monitor in the ongoing assessment of nutritional status include: weight changes not associated with changes in fluid status, adequacy of nutrient
intake and the patients clinical condition.
The most optimal method of determining caloric requirements in the critically ill
obese patient is with indirect calorimetry, utilizing a metabolic cart. A study of obese
patients (who were not critically ill) using indirect calorimetry revealed that their
energy 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 patients, 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 caloric
requirements in the non-obese population, its use for the obese patient is limited. If the
patients ideal body weight (IBW) is utilized in this equation, its use may seriously
underestimate actual requirements. Some practitioners increase the determined resting
energy expenditure (REE) by 120 to 150 percent to allow for higher requirements caused
by 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 in
lean body mass, as shown below.

Determining Adjusted Ideal Body Weight


[(actual weight IBW) x .25] + IBW = adjusted IBW
Example: actual weight = 90 kg
IBW = 50 kg
90 50 = 40 x .25 = 10 + 50 = 60 kg adjusted IBW

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Caloric needs can also be determined by utilizing a factor of 22 to 25 kcal/ideal


body weight or 11 to 14 kcal/kg actual body weight. After determining caloric requirements, the patient should be closely monitored to assure that he is not being over- or
underfed.
Protein requirements should be determined by using the patients ideal body
weight. In order to allow for protein sparing and to reduce the risk for protein depletion, 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 patients
nutritional status with nitrogen balance studies and laboratory data. Nitrogen balance
studies may be of limited value in the critically ill patient. However, they do provide a
baseline and can be used to show that nutrition support is not working to improve
nutritional status. Remember that a high protein intake can increase nitrogen output.
Requirements for trace elements, vitamins, minerals, and electrolytes are the same
as for other critically ill non-obese patients. These requirements have been outlined in
earlier chapters.

LONG-TERM CARE
Because the obese patient may be at risk for associated cardiac and respiratory
problems, he may often be critically ill for extended periods of time. Some researchers
have suggested that the use of hypocaloric nutrition support in the obese patient may
be of benefit (Baxter and Bistrian, 1989). Obese patients are often insulin-resistant and
glucose-intolerant. Use of a hypocaloric formula (approximately 60 percent of predicted
energy expenditure) may be of use in improving glucose tolerance.
In the critically ill obese patient, the need for some nonprotein calories, in addition
to protein calories, appears necessary to improve nitrogen balance. While hypocaloric
nutrition 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 hypocaloric
feedings can be made by subtracting 300 to 500 kcal from the REE, up to a limit of 2000
kcal/day. Protein needs remain the same, utilizing the estimate at the upper end of the
range 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 United
States (Mahler and Adler, 1999). Diabetics comprise approximately 10 percent of hospital discharges; their length of stay is 30 to 50 percent longer than their nondiabetic
counterparts. Approximately 100,000 diabetics receive TPN on an annual basis; about
the same number receive enteral nutrition support annually (Holdy, 1995).
Diabetes mellitus involves not only an alteration in the metabolism of carbohydrate, but also an alteration in the metabolism of protein and fat.
Alterations of carbohydrate metabolism include: a decrease in peripheral glucose
uptake, an increase in exogenous glucose production; a decrease in the ability to suppress hepatic glucose production; and a decrease in the ability to oxidize infused glucose.

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Alterations in fat metabolism include: a increase in lipolysis with resultant increases 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 to
suppress 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 decrease in the uptake of branched chain amino acids by the muscle tissue, and an increase in the release of amino acids from muscle tissue (Ziegler and Smith, 1994).
Diabetes mellitus also causes primary or secondary disturbances in the secretion
and/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 in
caused by diabetes mellitus, occurs with pregnancy, or occurs with stress or sepsis.
Elevated glucose levels impair leukocyte function and complement function. Both of
these complications can impair immune function. Growing evidence suggests that
hyperglycemia increases the risk of nosocomial infection (Holdy, 1995; McMahon, 1995).
Several studies have shown that the rate of central catheter-related infections is five
times higher in diabetic patients on TPN and that hyper-glycemia is the most common
risk 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 the
nosocomial infection rate was five times greater than what would have been expected.
Clearly, tight glucose control is important in all patients, not just the diabetic
patient. Glycemic control can be improved. Serum glucose should be maintained at
between 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 glucose
administration 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 glycemic
control. The insulin can be included in the TPN at a level of approximately 0.1 units per
gram of dextrose (Holdy, 1995; McMahon, 1995).
Subcutaneous insulin may be given as needed to maintain a serum glucose level of
less 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 insulin
per 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 a
10 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 high
levels of insulin may indicate that the patient has become insulin resistant. Insulin
resistance 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 at
increased risk for depletion of protein stores. They should be monitored closely for
changes in nutritional status.

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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 at
1.5 to 2.0 gm/kg/day. Keep in mind that the diabetic patient may have renal compromise and may not tolerate this level of protein intake.
Nutrition support should be initiated as quickly as possible. Because of the intolerance to glucose and the goal of improving control of serum glucose, enteral feedings or
TPN of both glucose and fat sources should be utilized.
Enteral feedings can be utilized fairly readily in diabetic patients. Blenderized
formulas and high fiber formulas may be better tolerated in these patients because of the
effect of soluble fiber on glucose control. However, the amount and type of fiber in most
enteral formulas appears to have little impact on serum glucose levels. Little research
exists 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 percent 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 likely
benefit from the use of formulas that are isotonic or nearly so. However, the patient with
gastroparesis may better tolerate jejunal feedings because of the delayed gastric emptying and small bowel dysmotility (Kim, et al., 1991).
If the patient with gastroparesis is fed into the stomach, a high fiber intake may
further delay gastric emptying (Charney, 1997), as can formulas containing free amino
acids (Charney, 1997). Formulas that are restricted in carbohydrate and higher in fat may
be beneficial in controlling blood glucose levels, especially in patients with difficulty in
attaining tight control. Generally, isotonic feedings run continuously are best tolerated,
especially initially. Monitor glucose levels closely, adjusting additional administration of
insulin as needed.
The avoidance of overfeeding is the most important factor in the nutrition support
of the diabetic patient. Specialty formulas containing lower levels of carbohydrate and
higher levels of fat have been developed in the hope that the formulas could aid in the
level of glycemic control. However, the clinical significance of studies performed with
these formulas is unclear. The avoidance of overfeeding appears to be far more beneficial than the use of specialized diabetes formulas (Charney, 1997; McMahon, 1995).

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REVIEW QUESTIONS
1. A female patient has been admitted with sepsis and respiratory distress. She is 52"
and weighs 220 lb (100 kg). Determine her protein/calorie requirements.
2. A diabetic patient, 62", 198 lb (90 kg) was admitted to the CCU for an acute myocardial infarction and has subsequently been through surgery for a coronary artery
bypass and graft. Postoperative complications include acute renal failure and an
inability to wean from the ventilator. What are his needs and what mode of nutrition 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 12:149154, 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) and
American 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 5th
Annual 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.

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Chapter Seven:
Respiratory Failure

s 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-dependent patients are often the sickest patients in the ICU. They are at great risk for malnutrition and resulting complications, especially pneumonia. The early initiation of nutrition 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 is
adequate, and, therefore, other reasons for weight loss must be examined.
The normal, healthy person uses 36 to 72 kcal/day for breathing. A patient with
COPD, 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 their
healthy 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 and
decreased respiratory muscle efficiency (Rothkopf, 1989). Impaired gas exchange with
subsequent inadequate oxygen delivery to organs and tissue may also contribute to
malnutrition (Sridhar, et al., 1994). The hypermetabolic state may be related to the increased work of breathing and may be accompanied by inadequate intake, thereby resulting in weight loss (Wilson, et al., 1985; Schols, et al., 1991). Whatever the cause, pulmonary
disease presents a set of challenges and problems to the nutrition support dietitian.
If a COPD patient subsequently becomes acutely ill and develops anorexia and
decreased intake, he loses weight more rapidly than a person without respiratory
disease. The malnourished COPD patient has a higher incidence of respiratory mortal-

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ity than a well nourished person with COPD (Gray-Donald, et al., 1996). Since his caloric
requirements are so high, the patient may have difficulty regaining, or even maintaining, weight. This weight loss may be associated with a decrease in muscle mass, including respiratory muscle mass. The diaphragm loses muscle mass and strength, and, since
normal muscle mass is necessary for normal lung function, any weakening makes the
lungs less efficient.
Impaired pulmonary function may necessitate intubation, or complicate weaning
the 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).

Effects of Malnutrition





Respiratory rate
Tidal volume
Muscle mass
Muscle strength

 Minute ventilation
 Response to hypoxia
 Immune response
Affects pulmonary metabolism

The lungs are profoundly affected by malnutrition, as shown above. The immune
response is also affected: the rate of surfactant production decreases, immunoglobulin
levels drop and the production of new cells in the epithelial lining slows. Decreased
surfactant levels can contribute to atelectasis and possibly pneumonia. Alteration of the
epithelial lining impairs the lungs ability to fight off infection.
Macrophages in the lining defend against the invasion of foreign materials and
bacteria. If the number of macrophages is reduced, immune function is compromised.
Hypoalbuminemia can cause pulmonary edema because of decreased oncotic pressures
and fluid shifts (Schwartz, 1993).
Pulmonary disease affects immunocompetence to the extent that a patient who is
also malnourished is at greater risk for infection. Once an infection sets in, the patient
may begin a downward spiral in which he becomes more nutritionally depleted due to
poor appetite and intake, leading to further weakening and loss of respiratory muscle
mass. Clearly, early nutrition support of pulmonary patients is warranted.

ASSESSING NUTRIENT NEEDS


As mentioned earlier, energy expenditure is increased in patients with respiratory
disease. In order to determine nutritional requirements, indirect calorimetry can give an
accurate estimation of actual needs, but other measures can be utilized if a metabolic
cart is unavailable or not appropriate for use. REE is determined by the following
formula when a metabolic cart is utilized:
REE = (3.94 x VO2) + (1.11 x VCO2) - (2.17 x UUN)

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In the completion of an indirect calorimetry measurement, a 24-hour urine collection for UUN (urinary urea nitrogen) is necessary. Those patients receiving enteral
nutrition support or TPN should have a constant intake for 12 hours before the test is to
begin (McClave and Snider, 1992). The patient should then be kept NPO for greater than
two hours; the room must be quiet and thermoneutral; and the patient should be kept
quiet (Compher, 1993).
Indirect calorimetry can be determined with either the open-circuit method or the
closed-circuit method. The more accurate open-circuit method allows the patient to
breathe room air. Actual volumes of expired gas are measured; the fractions of oxygen
and carbon dioxide are then ascertained. From these measurements, oxygen consumption and carbon dioxide production are calculated and energy expenditures are determined. Patients who cannot remove supplemental oxygen to breathe room air and
patients who are intubated on high pressure support with low measured oxygen levels
are not candidates for metabolic cart measurements. The easier-to-perform closedcircuit method requires that the patient breathe from a controlled air system, allowing
us to know volume and oxygen concentration. Continuous 24-hour metabolic monitors
have recently become available and may reflect actual energy expenditure and respiratory quotient. The monitor reflects actual requirements for the patient and no formulas
are 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 is
the fractional concentration of O2 in inspired gas and FEO2 is the fractional concentration 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 in
expired gas and FICO2 is the fractional concentration of CO2 in inspired gas.
Metabolic measurement carts measure oxygen consumption and carbon dioxide
production. Many factors influence metabolic rate, including activity, posturing, hyperthermia, disease states, dialysis, hyperthyroidism, and surgery. Several factors (muscle
relaxants, sleeping, starvation, narcotics, hypothermia, and hypothyroidism) decrease
metabolic rate. Metabolic monitoring cannot be completed on patients with chest tubes
or 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 be
no 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 in
patients who are unable to increase ventilatory drive to compensate for excess carbon
dioxide production (Jolly, 1997). The Vencor (a national chain of hospitals for vent
dependent patients) metabolic studies showed that an estimation of 25 kcal/kg is often
appropriate; in fact, 67 percent of patients on the study had measured energy expenditures of less than 25 kcal/kg (McClave and Snyder, 1996).
Increased protein intake can cause increased minute ventilation and oxygen consumption and can increase ventilatory response to hypoxia and hypercapnia. In other
words, the increased protein can cause the lungs to work harder and consume more

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

Nutritional Requirements
Calories

Protein

Maintenance

1.2 - 1.3 X BEE


25 - 30 kcal/kg/day

1.2 - 1.5 gm/kg/day

Anabolism

1.4 - 1.6 X BEE


20 - 30 kcal/kg/day

1.5 - 2.0 gm/kg/day

Pulmonary patients should never be overfed! Patients overfed with a high carbohydrate formula produce more carbon dioxide and show increased blood carbon dioxide levels, putting them at risk for worsening respiratory failure. Increased carbon
dioxide 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 their
respiratory quotient (RQ), the ratio of carbon dioxide production to oxygen consumption. This can be determined using a metabolic cart. RQ increases with the oxidation of
carbohydrate (as shown below), so carbon dioxide production increases with high
carbohydrate intake. This increases the lungs workload (to expel the additional carbon
dioxide), thereby increasing minute ventilation.

Respiratory Quotient
RQ =

carbon dioxide production


oxygen consumption

Oxidation of fat:
Oxidation of protein:
Oxidation of carbohydrate:

RQ = 0.7
RQ = 0.8
RQ = 1.0

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

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Respiratory distress is defined as increased dyspnea, pO2 level below 90, pCO2
level above 50 and the inability to maintain normal respiration without support. Respiratory distress is usually a physicians diagnosis, and is so indicated on the patients
chart.

TREATMENT MODALITIES
Respiratory failure can affect patients with existing pulmonary disease, and also
may 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 respiratory
muscles and for infection in the lung caused by aspiration of gastric contents or fluids
through unprotected airways (Miller, 1986).
Therefore, the feeding route for these patients is very important. As a rule, enteral
feedings are the method of choice. The benefits of enteral feeding often outweigh the
risks, especially if care is taken to avoid complications. The feeding tube should be
placed in the duodenum or jejunum, if possible, and the patient should be positioned so
that his head is at a 45-degree angle to the rest of his body in order to reduce the risk of
aspiration of gastric contents.
However, if circumstances preclude the use of enteral feedings, TPN can be utilized effectively. TPN may be a better choice for the patient who cannot be fed enterally
because of altered gastrointestinal function (perhaps from surgery or trauma) or whose
GI function is slowed because of medications, like narcotics (which paralyze the
sympathetic nervous system to calm the patient and make ventilator treatment more
effective).

FORMULAS
Because of the increase in carbon dioxide production with high carbohydrate
intake, it has been suggested by nutrition support companies that the patient who
normally is a carbon dioxide retainer be treated nutritionally with a high-fat, lowcarbohydrate formula. In clinical practice, however, the use of these formulas is rarely
warranted (Jolly, 1997). I have found that these formulas may be of limited use in a
patient who is a CO2 retainer, rather than in all patients on ventilators. A.S.P.E.N. and
SCCM do not recommend the use of high-lipid, low-carbohydrate formulas designed to
manipulate respiratory quotient (McClave, et al., 2009).
A more important consideration is that the patient should not be overfed or
underfed. Hypocaloric intake can decrease metabolic rate, minute ventilation, and
response to hypoxia. Overfeeding can increase CO2 production, minute ventilation, and
response to hypoxia. By the avoidance of overfeeding, excess carbon dioxide production will not occur.
High-fat formulas often cause gastrointestinal side effects, such as belching, abdominal distention and diarrhea (Kuo, 1993). Abdominal distention can increase pressure on the diaphragm and may contribute to delays in ventilator weaning. Delayed
gastric emptying and high residuals can also occur with high fat formulas; high residuals can increase the risk of aspiration, already a risk in the ventilator dependent patient.

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Elemental enteral formulas which are extremely low in fat (about 4 percent), can
cause elevated carbon dioxide levels and metabolic acidosis (Schwartz, 1993), increasing
the lungs workload. A formula high in fat (60 percent calories from fat) and low in
carbohydrate may therefore benefit patients who are known carbon dioxide retainers or
who have difficulty weaning from the ventilator. Again, it varies from individual to
individual and the key issue is not to overfeed.
Many pulmonary patients, including most intubated patients (especially if weaning is not imminent or difficult) can be managed effectively on more conventional,
balanced formulas with 20 to 50 percent calories from fat. Considering the adverse
effects of a high-fat-content formula on gastrointestinal function and immune function, I
recommend the use of conventional formulas for most patients.
Recommendations for provision of glucose in TPN solutions vary from a limit of 2
to 4 gm glucose/kg/day (Rothkopf, et al., 1989) to a provision of 50 percent of nonprotein calories from carbohydrate (Wilson, et al., 1985; Miller, 1986; Schwartz, 1993)
with the remainder of required calories provided from fat and protein. A limitation on
carbohydrate can result in a decrease in carbon dioxide production and may enhance
weaning from the ventilator. A more important consideration, again, is to ensure that
the patient is not overfed.
While the provision of protein to the patient with respiratory disease or failure may
increase the respiratory workload, the benefits (in terms of nutrition support) of its
provision in appropriate amounts outweigh the drawbacks. A high protein intake may
result in increased minute ventilation and increased oxygen consumption in the respiratory-compromised patient.
Requirements for protein in the pulmonary patient are 1.2 to 1.5 gm/kg/d, ranging
up to 2.0 gm/kg/d in the severely stressed patient. Response to the provision of protein
should be closely monitored, and changes made if symptoms of worsening respiratory
distress, such as increased metabolic rate and minute ventilation, develop. Protein
intake should then be reduced to levels sufficient to meet the lower ends of estimated
needs, or at higher levels if respiratory distress lessens.
Fluid balance should be closely monitored in the pulmonary or ventilator-dependent patient. These patients are at increased risk for fluid retention and may develop
pulmonary edema (accumulation of fluid in the lungs caused by depressed cardiac and
pulmonary function), which further increases the work of breathing. Fluid restriction
may often be indicated. Symptoms of edema are shortness of breath and worsening
respiratory distress.
Adequate phosphorus is vital to these patients. Low serum phosphorus alters
oxygen transport and appears to reduce the strength of the diaphragm (Rothkopf, et al.,
1989; Schwartz, 1993). Phosphorus levels, therefore, must be closely monitored (at least
once or twice a week), with appropriate supplementation to achieve normal serum
values provided as needed. Changes in phosphorus, potassium, and magnesium levels
may 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 patient
in Chapter Four can be used as well.

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ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)


ARDS is the onset of severe acute lung injury resulting in acute hypoxemic respiratory 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, as
discussed earlier, is implemented with ARDS, with the same sequellae as exists in other
stressed states. Just as in the patient with COPD or who is ventilator dependent, the
patient with ARDS should not be overfed, especially with carbohydrate calories. Calorie
and protein requirements are similar to the those recommended in COPD (25 to 30
kcal/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 may
be of benefit. While enteral feedings are preferred, parenteral nutrition may be utilized
when 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 same
for the respiratory patient as for any other patient. An accurate admission weight and
knowledge of any recent weight considering fluid status changes are important tools in
the determination of nutrient requirements.
During nutrition support, laboratory data, such as albumin, transferrin,
prealbumin, total iron-binding capacity and total lymphocyte count should be periodically monitored to assess improvement in nutritional status. Other laboratory data of
use in determining tolerance to nutrition support should also be monitored. These
indicators have been discussed in earlier chapters. Clinical improvement in condition
should 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 consumption does not interfere as much with the actual act of breathing. (Solid foods
expand the stomach, causing it to press against the diaphragm, making it difficult to
both eat and breathe.) Be sure that the patient continues to maintain adequate oral
intake once he is tapered off TPN or enteral feedings.
Laboratory values of use in determining changes in respiratory status may or may
not be of use in determining appropriate nutrition support. Indirect calorimetry is
useful in determining respiratory quotient; this information can help you determine the
optimal 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 upon
admission. He presented with an accompanying history of alcoholism, staph pneumonia, COPD and developed acute renal failure.
On Day 3 of his stay, TPN was initiated with a formula of 400 ml D50, 400 ml 10
percent amino acids, and 200 ml of 20 percent lipid emulsion, to run at 60 ml/hr.

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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, K
3.3, glucose 153, albumin 1.6, PO4 6.3, WBC 13.8, and Hgb 10.8 with Hct 32.4. Needs
were assessed to be 2000 to 2400 kcal/day and 80 to 95 gm protein/day. Factors to
assess needs were 30 to 35 kcal/kg/day and 1.0 to 1.2 gm protein/kg/day. Acute renal
failure continued as evidenced by increased BUN, creatinine and phosphorus. (The
decreased albumin level likely was secondary to sepsis, decreased intake and possible
liver disease due to alcohol intake.)
By Day 6, TPN was increased to 90 ml/hr (2333 nonprotein kcal, 2678 total and 87
gm protein), meeting his needs. On Day 10, weight had increased to 85.1 kg, BUN was
112 and Cr was 6.2. Albumin levels had increased to 2.1 and hemoglobin and hematocrit
levels had improved. Dialysis was initiated at this point, with resulting improvements
in lab values.
On Day 17, pCO2 levels were noted to be elevated and the patient continued to
require high levels of ventilatory support. Recommendations were made to change the
TPN formula in order to lower the carbohydrate load and increase the fat content
provided in the hopes of improving RQ. The TPN was subsequently changed to a
formula consisting of: 300 ml D50, 400 ml 10 percent amino acids, and 300 ml 20 percent
lipid emulsion. This provided (at 90 ml/hr) 2398 nonprotein calories, 2744 total calories
and 87 gm protein. Percentage of calories from fat was increased to 57 percent. The
patient was also given 25 percent IV albumin to assist with dialysis.
By Day 19, improvement in response to ventilatory support was noted and pCO2
levels had decreased. Serum albumin levels had fallen to 1.8 secondary to increased
levels of stress and slow response to therapy caused by the long half-life of albumin. All
other lab values remained stable, in an acceptable range for this patient with ARF. On
Day 22, the patient was stabilized well enough to allow him to be transferred to another
facility.

CASE STUDY #2
JW was a 71 year old male admitted with respiratory failure. His history included
COPD, obesity, hypertension, and IDDM. He had experienced compression fractures
because of chronic steroid therapy. He also had a permanent pacemaker inserted. He
followed a 1700 kcal ADA diet at home and was allergic to milk, pork, and soy. He was
58 and weighed 83.8 kg (109 percent of IBW). His needs were assessed to be 2100 to
2500 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 was
75 to 85 ml/hr (the feeding was 1.2 kcal/ml and 53 gm protein/liter). The following
day, he developed increasing levels of agitation, which prevented a ventilator wean. The
enteral feeding was increased to 40 ml/hr. On the following day, the feeding was increased 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, ventilator
support was decreased, steroid administration was decreased, and insulin administration was increased. His glucose level remained elevated.

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He continued to tolerate the enteral feeding, which was increased to his goal rate of
85 ml/hr. He was gradually weaned from the ventilator and transitioned back to an oral
ADA diet. JW appeared to benefit from early enteral feedings. His weight and protein
parameters remained stable through his admission and he was weaned from ventilatory
support.

CASE STUDY #3
CL was a 71 year old male admitted with a GI bleed secondary to Coumadin
therapy and CHF. His history included COPD, paroxysmal atrial fibrillation, hypertension, CVA, a decubitus ulcer on his foot secondary to peripheral vascular disease,
alcohol abuse, and smoking. He was intubated with respiratory failure. He was 61 and
weighed 106.3 kg (115 percent of IBW). His needs were assessed to be approximately
2100 kcal/day and approximately 105 gm protein/day.
He was pharmacologically paralyzed because of his agitation on the ventilator. An
esophagogastroduodenoscopy (EGD) revealed gastritis and an ulcer. He then developed
encephalopathy and delirium tremens and his anemia worsened. He was started on
enteral feedings at 40 ml/hr. His albumin remained stable at 2.8, as did his weight
remain stable. He developed high residuals with the enteral feedings, likely related to
the pharmacologic agent utilized to paralyze him. As the drug was decreased, he became able to tolerate the feeding and the rate was increased to meet his needs. His
albumin level improved and his weight remained stable. Although his nutritional status
remained stable, he was not readily weanable from the ventilator and his ventilator
dependency 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 being
attempted)?
3. A 54", 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 149:818824, 1994.
Compher C: Calorimetry, body composition, nitrogen balance, labs. Address at A.S.P.E.N. 17th Clinical
Congress, San Diego, 1993.
Donahoe M, Rogers R, Wilson D, et al.: Oxygen consumption of the respiratory muscles in normal and
malnourished 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 Parenteral
Nutrition. 2nd ed. Boston: Little Brown; 203-216, 1991.
Gray-Donald K, Gibbons L, Shapiro S, et al.: Nutritional status and mortality in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 153:961-966, 1996.

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Hudson LD, Steinberg KP: Acute respiratory distress syndrome; clinical features, management and outcome. 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. 21st
Clinical Congress, San Francisco, 1997.
Kuo CD, Shiao GM, and Lee JD: The effects of high-fat and high-carbohydrate loads on gas exchange and
ventilation 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 pulmonary
disease 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
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.
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 Prac
4:166-172, 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 Rev
Respir Dis 143:1248-1252, 1991.
Schols AMWJ, Soetes PB, Dingemans AMC, et al.: Prevalence and characteristics of nutritional depletion
in 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 Support
Practice: 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 with
increased oxygen cost of breathing due to emphysema, scoliosis and thoracoplasty. Thorax 49:781785, 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 Supp
Serv 5:9:46-48, 1985.
Wilson DO, Rogers RM, and Hoffman RM: Nutrition and chronic lung disease. Am Rev Respir Dis
132:1347-1365, 1985.

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Chapter Eight:
Renal Disease

he kidneys maintain the normal homeostatic condition of the body. Their primary function is to regulate extracellular fluid through the formation of urine, which
involves regulation of serum sodium and potassium concentrations and maintenance of
an appropriate-base balance (Fox, 1987). The kidney is also involved in the regulation of
calcium in the blood by decreasing phosphate reabsorption when extracellular calcium
levels decrease. This increases calcium reabsorption (Liftman, 1989).
When patients with renal disease or acute renal failure lose these primary functions, a wide variety of metabolic changes occur, making nutrition support a challenging task.
The primary effects of altered renal function, shown on the following page, are
fluid retention, increased serum levels of potassium, magnesium, and phosphate, and
increased protein catabolism. Blood urea nitrogen levels increase with the catabolism of
protein stores and decreased filtering of waste products, such as urea. BUN levels can
increase with gastrointestinal bleeding and dehydration as well.
Serum creatinine rises as renal function deteriorates. In fact, serum creatinine levels
increase by 200 percent with each 50 percent decline in glomerular filtration rate
(Liftman, 1989). Patients with very little muscle mass have lower than normal serum
creatinine levels. Therefore, renal deterioration may be missed or diagnosed late in the
patient with reduced muscle mass.
Phosphate levels increase with as little as a 30 percent decrease in glomerular
filtration rate (GFR). Because phosphorus and calcium maintain a balance, this causes a
decrease in serum calcium. The general picture, then, is of a system severely out of
balance, making even basic nutrition assessment more complex.
Effects of reduced renal runction inlcude increased fluid retention, serum potassium, serum magnesium, serum phosphate, BUNand serum creatinine, as well as
decreased serum calcium.

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NUTRITION ASSESSMENT
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 an
acute or chronic renal failure patient difficult, obtaining a dry weight is important in
assessing his nutritional requirements. Dry weight is post-dialysis weight. From this, an
estimation of lean body mass can be made, utilizing anthropometric measurements.
Changes in weight are often due to fluid shifts and changes, so once this baseline
weight is established, weight should be monitored daily. Weight gain of more than 0.5
to 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 treatment of existing renal disease. With excess fluid gain or retention, the need for dialysis
or other means of fluid removal increases.
A patients protein status can be estimated from serum albumin, serum transferrin
or total lymphocyte count. Because of albumins half-life of about 20 days and the fact
that it is profoundly affected by fluid shifts, its use as a nutrition indicator of protein
stores is limited. Albumin is not uncommonly given during dialysis and may transiently become elevated.
Transferrins shorter half-life of 8 days makes it a more accurate indicator. However, transferrin levels are affected by hydration (to a lesser degree), surgery, sepsis and
iron deficiency, which is often present in patients with renal failure. Iron deficiency
causes a false elevation in transferrin levels. Total lymphocyte count is used as an
indicator of overall nutritional status, and can be an indicator of protein deficiency or
immunocompetence.
Other acute phase proteins, such as prealbumin and retinol-binding protein, are of
limited use in renal failure patients. Prealbumin is normally degraded by the kidney, so
levels may be abnormally elevated by renal failure. Retinol-binding protein is filtered
and metabolized by healthy kidneys, so these levels are elevated in kidney failure
patients. This elevation does not, however, reflect actual protein status.
Obviously, the assessment of protein status in the patient with renal failure is quite
difficult and frustrating. Taking all of the above factors into consideration and weighing
benefits and drawbacks of each, you must develop through experience the ability to
judge protein status well. The best thing to do is to estimate needs based upon clinical
judgement, give adequate protein and calories, and follow the clinical course.
Nitrogen balance studies are of limited value in renal patients; however, determination of protein catabolic rate and urea kinetic modeling can be of use in determining
protein requirements. (See Nutrition Assessment: Tools and Techniques and another Nutrition Dimension course, Renal Nutrition). Urea kinetic modeling, though, is difficult to do.

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CHRONIC RENAL FAILURE


The chronic renal failure (CRF) patient has probably already started on dialysis by
the time nutrition assessment and treatment is begun. Because of the changes in kidney
function, he requires controlled intake of protein, potassium, sodium, phosphorus and
fluids. He likely requires supplementation with calcium and water-soluble vitamins
(because of vitamin loss in the dialysate), as shown below.

Nutrition for Chronic Renal Failure


Limit

Supplement

Protein
Potassium
Phosphorus
Fluids
Sodium

Calcium
Folate
Vitamin B6
Vitamin C (limit duration)
Water-soluble vitamins

Do not supplement
Vitamin A , trace elements (not dialyzed)

Heavier supplementation of folate (1 mg/day), and vitamin B6 (10 mg/day), and


vitamin C (100 mg/day) is indicated. Care should be taken with lengthy vitamin C
supplementation during CRF, since oxalate deposition can occur (Liftman, 1989).
Vitamin A supplementation should be avoided or restricted to prevent toxicity, and
trace elements should not be supplemented because they cannot be cleared effectively.
The potential for developing toxic levels is very real. Symptoms of vitamin A excess
include headaches, nausea, hepatomegaly and hypercalcemia.
The chronic renal patient is often already protein-depleted because of losses in the
early stages of renal disease, poor intake, etc. This existing malnutrition places the
patient at increased risk for infection in the hospital.
Once a CRF patient is admitted with a critical illness, he usually has a very poor
appetite or may be unable to take any nutrients by mouth. The early initiation of nutrition support in this patient is important. If the gut is functional, enteral feedings should
be initiated as soon as possible.

ENTERAL FEEDINGS
Generally, a critically ill patient with CRF can tolerate a conventional or standard
enteral 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 a
more nutrient-dense formula.
If a patient does not receive dialysis, a formula which is nutrient-dense (2 kcal/ml),

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with reduced protein (30 gm/L) can be utilized. The mineral content has been altered to
meet 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 appropriate
for the patient who has higher protein requirements and/or who has already started
dialysis. These formulas are also nutrient-dense but are higher in protein and are
supplemented with vitamins and minerals that may be lost with dialysis.
Depending upon the patients acute illness, he may require a more defined formula, such as a peptide or elemental formula. Peptide and/or elemental formulas are
often necessary after severe bowel resection, other surgery or trauma that prohibits
normal bowel function. Peptide formulas are often better tolerated in the acutely ill
patient who is severely hypoalbuminemic.
Enteral formulas provided into the stomach are usually well tolerated, but the
duodenum is generally the preferred site, to reduce the risk of aspiration for the patient
who is intubated or has an altered level of consciousness.

Nutrition for Critically ill CRF Patients


Calories
Starvation/mild stress
Moderate stress
Severe stress
Sepsis

1.0 - 1.3 x BEE


1.2 - 1.5 x BEE
1.4 - 1.8 x BEE
1.4 - 1.8 x BEE

Protein
Hemodialysis
Peritoneal dialysis

1.0 - 1.2 gm/kg/day


1.2 - 1.5 gm/kg/day

TPN
Should TPN be required, the chronic renal failure patient can usually tolerate a mix
of essential and non-essential amino acids (Matarese, 1993; Matarese, 1997). Individualization of electrolytes, calcium and phosphorus is necessary, using a baseline level and
clinical judgment. A combination of calories from glucose and lipid can be utilized if the
patient does not have impaired triglyceride metabolism.
As mentioned earlier, water-soluble vitamins are supplemented (with additional
supplementation of folate, B6 and C). Trace elements are generally given every day if the
patient 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 any
other acutely ill patient. A factor of 25 to 30 kcal/kg (dry weight)/day can be utilized. If
the Harris-Benedict equation is used, factors appropriate for the acute illness should be
applied (See Chapter Five). Indirect calorimetry can be used if available (Matarese, 1997).

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In acute and critical illness, nitrogen balance often becomes negative because of
catabolism and decreased protein synthesis during stress. With the additional stress of
dialysis, the patient may lose an additional 9 to 12 gm of protein during hemodialysis
and 12 to 13 gm during peritoneal dialysis. Generally, protein requirements for these
patients are 1.0 to 1.2 gm protein/kg/day for hemodialysis patients; 1.2 to 1.5 gm
protein/kg/day for peritoneal dialysis patients if BUN is stable (<100). If BUN levels
are 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.

Protein Restriction
GFR

Protein allowed

25 - 70
< 25
<5

0.7 - 0.8 gm/kg/day


0.6 gm/kg/day
1.0 - 1.2 gm/kg/day (with dialysis)

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 an
increase in mortality risk (Goldwasser, et al., 1993). Prevention of this malnutrition is
important and may be achieved with aggressive use of supplements, etc. The use of
intradialytic parenteral nutrition (IDPN) has been studied to a small extent. This process
allows for the provision of calories and protein during dialysis. IDPN can be expensive
and, to date, no scientific evidence exists that shows that it is indicated or even optimal
in the provision of additional nutrients to the malnourished CRF patient (Wolfson and
Foulks, 1996; Charney, 1995).

ACUTE RENAL FAILURE


Acute renal failure (ARF) can occur in a previously healthy individual as a result of
many different factors. Among the most common factors is acute tubular necrosis
(ATN), which occurs in some patients subjected to nephrotoxic agents or a decrease in
renal perfusion a decrease in blood flow to the kidneys. This can occur during surgery, with injury or infection, and after myocardial infarction.
Catabolism increases in the ARF patient, caused in part by the increase in the
release of catecholamines, corticosteroids and glucagon during the stress response
(Feinstein, 1988). The increased catabolism causes a rapid increase in BUN, loss of
muscle mass, and decreased albumin and transferrin. During acute renal failure, urea
and 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).

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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

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 reduce
complications and improve survival rates.
Nutrition goals for ARF are: limit protein catabolism and wasting of lean body
mass; 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. Theory
suggests that patients should be given a higher percentage of essential amino acids to
allow 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 appearance 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 only
essential amino acids was hazardous, resulting in hyperammonemia, coma, and even
death, with marked derangements in the plasma amino acid pattern. Nonessential
amino acids are vitally important in the synthesis of proteins and other biologically
valuable compounds (Kopple, 1996). Thus, nonessential amino acids should also be
given to the patient with ARF.
It appears that the quality of protein provided in ARF does not affect renal recovery. However, the amount of protein does. Excessive protein intake can be directly
related to decreased weight gain, a progressive increase in BUN and a decrease in
glomerular filtration rate (GFR). Current recommendations for provision of protein to
ARF patients are a combination of essential and nonessential amino acids at moderate
levels (see amounts on the following page).
Because patients with ARF are often hypercatabolic, when protein is given at levels
below 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 with
improved nitrogen retention and balance (Macias, et al., 1996). The optimal energy and
protein level for the ARF patient is as yet unknown. Macias suggests that to achieve
nitrogen balance in the ARF patient, protein requirements are between 1.5 and 1.8 gm/
kg/day.

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Caloric requirements appear to be 25 to 30 kcal/day. Protein requirements are the


same as in any critically ill patient. The patient on continuous renal replacement therapy
(CRRT) can receive 1.1 to 2.5 gm/kg/day.

Nutrition for ARF Patients


Calories
25 - 30 kcal/kg/day
Protein
1.2 - 2.0 gm/kg/day

CRRT may involve continuous arteriovenous hemofiltration (CAVH) or continuous


veno-venous hemofiltration (CVVH) with or without dialysis. The use of CRRT may
reduce the risk of fluid and electrolyte disorders and hypotension during dialysis, and
allow 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 may
be avoided altogether (Kopple, 1996).
Protein losses into the dialysate are about 4 to 7 gm/day with CVVHD. The
CAVHD patient may lose from 9 to 12 gm/day. These losses are easily replaced with
oral, enteral, or parenteral nutrition.
The use of TPN is sometimes required during ARF because of the patients other
acute problems. A very concentrated base solution of 70 percent dextrose may be necessary to compound TPN solution in those patients requiring fluid restriction. Concentrated lipid emulsions (20 percent) can provide additional calories. Approximately 50
percent of ARF patients require insulin supplementation because of glucose intolerance
caused by diabetes mellitus, sepsis or steroid therapy.
Standard amino acid formulas can be utilized; however, total protein should not be
limited. Water-soluble vitamins, with additional folate, B6 and C, should be supplemented. Vitamin K may require supplementation weekly. Supplementation of other fatsoluble vitamins is usually not recommended. Vitamins A and E are not dialyzable and
patients supplemented with vitamin A may develop hypervitaminosis (Wolk, 1993).
Trace elements are generally limited because of clearance of zinc and chromium by
the kidney. Electrolytes, calcium and phosphorus should be individually monitored and
limited or supplemented as needed. A decline in serum potassium and phosphorus may
occur with nutrition repletion, requiring supplementation of adequate amounts to
return levels to normal.

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If possible, the gut should be utilized for provision of nutrients. Nutrient-dense


formulas are often necessary because of fluid restriction. A standard enteral formula
should 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. Continuous
feedings are better tolerated in the critically ill patient and can be monitored more
effectively. As the ARF patient recovers and regains function of his kidneys, nutrition
care can be modified.
Eventually, patients who regain renal function can return to a normal diet without
renal restrictions. If they do not regain normal renal function, however, they will require
the same restrictions as any CRF patient.

CASE STUDY #1
TL is a 37-year-old female admitted to the ICU with systemic lupus erythematosus
(SLE), gastrointestinal bleed, chronic renal failure, non-insulin dependent diabetes
mellitus, and anemia. She is 54 and weighs 129 lb. Her admitting labs included a BUN
of 88, Cr of 4.9, albumin of 2.6, triglycerides of 263, and Hgb of 8.7. Her medications
included prednisone, IV albumin, Os-Cal, Lasix, and sliding scale insulin coverage. On
admission, 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 protein
and 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. Pulmonary
infiltrates were noted on x-ray, indicating that she had developed an infection. Dialysis
was initiated later that day.
On Day 6, she was intubated as respiratory distress worsened, likely precipitated
by the presence of pulmonary infiltrates. She was diagnosed by the consulting
pulmonologist with pulmonary hypertension and Serratia (a type of infection). She was
started on full strength Suplena at 40 ml/hr. This provided 960 ml, 1920 kcal, 28 gm
protein. Her needs were assessed to be 1700 kcal/day (based upon a factor of 30 to 40
kcal/kg with increased levels of stress) and 35 to 50 gm protein/day (based on a factor
of 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 the
formula, as evidenced by high residuals (greater than 300 ml) of gastric contents. Unfortunately, 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 formula
of 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 and
trace elements were added every other day. (Long-term TPN was not anticipated, but
we continued to monitor for problems associated with vitamin A toxicity. It was felt that
the benefits of trace element supplementation outweighed the drawbacks.) The TPN
provided 1440 ml, 1751 total calories, and 48 gm protein.

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Recommendations were made to increase the TPN as tolerated to 70 to 80 ml/hour


to approach estimated needs. On Day 11, TPN was increased to 70 ml/hr, providing
1680 ml, 2043 total calories, and 57 gm protein. Her albumin had decreased to 2.5 (likely
related to the level of sepsis and other problems this patient is experiencing). BUN was
81 and Cr was 7.5 (improved with dialysis) and her glucose level was 199 (patient was
receiving steroids - Solumedrol - and was also being covered with sliding scale insulin
and an insulin drip as needed). She was receiving dialysis every other day and was
diagnosed 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, but
nothing was seen on CAT scan. Her amylase was 790 and she was diagnosed with
pancreatitis, 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 third
generation cephalosporin for treatment of her multiple problems. On Day 16, she complained 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 laboratory
values remained stable.
On Day 16, a 13 cm abscess was detected on her small bowel by CAT scan. The
abscess was drained and an exploratory laparotomy was scheduled for the following
day. TPN increased to 80 ml/hr and we continued to follow the available lab values to
monitor her tolerance to TPN and for improvement in nutritional status. Her albumin
level dropped with the surgery and because of the abscess. However, she continued to
receive IV albumin to assist with dialysis and to maintain oncotic pressures. Slow
enteral feedings were resumed over the next few weeks. TL improved and was able to
be weaned from the ventilator and TPN and was slowly transitioned to enteral (full
strength 50 ml/hr) and then oral feedings.

CASE STUDY #2
LA was a 68 year old woman admitted with ischemic cardiomyopathy, IDDM,
ARDS (adult respiratory distress syndrome) and a history of acute renal failure that had
progressed to chronic renal failure. Her surgical history included a CABG (coronary
artery bypass graft) and a redo CABG. Her needs were estimated to be 1700 kcal/day
and 70 to 80 gm protein/day. (She was 54 and weighed 68 kg.)
Her left leg wound (from the CABG) had never healed well and required debridement. A Barium swallow study revealed frank aspiration (because of vocal cord paralysis from intubation with the previous surgery). A PEG (percutaneous endoscopic gastrostomy) tube was placed. Her stormy course continued as she developed sepsis,
required intubation, and started hemodialysis.

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Two days after extubation, LA started on a cardiac diet with supplements but had
poor PO intake. Her ejection fraction (a measurement of the strength and effectiveness
of the heart) was noted to be only 10 percent. TPN was initiated with 6 percent amino
acid, D10, and lipid 4 percent (1647 kcal, 101 gm protein) final concentration. The higher
level of protein was possible because she was placed on CRRT (continuous renal replacement therapy); this treatment provided an additional 550 kcal.
PO intake remained poor; TPN continued. One month after admission, LA was
started on enteral feedings of Nepro 40 ml/hr (1728 kcal, 79 gm protein) due to electrolyte disturbances and TPN was decreased to one liter with dialysis. LAs lab values
remained stable throughout. Two weeks later, her repeat modified Barium swallow
revealed that it was safe for her to attempt PO intake; she was able to consume approximately 1000 kcal/day and about 60 gm protein/day (with supplements). Enteral
feedings were thus reduced to one can of Nepro each day.
Her course continued until she had a bout of emesis and aspirated and became
intubated. TPN was restarted (amino acid 4 percent dextrose 20 percent and lipids 4
percent at 70 ml/hr) which provided 2083 kcal and 67 gm protein. She required a
thrombectomy and developed pulmonary edema and was ventilator dependent. Three
days later, CVVHD (a type of CRRT) resumed and provided an additional 550 to 855
kcal/day. She was meeting her needs, assessed now to be 1600 to 2200 kcal/day and 65
to 95 gm protein/day. Her albumin was 2.3; LFTs were elevated; and her weight was
64.1kg.
The CVVHD was successful in removing excessive fluid. However, LA became
septic and required pressor support to maintain her blood pressure. Her lab values
remained stable. She continued to deteriorate and it appeared that she would be ventilator 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, continue
CRRT, and allow her to move out of the ICU. Her diet advanced from CL to FL; PO
intake 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 abdominal
aortic aneurysm. At two days post-op, he exhibits no bowel sounds as yet. Patient
is 61, 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 bypass
graft patient who now exhibits acute renal failure. BUN 111, creatinine 10.2, potassium 5.0, sodium 150, albumin 2.7, phosphate 8.0, cholesterol 139, triglycerides 90,
glucose 252. She is 54, 154 lb (70 kg).

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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 3:1:1013, 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: Dietitians 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 Francisco, 1997.
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) and
American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) JPEN 33(3): 277-316, 2009.
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.

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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 and
secretion of bile (Fox, et al., 1987).
Most nutrients must pass through the liver, where they are stored, used for energy
or processed into other substances. All essential amino acids, except the branched-chain
amino 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 liver
and 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, EpsteinBarr, and cytomegalovirus. Ischemic damage to the liver can occur after trauma or
surgery, while the liver can also be damaged with alcohol and/or drug abuse, by autoimmune diseases, and by cancer.
Nutrition therapy, while sometimes difficult, is of primary importance in the
treatment of the patient with diseases affecting the liver and will likely have an impact
on the patients final outcome.
Care of liver failure patients requires careful assessment of their nutritional requirements and provision of appropriate levels of nutrients to allow anabolism but
prevent complications from overfeeding. Assessment is difficult because damage to the
liver affects the metabolism, transport and synthesis of many nutrients.

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Metabolic Alterations with Liver Disease


Hypoglycemia (in acute)
Hyperglycemia (in chronic)
Decreased protein synthesis
Decreased fibrinogen levels
Decreased production of urea
Increased aromatic amino acids
Increased liver function tests
Thiamine deficiency
Folate deficiency
Iron deficiency
Manganese deficiency

Fat malabsorption
Fatty liver
Decreased serum albumin
Decreased prothrombin levels
Increased ammonia levels
Decreased BCAA
Fat-soluble vitamin deficiency
B6 deficiency
Niacin deficiency
Copper deficiency
Zinc deficiency

CARBOHYDRATE METABOLISM
In the normal liver, carbohydrate metabolism occurs without problems. After
ingestion, glucose and other simple sugars are converted into glycogen. If there is too
much simple carbohydrate for the liver to store, it converts the excess to fat. When the
body requires more glucose (as might happen several hours after a meal), the liver
initiates the process of glycogenolysis, and the resulting glucose is released into the
bloodstream. If the glycogen stores are depleted, as might happen overnight, gluconeogenesis begins, forming glucose from amino acids, lactate and glycerol.
The injured or diseased liver is often unable to maintain normal carbohydrate
metabolism. This is most often manifested as hypoglycemia in acute liver failure, and
hyperglycemia in chronic liver disease. The cause of these changes remains unclear, but
factors may include the inability of the liver to undergo glycogenesis and a reduced
ability for gluconeogenesis (Shronts and Fish, 1989, Guenter and Slocum, 1983; Wong, et
al., 1998).

FAT METABOLISM
The healthy liver secretes bile, which is transported to the gastrointestinal tract to
assist in the absorption of fats and fat-soluble vitamins. Triglycerides are transported to
the liver and are converted to fatty acids and glycerol. These substances are then oxidized for energy, reformed into triglycerides for transport and storage, or transformed
into 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, the
nutritional status of the patient. Without the normal production and secretion of bile
salts, malabsorption of fats and fat-soluble vitamins may occur. If normal fat metabolism does not occur, short-chain fatty acids accumulate in the liver, causing fatty liver.

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The causes of this alteration in fat metabolism are many and include increased amounts
of fat produced by the liver, reduced transport of these fats out of the liver, and reduced
oxidation of fats.
The steatorrhea that occurs with liver disease may cause as much as 30 to 60 per
cent of fat to be malabsorbed (Sokol, 1995).

PROTEIN METABOLISM
The liver plays a significant role in the normal metabolism of protein. Absorbed
protein passes through the portal system to the liver. Nonessential amino acids and
other important compounds, including albumin, are formulated there. Urea, made in
the liver, is vital to the removal of ammonia formed in the body. Fibrinogen and prothrombin 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 for
healing. Several functions are impaired, as shown in the following chart.

Liver Dysfunction
Decreased urea production

Increased serum ammonia levels

Increased AAA Levels

Decreased BCAA levels

Production of
false neurotransmitters

Confusion, reduced consciousness

Decreased production of urea decreases ammonia removal, thus boosting the level
of serum ammonia, which is toxic to the brain. This may contribute to the development
of hepatic encephalopathy. In severe liver disease, the increase in serum ammonia is
caused from secretion of glucagon and its stimulus of gluconeogenesis from amino
acids. The increased use of protein for calories results in diminished plasma levels of
branched chain amino acids. Serum levels of aromatic amino acids (AAA) rise when the
liver decreases metabolism of AAA. The elevation in blood ammonia results in increased uptake of ammonia by the brain. Influx of AAA increases into the brain the
AAA substitute for norepinephrine and dopamine to form octopamine and
phenylethanolamine. These altered compounds cause encephalopathy and resultant
confusion and reduced levels of consciousness (Sokol, 1995).

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MICRONUTRIENTS
The liver normally plays a significant role in the storage, synthesis, and transport
of 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 are
stored in the liver include iron, copper, and cobalt. Thiamine, B6, and vitamin D are
converted to their active forms in the liver. Transport of vitamin A is dependent upon
normal liver function, as well. The steatorrhea that may occur with liver disease may
cause malabsorption of calcium, magnesium, zinc, and fat-soluble vitamins.
As mentioned earlier, liver disease or failure can result in decreased absorption of
fat-soluble vitamins. Deficiency of vitamin A may occur due to a decrease in the amount
of transport proteins available, while vitamin D levels may fall because of alterations in
conversion of vitamin D to its active form. The inability of the diseased liver to convert
thiamine and B6 to their active forms may result in deficiencies of these vitamins. A
significant decrease in folate stores may also occur, especially in liver disease associated
with alcohol intake.

NUTRITION ASSESSMENT
Nutrition assessment may be difficult because of the wide variety of effects of liver
disease or injury. The patient may be edematous with ascites or anasarca or dehydrated
due to diuretic therapy, making determination of weight difficult. Weight may be
further impacted by increased interstitial fluid associated with hypoalbuminemia and
by 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 increased risk of complications, such as peritonitis. Factors contributing to this malnutrition include anorexia with poor intake, maldigestion and malabsorption, and the
changes in metabolism associated with liver disease.
Since many of the serum proteins (including albumin, transferrin, prealbumin, and
retinol-binding protein) are synthesized by the liver, their use in nutrition assessment is
invalid. Although only 25 percent of normal liver function is required to maintain normal 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 of
lean body mass, but its use may be limited because CHI can be affected by age, malnutrition and hepatorenal syndrome (failure of the hepatic and renal systems) (Shronts and
Fish, 1989; Shronts, 1988).
Thus it is difficult to accurately assess the nutritional status of the patient with
severe liver disease. Laboratory values will likely be skewed with liver disease. Total
bilirubin will increase and liver function tests (aspartate aminotransferase [SGOT],
alanine aminotransferase [SGPT], alkaline phosphatase) will increase dependent upon
the severity of the disease and type of disease (Shronts and Fish, 1993). Prothrombin
time will likely be lengthened.

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Liver disease patients have increased energy requirements for anabolism and
healing of the injured liver. Adequate calories to allow for protein sparing should be
provided perhaps as much as 25 to 35 kcal/kg/day (utilizing the estimated dry
weight) (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 of
the non-protein calories should be given as fat. Since overfeeding of calories may exacerbate fatty liver, care should be taken to provide the appropriate level of calories.

Calorie Requirements
25 - 35 kcal/kg/day
or
1.3 - 1.5 X BEE
(25 to 40% as fat)

Protein requirements vary with the severity of the disease and presence or absence
of symptoms. The patient with acute and chronic liver failure should have no protein
restriction protein should not be restricted in an effort to manage hepatic encephalopathy (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 without
encephalopathy.
Several studies have shown that the supplementation of protein with BCAA may
be of benefit in the treatment of encephalopathy (Hiyama and Fischer, 1988; Cerra, et al.,
1985; OKeefe, 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, especially
with long term use. In refractory hepatic encephalopathy, use of BCAA formulas may
improve coma grade.

MICRONUTRIENTS
Because of alterations in vitamin and mineral absorption, metabolism and transport in liver disease, supplementation is often warranted. However, the liver may be
unable to metabolize or transport certain vitamins and minerals, and toxicities may
develop, especially in end-stage liver disease. Any supplementation should be judicious
and closely monitored. Fat-soluble vitamin status should be evaluated regularly and
supplemented when deficiency occurs. Water-soluble vitamin E can be given at a dose
of 15 to 25 IU/kg/day; vitamin D can be supplemented at a level of 2 to 4 mcg/kg/day
if the patient is also exposed to sunlight.

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Vitamin K can be given as a 2.5 to 5 mg oral dose twice per week. Vitamin A can
become toxic if supplemented.
Other nutrients that may require supplementation include zinc, magnesium,
phosphorus, and calcium (Sokol, 1995). Copper and manganese should not be supplemented in patients with liver disease who are receiving TPN. Copper may be stored
excessively in the diseased liver; both copper and manganese are excreted in bile (excretion via bile would be decreased with cholestasis) (Fell, et al., 1996).
Individual dosages should be based upon the patients symptoms of clinical deficits and subsequent evidence of deficiency, through biochemical measurements. In other
words, in end-stage liver disease, vitamin-mineral supplementation especially fatsoluble vitamins stored in the liver should be limited. Supplementation of watersoluble vitamins is less risky and often warranted, such as 25 to 50 mg thiamine, 400 to
800 mg folate and the RDA for vitamin C.

NUTRITION SUPPORT
The patient with hepatitis, either acute or chronic, can usually be maintained on a
normal diet, with 25 to 35 kcal/kg/day and 1.0 to 1.5 gm protein/kg/day. The cirrhotic
patient especially needs adequate calories and protein (needs can be determined from
recommendations above).
If esophageal varices from cirrhosis prevent oral intake or placement of a
nasogastric tube, TPN is indicated. Enteral nutrition support is recommended over TPN
if the patient is unable to ingest nutrients orally and has a functional gastrointestinal
tract. Small-bore feeding tubes should be used to prevent irritation of varices and
subsequent hemorrhage (Shronts and Fish, 1989).
Most patients with esophageal varices can tolerate a normal diet. The presence of
ascites 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 for
encephalopathic patients. Most standard enteral formulas may be well tolerated.
Often, a calorie-dense formula is recommended because of the need for fluid
restriction. Since these types of formulas are often hypertonic, they should be well
tolerated if initiated and advanced slowly.
Initially, the formula should be given continuously at a low rate, with gradual
increase as tolerated by the patient (Shronts and Fish, 1989). Certain medications, such
as lactulose, given to bring down serum ammonia levels, will cause diarrhea; this
should not be attributed to the enteral feedings.
TPN support can be used in the patient with a nonfunctioning GI tract. It may also
help a patient with encephalopathy who has difficulty protecting his airway, and who
therefore may be at risk for aspiration.
As mentioned previously, 25 to 30 percent of nonprotein calories should be provided as fat, with additional calories from carbohydrate in the form of 50 to 70 (initial
concentration) 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).

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As mentioned earlier, any supplementation of vitamins and minerals should be


monitored carefully to prevent toxicities (especially copper and manganese).
The liver failure patient presents many challenges to those responsible for nutrition
care. There is often a fine line as to the level of protein a patient can tolerate. Finding
that level is challenging and frustrating. Because of varices, enteral feedings may be
next to impossible, unless a G-tube is placed. TPN is not always well tolerated because
of the complex role of the liver in metabolism. And, once the patient with alcoholic liver
disease recovers from the acute phase, he or she is often very difficult to work with due
to altered mental status.

CASE STUDY
CW was a 53-year-old female admitted to the hospital with hepatic encephalopathy and a gastrointestinal bleed. Her history also revealed the following medical problems: ARDS, COPD (steroid-dependent), sepsis syndrome, cholestasis, and a history of
alcohol abuse. She was 52" and weighed 140 lb and had a recent 10 lb weight loss. Her
admitting albumin was 2.5. Her needs were assessed to be 1300 to 1500 kcal/day and 60
to 90 gm protein/day because of her level of encephalopathy, which had been refractory
to intervention. Her elevated ammonia level (100) fell to 63 after administration of
Lactulose.
Enteral feedings were initially attempted but were poorly tolerated as the patient
had high residuals and diarrhea. She was intubated and an open lung biopsy was
performed. She had developed a decubitus ulcer on her sacral area. Portal hypertension
was diagnosed. Enteral feedings were again attempted with a hepatic formula, in the
thought that the higher branched-chain amino acid level would aid in reducing her
level of encephalopathy. Her albumin level remained stable but she was poorly responsive. High residuals from the enteral feedings continued so TPN was initiated with final
concentrations of D18 and a hepatic amino acid source at 4 percent with lipid 20 percent
500 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 protein
because of the utilization of a branched-chain amino acid formula.
CWs BUN and Cr began to rise and her hemoglobin and hematocrit levels began
to fall. She was diagnosed with sepsis from Candida albicans and Aspergillus fumigatus
(opportunistic infections are not uncommon as the liver fails); ARDS continued; and
thrombocytopenia developed. Her condition continued to worsen and little hope was
offered 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 hepatic
failure?
2. An encephalopathic patient presents to the ICU. He is comatose. Height 51", weight
132 lb. Determine his nutrient needs.

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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 parenteral
nutrition. Lancet 347(9010):1218-1221, 1996.
Flores DA, Aranda-Michel J: Nutritional management of acute and chronic liver disease. Semin
Gastrointest 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. J
Hepatology 27:239, 1997.
Marchesini G, Bianchi G, Merli M, et al.: Nutritional supplementation with branched-chain amino acids in
advanced 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
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.
Muto Y, Sato S, Watanabe A, et al.: Effects of oral branched-chain amino acid granules on event-free
survival in patients with liver cirrhosis. Clin Gastroenterol Hepatol 3: 705-713, 2005.
OKeefe SJ, Ogden J and Dicker J: Enteral and parenteral branched chain amino acid-supplemented
nutritional support in patients with encephalopathy due to alcoholic liver disease. JPEN 11:5:447253, 1987.
Plauth M, Cabre E, Riggio O, et al.: ESPEN guidelines on enteral nutrition: liver disease. Clin Nutr 25: 285294, 2006.
Shronts EP and Fish JA: Hepatic failure. In: Nutrition Support Dietetics, 2nd ed. Gottschlich MM, Matarese
LE, 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 Dietitians
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 branchedchain amino acid granules on the prognosis of liver cirrhosis. Gastroloenterol Jpn 24: 692-698, 1989.

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Chapter Ten:
Cancer Patients

ancer patients can face a multitude of nutrition-related problems, both from


cancer itself and from therapy. Incidence of malnutrition in the cancer population
ranges from 30 to 87 percent (Heber and Tchekmedyian, 1992; Heber, 1995).
Surgery, radiation therapy, and chemotherapy all profoundly affect a patients
ability to ingest adequate nutrients. These effects will be discussed briefly. This chapter
will focus primarily on the appropriateness of extensive nutrition support and recommendations for patients with various complications related to the cancer or therapy.
Maldigestion and malabsorption occur in cancer patients and can be related to the
tumor itself or to the changes in distribution of nutrients that occurs with cancer. Muscle
and fat reserves appear to be redistributed to the liver and bone marrow and protein
conservation does not occur.

SURGERY
Depending on the type of cancer, a patients ability to chew or swallow may be
impaired. If the gut works, use it, but these patients may be best served with enteral
nutrition support, with placement of a gastrostomy or jejunostomy tube during the
primary surgery. The incidence of malnutrition in patients with head and neck cancer is
estimated at 25 to 74 percent (Lee, 1999; Mekhail, et al., 2001).
Complications that may occur after esophagectomy include reduced motility and
gastric acid production, steatorrhea or fistulas related to the associated vagotomy, and
stenosis of the esophagus (Kouba, 1988; Bloch, 1989).
Gastrectomy may cause the development of dumping syndrome (discussed in
Chapter Four) and hypoglycemia, and malabsorption, with the potential for related
deficiencies of calcium, iron, B12 and fat-soluble vitamins. Post-gastrectomy patients

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may be able to attain and maintain adequate intake with feedings through a jejunostomy tube until they can resume oral intake.
Resection of the small bowel may cause malabsorption, diarrhea and deficiencies
of B12, fat-soluble vitamins, magnesium, calcium, and electrolytes. Adequate nutrition
therapy may be attainable with oral intake, enteral feedings utilizing elemental or
peptide 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 necessary
initially, with transition to enteral feedings (utilizing elemental formulas) and, eventually, oral feedings as tolerated by the patient.

RADIATION
Radiation therapy can have a vast effect on a patients ability to ingest and absorb
nutrients. Taste and smell may be diminished, and difficulty in chewing and swallowing is a frequent side effect (this may be associated with stomatitis, mucositis and
decreased salivation) (Kouba, 1988; Bloch, 1989; Burgess, 1989). The formation of strictures and fistulas is possible, and malabsorption, diarrhea, nausea and vomiting are
often present.
Acute reactions occur within 10 to 17 days of radiation therapy. These reactions
include: mucositis, xerostomia, esophagitis, dysphagia, otitis media, fungal, bacterial,
and viral infections (Hunter, 1996). Delayed reactions can include necrosis of the mandible, ulceration of the mucosa, dental caries, endocrine dysfunction, and laryngeal
edema (Hunter, 1996).
These complications can preclude adequate intake and necessitate enteral support,
when possible, or parenteral support as necessary. Enteral support is indicated if the
patient exhibits progressive weight loss with oral intake alone, has received radiation
therapy of the mouth or throat, has received extensive radiation therapy or is being
treated with adjunctive chemotherapy or surgery.
Isotonic enteral or nutrient-dense formulas are often well tolerated in the patient
with head, neck or esophageal cancer; more elemental formulas may be required for
patients receiving radiation therapy to the stomach or small bowel. TPN may be the
only means available to provide adequate nutrition support and may help the patient
withstand 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 patients ability to maintain
adequate 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 be
considered if all other methods of nutrition support fail. Many chemotherapeutic agents
can cause metabolic changes as well. (See chart on the following page).

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Effects of Chemotherapy Drugs


Drug

Metabolic change

Asparaginase
Chlorotrianisene
Cisplatin
Diethylstilbestrol
Methotrexate
Mithramycin
Streptozocin
Tamoxifen
Taxol
Tretinoin
Vincristine

hyperglycemia, pancreatitis
hypercalcemia
hyperuricemia, hypomagnesemia
hypercalcemia
deficiency of folate and calcium
hypocalcemia, hypokalemia
hypoglycemia
hypercalcemia
nausea, emesis, mucositis
hypertriglyceridemia, elevated LFT
SIADH, hyponatremia
Bloch AS, 1998

NUTRIENT NEEDS
Cancer cachexia is a well described phenomenon. Weight loss may occur in up to
40 percent of patients, while as many as 80 percent of patients with endstage disease
will develop cancer cachexia syndrome (DeWys, 1979, 1980; Barber, 2002). The cachexia
appears to be caused by decreased intake of nutrients along with increased nutrient
losses and increased or inefficient energy metabolism (Hunter, 1996). The patient with
cachexia generally has a further decline in nutritional status because of associated
anorexia and early satiety which then causes weight loss, immunosuppression, and
other 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. For
instance, some patients exhibit an increase in resting energy expenditure, but others
show a decrease in energy requirements (Hearne and Daly, 1986). The resting energy
expenditure 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 the
altered metabolism associated with solid tumors. Lean body mass is depleted, primarily
from skeletal muscle.
For patients who are hypermetabolic, who would benefit from weight gain, or who
undergo catabolism after surgery, radiation therapy or chemotherapy, a general rule of
thumb is the provision of 25 to 30 kcal/kg/day. At least 35 kcal/kg/day should be
provided 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 of
the patient. Supplementation with vitamins and minerals should be considered for the
patient with inadequate intake or one who has undergone surgery or therapy that may

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112

cause deficiencies. Folate levels may fall in acute leukemia, lymphoma, and metastatic
carcinoma. Vitamin B6 levels drop in Hodgkins disease and zinc levels decrease with
diarrhea, 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 probably not be considered as a nutrition support candidate. But nutrition support may
enhance therapy by improving nutritional status, and the prevention of malnutrition
may reduce other complications. Most importantly, the quality of life can be vastly
improved 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 nutrition
support (McCann, et al., 1994; Hill, 1998).
A.S.P.E.N. guidelines suggest that one to two weeks of preoperative nutrition
support may be of benefit in moderately to severely malnourished patients and in
malnourished patients undergoing anticancer therapy if they are unable to adequately
consume or absorb nutrients.
Provision of nutrition support to the patient whose life would be prolonged but
not enhanced should be carefully considered, weighing both benefits and burdens for
the patient and his care. Nutrition support may be highly beneficial to the patient with
gastrointestinal cancer or problems related to the GI tract that have occurred after
radiation, surgical, or chemotherapeutic intervention.
Typically, what works for other, non-cancer, patients in assessing needs works for
cancer patients as well, as long as circumstances (such as surgery) are similar. Because
cancer patients undergoing radiation or chemotherapy are often unable to eat due to
nausea and vomiting, oral supplementation is difficult. However, these patients are
often more highly motivated, making them more receptive to oral supplementation.
Relaxed, frequent small meals are often best tolerated. Between-meal supplements
or nourishments of high calorie, high protein foods are suggested. Modification in
consistency of foods is often helpful, depending upon the problem.
Since nausea and emesis are a frequent complication to the therapies for various
types of cancer, antiemetics are often utilized with some success. Chronic nausea, which
can occur with advanced cancers, is more difficult to treat, but metoclopramide is used
initially (Hardin, 1994). Megestrol acetate has been utilized to stimulate appetite for a
number of years and, in several studies, has been suggested to increase weight and
improve nutritional status in those patients treated (Feliu, et al., 1992; Tchekmedian, et
al., 1992; Loprinzi, et al., 1990).
Enteral and parenteral nutrition support is sometimes of benefit, but should not be
considered a therapy.

CASE STUDY #1
JG 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 with
chemotherapy. After starting chemotherapy, JG was beginning to develop anorexia and
had experienced some weight loss when he was referred to a home care agency for home
TPN to supplement his oral intake. He had refused invasive jejunal tube placement for
enteral feedings. Home TPN was initiated, to be given over 10 to 12 hours each night.

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His physician had given JG approximately 6 weeks to live as a prognosis. JGs


weight was within normal limits for his height of 61"; he weighed 178 lb upon initiation
of TPN.
He received adequate protein and caloric intake to meet his needs and his weight
and labs were monitored on a weekly basis. We consulted with him and his family
regarding his oral intake. JG was still able to consume approximately 1200 kcal and 40
to 60 gm protein each day, thus we adjusted his TPN accordingly. He complained of
excessive weight gain and desired a reduction in his TPN to 5 days/week; this was
allowed 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 values
remained within normal limits.
Six weeks passed and JG was able to reach his goal of spending the Christmas
holidays with his family. He then set his next goal of attending his daughters wedding
in June. During the next 6 months, he vacationed, always assuring that he would have
his TPN available. He continued to eat fairly well, although he noticed more anorexia
and complained of early satiety. He was reminded to take his meals in small frequent
feedings and was encouraged to try any of a variety of supplements. He continued to
do well, with the only changes in his weight occurring after chemotherapy. He proudly
walked his daughter down the aisle at her June wedding. He promptly set another goal
of attending another family wedding in October.
JGs nutritional status remained stable until he had another course of chemotherapy. At that time, he experienced nausea, vomiting, and diarrhea to a greater degree. 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 travel
to the wedding in October, but returned quite fatigued. His nutritional status remained
about the same, but his general health continued to decline.
JGs battle with cancer ended in November, 13 months after he was first diagnosed
and given a prognosis of 6 weeks to live. Clearly, nutrition support played a significant
role in not only extending his life, but also improving his quality of life.

CASE STUDY #2
PT 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 57" 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 and
amino acid 5 percent at 60 ml/hr along with a regular diet. The TPN was then increased
to 90 ml/hr (2186 kcal and 108 gm protein). His needs had been assessed at 1800 to 2100
kcal/day and 85 to 120 gm protein/day. On hospital day #3, he underwent an
esophagogastrectomy. Two thirds of the proximal stomach and one third of the distal
esophagus were removed. He also had a pyloroplasty and a jejunostomy tube was
placed. TPN continued until post op day 3 when a fiber-containing enteral formula was
started at 20 ml/hr; TPN rate was decreased to 80 ml/hr.

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The plan was for the enteral feeding to be gradually increased to 65 to 75 ml/hr to
meet his needs (formula was 1.2 kcal/ml and 53 gm protein/l). He started on clear
liquids the following day. On post op day 5, the enteral feeding was at 70 ml/hr and the
TPN was reduced to 30 ml/hr. He tolerated the j-tube feeding well.
PTs course did not remain so smooth, however. His diet was advanced to soft; he
did not tolerate the diet and was placed back on enteral feedings with supplemental
TPN. 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 revealed near adequate intake as his appetite and intake continued to improve with the
pureed diet and supplements. He was discharged home on a soft diet with supplements
with a reasonable quality of life.

REVIEW QUESTIONS
1. Evaluate the calorie/protein needs for a 25-year-old female with leukemia. Height,
55", weight 110 lb.
2. Describe the nutrition problems that might be associated with radiation therapy of
the 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.

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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.

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Chapter Eleven:
AIDS and
HIV-Positive Patients

s we are all well aware, the incidence of AIDS and HIV infection continues
to increase; now AIDS and HIV infection are perceived as chronic and long-term
diseases. This population of patients will continue to be at risk for malnutrition
and, thus, may benefit from our early intervention and assistance. What causes the
malnutrition seen with the AIDS and ARC (AIDS-related complex) patient? These
patients appear to have increased nutrient demands but have decreased intake and
alterations in digestion, absorption, utilization and metabolism of the foods they
do ingest.
HIV, a retrovirus, acts by making its own DNA by utilizing genetic material
from the host cell. Once the virus penetrates into the cell, it eventually replicates
and destroys the functioning ability of the host cell. The virus also alters the cell
membrane and causes it to fuse to other cells, passing the virus from healthy cell to
healthy cell.
HIV affects cells that contain the glycoprotein receptor, CD4; these cells include T
helper cells, macrophages, monocytes, some B cells, and cells found in the central
nervous system. Obviously, the immune system is profoundly affected by HIV. Some
effects are shown in the chart on the following page.
Once the immune function of the patient has been impacted, the patient is at
increased risk for opportunistic infections such as protozoa, fungi, bacteria, and viruses.
Some of these opportunistic infectious agents are listed on the next page.

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Immune System Abnormalities in AIDS


Abnormalities characteristic of AIDS
Depletion of CD4 helper T cells
Elevated, normal or decreased CD8 (suppressor) cells
Decreased proliferative responses to mitogens and antigens in vitro
Impaired delayed-type hypersensitivity reactions
Decreased gamma-interferon production in response to antigens
Decreased humoral response to immunization (mainly primary)
Decreased helper function for B-cell immunoglobulin production
Decreased macrophage-dependent T cell proliferation
Decreased virus-specific cytotoxic lymphocyte function in vitro
Commonly detected abnormalities
Lymphopenia
Decreased proliferative responses to T cell and B cell specific antigens
Decreased IL-2 production
Decreased: cytotoxicity to virally infected cells; monocyte chemotaxis;
immune complex formation; natural killer cell activity with normal
binding to cell
Decreased MCH class II antigen expression on monocytes & macrophages

Infectious Agents Common in AIDS Patients


Bacteria
Mycobacterium:
avium-intracellulare,
tuberculosis, kansasii
Legionella
Salmonella
Listeria
Shigella
Campylobacter
Pneumococcus

Fungi
Candida
Cryptococcus neoformans
Aspergillus species
Coccidioides immitis
Histoplasma capsulatum

Viruses
Cytomegalovirus(CMV)
Herpes simplex
Varicella-zoster (VZV)
Epstein-Barr (EBV)
Hepatitis B
Papillomavirus
Polyomavirus
Protozoa
Pneumocystis carinii
Toxoplasma gondi
Cryptosporidium species
Isospora belli

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The patient also has increased susceptibility to neoplasms, such as Kaposis sarcoma, non-Hodgkins lymphoma, squamous cell carcinoma, and small-cell undifferentiated carcinoma. Finally, because of the CNS involvement, the patient may develop AIDS
dementia complex.
The most common gastrointestinal fungal infection is candidiasis; it generally
occurs in the mouth and throat. Cytomegalovirus and herpes simplex virus also occur
in the mouth and throat. Cytomegalovirus can also cause inflammation of the entire GI
tract and exhibits itself with diarrhea, steatorrhea, etc. (Moorwessel, et al., 1993).
Protozoa, such as Cryptosporidium parvum, cause watery diarrhea and malabsorption. Other protozoa cause similar symptoms of malabsorption and diarrhea. This
malabsorption causes weight loss, tissue-wasting and decreased levels of nutrition
indices (Kotler and Grunfeld, 1995). The prevalence of HIV-related diarrhea may range
from 30 to 60 percent (Wanke, 1994). In 15 to 30 percent of patients, no pathogenic cause
is found.
Antiviral therapy has advanced tremendously with the discovery of protease
inhibitors. The drugs previously used to treat HIV, known as nucleoside analogues,
inhibit the reverse transcriptase enzyme, inhibiting HIV, reducing viral load, and increasing CD4 T cell counts in serum (Bartlett, 1996). The newer drugs, protease inhibitors, prevent the HIV virus from attaching the polyproteins into a functional virus, in
essence creating an immature virus that is unable to infect new cells. In patients taking
protease inhibitors, viral loads drop to undetectable levels.
As the viral load drops, so do many problems associated with HIV: immune dysfunction, opportunistic infections, diarrhea, weight loss, malnutrition and death. Only
10 percent of HIV+/AIDS patients take the protease inhibitors. Some of those that do
find the virus mutates and the drugs may no longer work effectively or at all. Once
protease inhibitors are stopped, viral load again increases and the disease progresses.

NUTRITION ASSESSMENT
Various studies have reported weight loss of 10 percent or more of usual body
weight in 62 to 92 percent of AIDS patients studied (OSullivan, et al., 1985; Chelluri and
Jestremski, 1989; Ysseldyke, 1991). The weight loss appears to not be acute; rather, it
occurs with the presence of secondary infection averaging 5 percent of body weight
in 28 days (Grunfeld, et al., 1992). This weight loss results not only from the malabsorption mentioned above, but also from decreased intake caused by anorexia and increased
energy 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, depending 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, depending
upon the patients individual needs (see Chapters Four and Five). Typically, stable
patients require 30 kcal/kg (Hellerstein, 1996). Protein needs vary from 0.8 to 1.25 g/kg
for stable patients and 1.5 to 2 gm/kg for symptomatic patients (Gerrior, et al., 1997).

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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 of
AIDS but may alter the patients sense of taste and cause nausea and/or vomiting.
Many of the antibiotics utilized to treat the opportunistic infections (i.e. sulfadiazine, pyrimethamine, ampicillin, chloramphenicol, amphotericin B, nystatin, ganciclovir,
acyclovir, etc.) can cause anorexia, nausea, vomiting, and diarrhea. Chemotherapeutic
agents utilized to treat the various malignancies that may occur can all have effects on
the 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 swallowing due to an infection in the mouth or esophagus or because of medication which
causes stomatitis.
Dietary treatment of diarrhea depends upon the cause of the diarrhea. Supplementation 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 tract
problems 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 least
initially. Other more experimental drugs that have been used for the treatment of anorexia, both in this population and in patients with cancer, include dronabinol and
Megace. Dronabinol naturally occurs in marijuana and has been given in a dose of 2.5
mg before lunch and dinner (VonRoenn, 1993). However, no significant weight gain has
been associated with treatment with dronabinol. Megace appears to stimulate appetite, significantly increase food intake and cause weight gain in about one-third of
treated patients (Gregory, et al., 1985; Kotler, 1997). However, the weight gain appears to
be in fat rather than in lean body mass (Kotler, 1997).
Because the AIDS patient is at risk for opportunistic infections, he or she is at
increased risk for food-borne illnesses. Care should be taken in food preparation to
assure that the patient is not exposed to food-borne illnesses.
If the patient is unable to adequately consume enough nutrients orally, enteral
feedings may be of benefit. Only commercially prepared sterile products should be
utilized. The patient may well tolerate intact nutrient formulas, but may require peptide
or elemental formulas. High fiber formulas may be helpful.
Several formulas that appear to be well tolerated and may enhance immune function are available. [Impact (Sandoz Nutrition), Advera (Ross Labs), and Immun-Aid
(Clintec)]. While Advera has been studied specifically on AIDS patients, Impact has
not. Take care to assure that the formula does not become contaminated (closed tube
feeding systems may be beneficial).

121

Nutrition Support

Parenteral nutrition support may be utilized to supplement oral or enteral intake


or provided instead of oral or enteral intake if the gastrointestinal tract is not functional
or the individual does not tolerate enteral nutrition support.
AIDS is known to affect metabolism as well, as indicated in the chart below

Metabolic Abnormalities in AIDS


Starvation
Early
Adapted
REE
Glucose use
Fat use
Amino acid use
Weight loss
+ = mild



+++
+
++
+

+
+++
+
+

++ = moderate +++ = severe

Hypermetabolism
++
+
+
++
++

Organ Failure
Early
Late
++
+
+
++
++

++
+

+++
+++

Adapted from Cerra, 1987

Guidelines suggested for other disease states apply here in that adequate, but not
excessive, calories from dextrose and fat are given and that adequate protein intake is
provided. Requirements for calories are 25 to 35 kcal/kg in the acutely ill patient; with
40 kcal/kg in the chronic patient to promote weight gain. Protein intake should be 1 to
1.5 gm/kg/d (Bell, et al., 1998). Multivitamins and trace elements should be added as
well. The diarrhea and steatorrhea associated with AIDS may cause increased losses of
B6, B12, folate, selenium, zinc, calcium, and magnesium (Bell, et al., 1998). TPN is given
and monitored in much the same way as with other illnesses.
Pharmacological intervention may stimulate protein anabolism or reverse metabolic abnormalities (Hellerstein, 1996). Growth hormone (GH) supplementation resulted in positive nitrogen balance and increased fat oxidation with a resultant increase
in 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 in
his or her medical care. They often do well with home nutrition support and tend to be
very compliant with whatever is suggested and works. Nutrition assessment and
support of the HIV and AIDS patient is often very beneficial to the patient and rewarding 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 1993
when he presented with Pneumocystis carinii pneumonia.

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Upon this admission, he related a three-week history of anorexia, nausea, vomiting, and headache; he had chronic diarrhea. He had lost 10 lb over the previous month
and was 68 kg on a 61" 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 and
80 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 and
rifampin 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). His
neurological status began to deteriorate and he developed intractable hiccups. His
albumin dropped to 3.4.
TPN was increased to 75 ml/hr (1822 kcal, 90 gm protein) with a goal rate of 100
ml/hr (2428 kcal, 120 gm protein) to accompany his limited PO intake. His headache
continued, causing worsening of his symptoms of nausea and vomiting.
He then became confused and dysarthric and was consuming only liquids. His
albumin dropped to 2.5. He developed chills and fever, along with projectile vomiting
and ileus. TPN continued, with a goal of 100 to 115 ml/hr.
Comfort care was recommended when evidence of progressive invasion of the
Aspergillus in his brain appeared and he suffered a pontine infarct. TPN and the antibiotics were discontinued and a morphine drip was initiated. Cheyne-Stokes respirations
became 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: Dietitians 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 syndrome. 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-containing
formula. 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.

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123

Hellerstein M: The spectrum of nutrition support for AIDS. Address at 5th Annual Nutrition Support
Update, San Diego, 1996.
Kotler DP, Tierney AR, Ferraro R, et al.: Enteral alimentation and repletion of body cell mass in malnourished 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.
OSullivan 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. Current
Nutritional Consultations. Mead Johnson & Company, Evansville, IN, 1994.
Ysseldyke LL: Nutritional complications and incidence of malnutrition among AIDS patients. JADA
91(2):217-218, 1991.

Nutrition Support

Notes

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Nutrition Support

125

Chapter Twelve:
Transition to Home Care

Once your patient is no longer in crisis, the road to complete recovery is just

beginning. While most patients are able to resume oral intake and eventually return to a
somewhat normal lifestyle, some patients will require long-term enteral or parenteral
nutrition 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 excellent
resources for determining the best possible choices for the patient going home with
nutrition support.
Home care providers are widespread, but vary in the type and quality of care
provided. Both the hospital resource people (discharge planners and social workers)
and these home care agencies should be familiar with what is required by the Health
Care Financing Administration (HCFA) for determining eligibility for home care.
HCFA has also developed guidelines for reimbursement for home nutrition support, which should be monitored when considering a patient for home nutrition support. Home nutrition support can be very expensive and care should be taken to assure
that the patient has adequate insurance coverage or other resources to be able to afford
the home nutrition support regimen.
A.S.P.E.N. has developed Standards for Home Nutrition Support (Standards for
Home Nutrition Support, 1988). The standards cover guidelines for provision of home
nutrition support, patient selection, care plans, implementation, monitoring and guidelines for termination of therapy.
The Dietitians in Nutrition Support practice group of ADA has developed a starter
kit for dietitians involved with home care this packet is very helpful and can be
ordered through the American Dietetic Association. Nutrition in home care and home
nutrition support are also covered in other Nutrition Dimension home study courses.

Nutrition Support

126

GUIDELINES FOR HOME NUTRITION SUPPORT


Patients unable to meet their nutrient requirements with oral intake are candidates
for enteral nutrition support. Those unable to meet nutrition needs with enteral nutrition because of inadequate gut function are candidates for parenteral nutrition support.
The patients home environment must be safe and stable and the patients medical
condition must be stable enough to allow for discharge. The formula and the mode of
nutrition support utilized for home care must be appropriate for the medical condition
of 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 be
tolerating the chosen method of support at adequate levels to meet his or her nutrition
needs before discharge. Changes should be made while the patient is in the hospital. For
example, if a patient is to receive all of his enteral feedings while he sleeps, a more
nutrient-dense formula might be in order (to insure that adequate nutrients are provided during a shorter time span). This change in formula should be accomplished
while the patient is still hospitalized so that problems and any necessary alterations can
be identified. TPN/enteral feedings can be initiated at home with appropriate education
and follow-up, if necessary.
Patient education is important. A.S.P.E.N. has identified these key areas: The
patient must know the type and amount of formula he is to receive, should understand
the method of infusion and should be taught proper technique for administration of
feedings or TPN.
He should be taught that enteral feedings should not hang for longer than 8 to 12
hours (or 24 hours if a closed feeding system is utilized) or that parenteral formulas should
not be left at room temperature for longer than 24 hours. He must be shown how to inspect 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, after
feeding to maintain patency.
Instruction on care of the TPN access route should be emphasized. Dietitians and
nurses 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 with
care of the equipment or complications associated with the provision of nutrition support. He should have a contact to call with problems or questions and a health care
provider on 24-hour availability.
Routine monitoring systems should be set up for the patient. Monitoring can
include home visits, telephone calls, return visits to the hospital or physicians office,
etc. Monitoring should include adequacy of nutrient intake, investigation for possibility
for drug-nutrient interactions, weight changes, biochemical and other assessment data
to determine tolerance to therapy, and physical examination (Standards, 1988).
Ideally, the patient will be followed by a home nutrition support team, comprised
of a physician, registered nurse, registered dietitian, and registered pharmacist. Nutrition care plans should be routinely reviewed and revised to best and most appropriately
meet the patients nutritional requirements.

Nutrition Support

127

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 patients 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
patients 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

Nutrition Support

128

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 of
the patients care. The patients nutritional status must be assessed. (This can be
completed by a qualified health care provider, i.e. a nurse, dietitian, physician,
or pharmacist.)
Authorized individuals (i.e. physician) prescribe or order food and nutrition
therapies.
Responsibility for the preparation, storage, distribution, and administration of
oral, enteral, and parenteral nutrition is defined and assigned.
Food and nutrition therapies are prepared and stored under proper conditions of
sanitation, temperature, light, moisture, ventilation, safety, and security to
prevent 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 or
ordered.
The organization has a process for providing food or nutrition therapy when diet
or diet schedules are altered, i.e. transitional feedings.
Each patient is monitored on an ongoing basis for the effectiveness and appropriateness of nutrition therapies (JCAHO, 1997).
Each home care company or provider must interpret these guidelines and define
how each standard will be met. Potentially, the nutrition screening initiative
could be utilized to determine those patients at risk. The Level I screen is a basic
screen that can be utilized by nursing on their initial visit to identify patients at
nutrition risk. The Level II screen can then be utilized to identify specific risk
factors for moderate to high risk patients (NSI, 1992).

COMPLICATIONS OF LONG-TERM TPN


Complications of long-term TPN include metabolic bone disease, cholestasis,
chronic liver disease, carnitine and taurine deficiency, and changes in vitamin and trace
element nutriture. We should be aware of the possibility of these complications and
monitor for changes accordingly with laboratory testing, as shown on the following
page.
Metabolic bone disease is difficult to treat. Liver complications can be reduced by
avoiding overfeeding, and scheduling cycled feedings, oral or enteral feedings to prevent cholestasis, and discontuining TPN. Supplementation of necessary carnitine,
taurine, vitamins and trace elements can prevent deficiencies (McCrae, 1989).

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129

Lab Monitoring for Long-term TPN


Metabolic bone disease
Test for vitamin D nutriture, calcitonin & parathyroid hormone
Ionized calcium, biochem panel
Urinary calcium, phosphorus, urea
Urinary sodium and creatinine
Liver complications
Liver function tests
Biopsy
Carnitine deficiency
Plasma carnitine

Taurine deficiency
Plasma taurine
Vitamins and trace elements
Plasma levels

Home nutrition support is growing by leaps and bounds. More and more of our
patients will require and receive home nutrition support in the future. Our job is to
insure that this therapy is of benefit to them, is safe, and provides adequate nutrients to
them to sustain their lives.

REFERENCES
Accreditation Manual for Home Care, 1997-87. Joint Commission on Accreditation of Health Care
Organizations, 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. Dietitians Handbook of Enteral and Parenteral Nutrition. Skipper A,
Ed. A.S.P.E.N. Publ., Rockville, MD, 1989.
Nelson JK and OShea 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 OShea 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.

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Notes

130

Review Question Answers

131

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, postoperative status, stress, fluid imbalance, renal disease and dialysis.
4. Utilizing actual weight (within range for IBW) of 59 kg x 25 kcal/kg = approximately
1500 kcal/day. Protein needs are based upon 150:1 Kcal/N ratio; therefore are
1500/150 = 10 x 6.25 = 62.5 gm protein. However, in trauma patients, protein needs
are 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 a
nasogastric tube into the duodenum would likely be well tolerated.

1991-2009 Nutrition Dimension, Inc.

3. A nutrient-dense formula should be used to assure adequate provision of nutrients


with 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 from
the addition of fiber to the diet, either by utilizing a fiber-rich formula or by adding
fiber to the existing formula. Make sure that the feeding is at isotonicity. Stools could
be tested for growth of pathogenic bacteria. Recommendations for anti-diarrheal
medications could be made, as well.
5. For the critically ill patient, feedings should be given continuously into the duodenum or jejunum (distal to the ligament of Treitz).

132

Review Question Answers

6. With high gastric residuals, the feeding may be held. You should assure that the
feeding is isotonic. You could recommend that feedings should be into the small
bowel since obstruction in the stomach does not necessarily mean there is also an
ileus in the small bowel.
7. A patient in a long-term care facility may best tolerate intermittent feedings, utilizing
a 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, and
since the patient had been receiving nothing by mouth for five days The patient is
already underweight and would benefit from TPN until enteral feedings can be
implemented. Transition to enteral feedings should be made as early as possible.
2. Recommend that central venous access be attained or recommend that a formula
with a final dextrose concentration of less than D10 be utilized. A formula with a
final dextrose concentration of more than 10 percent will not be tolerated in a peripheral vein. The final concentration of the TPN formula ordered is greater than
10%.
3. First check for signs of infection (reddening, puffiness) around IV site and change
site, as necessary, culturing for growth of bacteria. Since the patient is not tolerating
fat, you could recommend removal of lipid from TPN regimen. Suggest insulin
coverage for increased glucose levels and monitor BUN and creatinine levels for
further alteration in renal function, because current levels are acceptable and may
return to normal as renal function improves (but no change in formula is indicated
for now).

1991-2009 Nutrition Dimension, Inc.

4. Attempt enteral or oral feedings as soon as possible. Make sure that the patient is not
being 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% calories
from fat), with calories from dextrose decreased. Increased calories from fat are often
beneficial in efforts to decrease carbon dioxide production, improve respiratory
quotient and improve the patients chances of weaning from the ventilator. Assure
that patients nutrient requirements are met, but that patient is not overfed. If you
have a metabolic cart, measure CO2 production and O2 consumption to determine
the appropriate mix of nutrients. If CO2 production is greater than it should be, you
may be overfeeding the patient in total calories and/or carbohydrate calories.

Review Question Answers

133

6. 80 ml/hour x 24 hours = 1920 ml or 1.92 liters


400 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: 2443
Nonprotein kcal: 2075
Protein: 92 gm

768 kcal from fat 2443 kcal = 31% kcal from fat
92 gm protein 6.25 = 14.7 gm nitrogen
Calorie:nitrogen ration 141:1

7. 50 ml /hour x 24 hours = 1200 ml or 1.2 liters


1200 ml total = 600 ml each of dextrose and amino acid
600 ml x 0.5 (% dex) = 300 gm x 3.4 kcal = 1020 kcal from dextrose
600 ml x 0.10 (% amino acid) = 60 gm protein x 4 kcal = 240 kcal from protein
500 ml x 2.0 (kcal/ml in 20% lipid) = 1000 kcal from lipid
Total calories: 2260 kcal
Nonprotein kcal: 2020 kcal
Protein: 60 gm

1000 kcal from fat 2260 kcal = 40% kcal from fat
60 gm pro 6.25 = 9.6 gm nitrogen
2020 nonprotein kcal 9.6 = 210
Calorie: nitrogen ration 210:1

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 patients oral
intake increases through intake of antidumping diet and/or small frequent feedings.

1991-2009 Nutrition Dimension, Inc.

2. Dumping syndrome may occur with decreased tolerance to concentrated sweets and
sugars and the need to limit fluid intake with meals. Slow feedings and/or small
frequent meals will be necessary initially, advancing later to a less restrictive regimen.
3. TPN may be required initially after surgery. Taper TPN as other modes of feeding are
tolerated. 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 a
continuous feeding. Patient can later be transitioned to oral intake, slowly with a lowresidue, lactose-free diet in frequent small feedings. Consider supplementation with a
multivitamin/mineral.

134

Review Question Answers

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 decreased
insulin and increased glucagon; increased secretion of ACTH; increased glucocorticoids and mineralocorticoids (which later return to normal); increased synthesis (but
decreased 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 be
used. Optimally, fat should be provided with a mix of -3 and -6 fatty acids. If
CHO-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 because
of the increased level of stress.
Notes:

CHAPTER SIX: OBESITY AND DIABETES MELLITUS

1991-2009 Nutrition Dimension, Inc.

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 ideal
body weight to determine protein requirements: 75 - 100 gm pro/day (using factors
of 1.5 - 2 gm pro/kg/day.)
2. Patient is at his Ideal Body Weight.. Needs are estimated at 2250 kcal/day, based
upon 25 kcal/kg and considering that we do not want to overfeed this patient who
is facing a difficult wean from the ventilator. Protein needs are estimated at 90-135
gm protein/day (using a factor of 1.0 1.5 gm protein/kg/day with acute renal
failure). Enteral feedings should be attempted with the usual isotonic formula not
a renal formula, unless electrolyte disturbances are noted.
Notes:

Review Question Answers

135

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 patients head should
remain 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 with
about 60% calories from fat would be used. Care should be taken not to overfeed the
patient either calories or protein.
3. Caloric requirements for this 45 kg female would be about 1100 - 1300 kcal (25-30
kcal/kg), with reduced calories given if respiratory distress increases (increased
dyspnea, decreased pO2, increased pCO2, etc). Protein requirements would be 68 - 90
gm/day. Recommend enteral feedings if possible with an isotonic, intact protein
formula through the duodenum or jejunum.
Notes:

CHAPTER EIGHT: RENAL DISEASE


1. Nutritional parameters of use in assessing the renal failure patient would include
height and weight, weight changes, transferrin levels and physical exam.
2. All water soluble vitamins should be supplemented in renal failure, with increased
amounts of B6 (10 mg), C (100 mg) and folate (1mg) over the RDA.

1991-2009 Nutrition Dimension, Inc.

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 acid
formula or solution. A possible formula might be: : 400ml D18, 400ml amino acids
5%, 200 ml 20% intralipid @ 85ml/hr. This would provide about 2600 nonprotein
calories, 77 gm of protein, and 2900 total calories. Supplement with water soluble
vitamins, and monitor trace elements if on TPN for an extended period. Limit addition of phosphorus and potassium. Begin low rate enteral feedings with isotonic
conventional formula as soon as possible. Transition off TPN and enteral feedings as
able to tolerate normal renal diet.
4. Caloric requirements: Adjusted body weight 62 kg x 25 = 1550 kcal. Protein needs
are 59kg (based on IBW) x 1.2 = 71 gm protein. If the patient is able to tolerate enteral feedings, recommend conventional formula, adjusting to a renal formula if
electrolyte disturbances persist.
Notes:

136

Review Question Answers

CHAPTER NINE: LIVER DISEASE


1. You must consider changes in CHO metabolism and the possibility of hypo- or hyperglycemia, changes in fat metabolism and development of fatty liver, increased
protein 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 1700
kcal/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/day
and 1.0 - 2.2 gm pro/kg/day as indicated by increased stress level. Additional
calories can be added to allow for weight gain.
2. Alterations in taste and smell; difficulty in swallowing; decreased secretions leading
to dry mouth.
Notes:

CHAPTER ELEVEN: AIDS & HIV-POSITIVE PATIENTS


1. The following diseases appear to opportunistically impact the GI tract in the AIDS
patient: candidiasis, cytomegalovirus, herpes simplex and various protozoa.

1991-2009 Nutrition Dimension, Inc.

2. The drugs used to increase appetite are Dronabinol and Megace (megastrol acetate).
Notes:

136

Review Question Answers

CHAPTER NINE: LIVER DISEASE


1. You must consider changes in CHO metabolism and the possibility of hypo- or hyperglycemia, changes in fat metabolism and development of fatty liver, increased
protein 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 1700
kcal/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/day
and 1.0 - 2.2 gm pro/kg/day as indicated by increased stress level. Additional
calories can be added to allow for weight gain.
2. Alterations in taste and smell; difficulty in swallowing; decreased secretions leading
to dry mouth.
Notes:

CHAPTER ELEVEN: AIDS & HIV-POSITIVE PATIENTS


1. The following diseases appear to opportunistically impact the GI tract in the AIDS
patient: candidiasis, cytomegalovirus, herpes simplex and various protozoa.

1991-2009 Nutrition Dimension, Inc.

2. The drugs used to increase appetite are Dronabinol and Megace (megastrol acetate).
Notes:

Appendix #1

137

1991-2009 Nutrition Dimension, Inc.

Physical Changes with Malnutrition


Condition

Deficiency

Hair
easily pluckable, dyspigmented

Protein-calorie malnutrition

Eyes
Bitots spots
xerophthalmia
night blindness
angular palpebritis

Vitamin A
Vitamin A
Vitamin A
Riboflavin, niacin

Gums
bleeding, spongy

Vitamin C

Lips
angular stomatitis
cheilosis

Riboflavin, B6, iron


Riboflavin, B6, niacin

Tongue
magenta
glossitis

Riboflavin
Niacin, folate, iron, B6, B12

Skin
xerosis
follicular hyperkeratosis
petechiae, ecchymoses

Vitamin A, essential fatty acids


Vitamin A, essential fatty acids
Vitamin C, Vitamin K

Nails
koilonychia

Iron

Muscle wasting

Protein-calorie malnutrition

Beading of ribs

Vitamin D and calcium

Appendix #2

138

Metropolitan Life Height-Weight Tables


Ht.
(inches)

Small
Frame

62
63
64
65
66
67
68
69
70
71
72
73
74
75
76

128-134
130-136
132-138
134-140
136-142
138-145
140-148
142-151
144-154
146-157
149-160
152-164
155-168
158-172
162-176

Men (age 25-59)


Medium
Frame
131-141
133-143
135-145
137-148
139-151
142-154
145-157
148-160
151-163
154-166
157-170
160-174
164-178
167-182
171-187

Large
Frame

Ht.
(inches)

138-150
140-153
142-156
144-160
146-164
149-168
152-172
155-176
158-180
161-184
164-188
168-192
172-197
176-202
181-207

58
59
60
61
62
63
64
65
66
67
68
69
70
71
72

Men are wearing 5 lb of clothing, and shoes with 1-inch heels


Source: Metropolitan Life Insurance Company, 1983.

1991-2009 Nutrition Dimension, Inc.

62
63
64
65
66
67
68
69
70
71
72
73
74
75
76

Large
Frame

109-121
111-123
113-126
115-129
118-132
121-135
124-138
127-141
130-144
133-147
136-150
139-153
142-156
145-159
148-162

118-131
120-134
122-137
125-140
128-143
131-147
134-151
137-155
140-159
143-163
146-167
149-170
152-173
155-176
158-179

102-111
103-113
104-115
106-118
108-121
111-124
114-127
117-130
120-133
123-136
126-139
129-142
132-145
135-148
138-151

Women are wearing 3 lb of clothing and 2-inch heels

Creatinine Height Index

Men
Height
(inches)

Women (age 25-59)


Small
Medium
Frame
Frame

Women

Ideal
Weight
(lb)

Creatinine
Excretion
(mg/24 hrs)

Creatinine
Height Index

Height
(inches)

Ideal
Weight
(lb)

Creatinine
Excretion
(mg/24 hrs)

Creatinine
Height Index

124
127
130
133
137
141
145
149
153
158
162
167
171
176
181

1288
1325
1359
1386
1426
1467
1518
1555
1596
1642
1691
1739
1785
1831
1891

8.17
8.28
8.36
8.40
8.51
8.62
8.76
8.86
8.98
9.11
9.24
9.38
9.49
9.61
9.80

58
59
60
61
62
63
64
65
66
67
68
69
70
71
72

101
104
107
110
113
116
119
123
128
132
136
139
143
147
151

830
851
875
900
925
949
977
1006
1044
1076
1109
1141
1174
1206
1240

5.63
5.68
5.74
5.81
5.87
5.93
6.01
6.09
6.23
6.32
6.42
6.51
6.60
6.69
6.78

Appendix #3

139

Anthropometric Measurement Standards


Triceps Skinfold Percentiles (mm)
Male
%

A
G
E

Female

10

25

50

75

90

95

10

25

50

75

90

95

18

13

20

24

10

12

15

18

22

26

30

19

10

15

20

22

10

11

14

18

24

30

34

25

12

16

20

24

10

12

16

21

27

34

37

35

12

16

20

23

12

14

18

23

29

35

38

45

12

16

20

23

12

16

20

25

30

36

40

55

11

14

19

22

12

16

20

25

31

36

38

65

11

15

19

22

12

14

18

24

29

34

36

Arm Muscle Circumference (mm)


Male

1991-2009 Nutrition Dimension, Inc.

Female

10

25

50

75

90

95

10

25

50

75

90

95

18 226

237

252

264

283

298

324

174

179

191

202

215

237

245

19 238

245

257

273

289

309

321

179

185

195

207

221

236

249

A 25 243
G
E 35 247

250

264

279

298

314

326

183

188

199

212

228

246

264

255

269

286

302

318

327

186

192

205

218

236

257

272

45 239

249

265

281

300

315

326

187

193

206

220

238

260

274

55 236

245

260

278

295

310

320

187

196

209

225

244

266

280

65 223

235

251

268

284

298

306

185

195

208

225

244

264

279

Source: Frisancho, A.R..American Journal of Clinical Nutrition, 1981, 34:2540-2545

140

Appendix #4

Non-nutritional Factors Affecting Serum Proteins


Albumin

Transferrin

Prealbumin

hydration status
nephrotic syndrome
burns
liver disease
acute stress
eclampsia
infection
trauma
surgery
chronic illness

iron deficiency
pregnancy
chronic illness
blood loss
infection
liver disease
uremia
nephrotic syndrome
increased iron stores
hydration status
surgery

renal disease
liver disease
stress
surgery
infection
dialysis
chronic illness
hydration status

Appendix #5
Nutrient Absorption
Stomach

Intrinsic factor secretion

Duodenum

Vitamin A, B1, iron, calcium, glycerol and fatty acids, monoglycerides,


amino acids, mono- and disaccharides

Jejunum
Entire:

Glucose, galactose, ascorbic acid, amino acids, glycerol and fatty acids,
monoglycerides, folic acid, biotin, copper, zinc, potassium,
vitamins D, E, B1, B2, B3, B6, iodine, magnesium, calcium, phosphorus
Proximal: Vitamin A, folic acid, iron, disaccharides
Distal:
Disaccharides, dipeptides
Ileum

1991-2009 Nutrition Dimension, Inc.

Entire:

Sodium chloride, vitamins D, E, B1, B2, B3, B6, iodine, magnesium,


calcium, phosphorus
Proximal: Disaccharides, potassium
Distal:
B12 and intrinsic factor

Colon
Entire: Water, Vitamin K
Transverse: Water, biotin

Appendix #6

141

TPN Monitoring Form


Name_______________________________
Doctor______________________________
Formula_____________________________
____________________________________
____________________________________
Patient Needs: Calories/day_____________
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

1991-2009 Nutrition Dimension, Inc.

Cholesterol
Triglycerides
WBC
Total Lymphocytes
PT
UUN
Nitrogen Balance
Other
Charted

Rm#____________________________
Diagnosis_______________________
IV Rate____________ ml/hr
Calorie/Nitrogen ratio______________
Height ________
Protein gm/day____________

Appendix #7

142

Dietary Reference Intakes:

)
2

B1
in

e(

Vit

lat
Fo

am

mc

g) f

(g

g)
(m
in
Vit

am

(m
cin
Nia

avi
ofl
Rib

B6

g) e

mg
n(

g)
(m
in
Th

iam

in

45

5*

11

60*

0.9

0.9

12

1.0

300

1.8

14-18

59

900

75

5*

15

75*

1.2

1.3

16

1.3

400

2.4

19-30

58

900

90

5*

15

120*

1.2

1.3

16

1.3

400

2.4

31-51

63

900

90

5*

15

120*

1.2

1.3

16

1.3

400

2.4

51-70

63

900

90

10*

15

120*

1.2

1.3

16

1.7

400

2.4h

70+

63

900

90

15*

15

120*

1.2

1.3

16

1.7

400

2.4h

9-13

46

600

45

5*

11

60*

0.9

0.9

12

1.0

300

1.8

14-18

44

700

65

5*

15

75*

1.0

1.0

14

1.2

400i

2.4

19-30

46

700

75

5*

15

90*

1.1

1.1

14

1.3

400i

2.4

31-50

50

700

75

5*

15

90*

1.1

1.1

14

1.3

400i

2.4

51-70

50

700

75

10*

15

90*

1.1

1.1

14

1.5

400

2.4h

70+

50

700

75

15*

15

90*

1.1

1.1

14

1.5

400

2.4h

Vit

600

Vit

34

Vit

Vit

am

in
am

g)
K(

mg
E(

D(
in
am

mc

)d

g ) b,c
mc

mg
in
am
Vit

am

in

A(

C(

mc

)
gm
n(
tei
1991-2009 Nutrition Dimension, Inc.

F
E
M
A
L
E
S

Pro

9-13

Ag

M
A
L
E
S

g) a

Recommended Dietary Allowances & Adequate Intakes


Vitamins

NOTE: This table (taken from the DRI reports, see www.nap.edu) presents Recommended Dietary Allowances (RDAs) in bold type and
Adequate Intakes (AIs) in ordinary type followed by an asterisk (*). RDAs and AIs may both be used as goals for individual intake. RDAs are
set 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 other
life 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 being
able 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 -carotene, 24 mcg -carotene, or 24 -cryptoxanthin. The RAE for
dietary 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 -Tocopherol includes RRR--tocopherol, the only form of -tocopherol that occurs naturally in foods, and the 2R-stereoisomeric
forms of -tocopherol (RRR-, RSR-, and RSS--tocopherol) that occur in fortified foods and supplements. It does not include the 2Sstereoisomeric forms of tocopherol (SRR-, SSR-, SRS-, and SSS--tocopherol), also found in fortified foods and supplements.

Appendix #7 cont.

25*

1,300* 1,250

410

11

11

150

55

890

2.2*

5*

30*

1,000*

700

400

11

150

55

900

2.3*

5*

30*

1,000*

700

420

11

150

55

900

2.3*

5*

30*

1,200*

700

420

11

150

55

900

2.3*

5*

30*

1,200*

700

420

11

150

55

900

2.3*

4*

20*

1,300* 1,250

240

120

40

700

5*

25*

1,300* 1,250

360

15

150

55

5*

30*

1,000*

700

310

18

150

5*

30*

1,000*

700

320

18

5*

30*

1,200*

700

320

5*

30*

1,200*

700

320

cg)
(m

g) g

(m

cg)
(m

de

ium

ne

g)
(m

nu

oli

5*

lyb

1.9*

34

375*

3*

35*

43

550*

4*

35*

45

550*

4*

35*

45

550*

4*

30*

45

550*

4*

30*

45

550*

1.6*

2*

21*

34

375*

890

1.6*

3*

24*

43

400*

55

900

1.8*

3*

25*

45

425*

150

55

900

1.8*

3*

25*

45

425*

150

55

900

1.8*

3*

20*

45

425*

150

55

900

1.8*

3*

20*

45

425*

Ch

25*

Co

2*

Se

Mo

700

rom

40

Ch

120

ori

Flu

de

an
ng
Ma

(m
er
pp

len

ese

cg)

g)
(m
ium

cg)
Iod

ine

(m

)
mg
Zin

c(

)
mg

240

Ph

1,300* 1,250

Ca

20*

Bio

4*

Pa

Iro

n(

(m

g)

cg)
(m
um
esi
gn

ho
osp

Ma

rus

g)
lci

um

(m

cg)
(m
tin

(m

id

g)

(m

cg)

Minerals

Ac
nic
the
nto

143

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
1991-2009 Nutrition Dimension, Inc.

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 B , it is advisable for those older than 50 years to meet their RDA mainly by
12
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

Appendix #8

144

Example of Standard TPN Admixtures


Standard Central TPN Formula
Nutrient Content of One Liter of TPN
Final concentrations
Amino Acids
5%
Dextrose
18%
Lipid
2%

Nutrient Composition
Amino 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
Electrolyte Concentration (each 20 ml contains): The following electrolytes will be present in solution:
Na
35 mEq
Na+ 55 mEq
Cl61 mEq
Cl
35 mEq
K
20 mEq
K+
30 mEq
Ac
64 mEq
Ca
4.5 mEq
Mg
5 mEq
Ac
30 mEq
Vitamins and Minerals
MVI-12
10 ml/24 hours
Trace elements 3 ml/24 hours

Standard Peripheral TPN Formula


Nutrient Content of One Liter of TPN
Final concentrations
Amino Acids
Dextrose
Lipid

4%
8%
3%

Nutrient Composition
Amino Acids
40 gm (6.4 gm Nitrogen)
Dextrose
80 gm (275 kcal)
Lipid
30 gm (300 kcal)

1991-2009 Nutrition Dimension, Inc.

Nonprotein to calorie ratio: 90:1; 40% of total calories come from fat
Electrolyte Concentration (each 20 ml contains): The following electrolytes will be present in solution:
Na
35 mEq
Na+ 55 mEq
Cl61 mEq
Cl
35 mEq
K
20 mEq
Ca
4.5 mEq
K+
30 mEq
Ac
64 mEq
Mg
5 mEq
Ac
30 mEq
Mg++ 5 mEq
PO4
12 mMol
Ca++ 4.5 mEq
Vitamins and Minerals
Osmolality
MVI-12
10 ml/24 hours
980 mOsm/L with additives
Trace elements 3 ml/24 hours

Appendix #9

145

Determining Nutritional Values from TPN


Hydrated dextrose = 3.4 kcal/gm*
20% lipid = 2 kcal/ml
10% lipid = 1.1 kcal/ml
Protein = 4 kcal/gm**

Computation of Nutrition Content


TPN Solution #1: 400 ml D50, 500 ml a.a. 10%, 100 ml lipid 20% @ 100 ml/hr
(per liter)

400 ml D50:
500 ml aa 10% :

100 ml lipid 20%:

100 ml/hr X 24 hrs = 2400 ml or 2.4 liters


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 kcal
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 pro
50 gm pro X 2.4 liters = 120 gm pro
100 ml X 2 kcal/ml = 200 kcal lipid
200 kcal X 2.4 liters = 480 kcal lipid

Total calories:
Nonprotein calories:
Grams of nitrogen:
Calorie/Nitrogen ratio:
Percent calories from fat:

1632 (dex)+480(pro) + 480(lipid) = 2592 total kcal


1632 (dex) + 480 (lipid) = 2112 nonpro kcal
120 gm pro 6.25 = 19.2 gm N
2112 (nonpro kcal) 19.2 (gm N) = 110:1 (kcal/N)
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

1991-2009 Nutrition Dimension, Inc.

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 dex
720 ml X .10 (% aa) = 72 gm pro X 4 kcal/gm = 288 kcal pro
500 ml X 1.1 (lipid) = 550 kcal lipid
Total calories:
Nonprotein calories:
Grams of nitrogen:
Calorie/Nitrogen ratio:
Percent calories from fat:

1224 +288 + 550 = 2062 total kcal


1224 (dex) + 550 (lipid) = 1774 nonpro kcal
72 6.25 = 11.5 gm N
1774 nonpro kcal 11.5 gm N = 154:1 (kcal/N)
550 (kcal lipid) 1774 (nonpro kcal) = 31% fat kcal

*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)

Appendix #10

146

Metabolic Complications of TPN

1991-2009 Nutrition Dimension, Inc.

Condition

Probable Causes

Treatment

Refeeding Syndrome

Overfeeding patients who haven't eaten in


over 2 days or are severely malnourished.
Rapid drop in serum PO4, Mg, K

Correct electrolytes in formula, slow down


the rate of feeding and monitor carefully

Hyperglycemia

Glucose intolerance, insulin-resistance,


sepsis, diabetes

Monitor glucose 6x/day, adjust insulin


dose, increase lipid calories, decrease
CHO calories if possible

Hypoglycemia

Too much insulin, too abrupt discontinuation


of TPN

Immediate glucose infusion; monitor


glucose; taper off TPN gradually

Hyperlipidemia

Severe sepsis, stress, familial condition

Limit lipid emulsions to every other day, if


tolerated and meets caloric needs

Hyperkalemia

Renal insufficiency

Decrease potassium in formula

Hypokalemia

Protein anabolism; insufficient K+ in TPN


especially during initial refeeding; diarrhea,
vomiting, fistulas; side effects of drugs; losses
from gut or kidneys

Increase potassium in TPN; determine if


there are unrecognized losses

Hypophosphatemia

Inadequate PO4 in TPN, especially during


initial refeeding, alkalosis, metabolic acidosis,
antacids, hypomagnesemia and hypokalemia,
uncontrolled diabetes

Increase PO4 supplementation (can be


done in the TPN). Monitor other minerals.

Hyperphosphatemia

Renal insufficiency or renal failure

Decrease PO4 in TPN. Individualize. Often


no PO4 is given.

Hypermagnesemia

Chemotherapy, aminoglycosides

Adjust formula

Hypomagnesemia

Inadequate Mg in TPN: renal insufficiency,


increased losses, impaired absorption in GI
tract

Increase Mg in formula

Elevated LFTs

Overfeeding or cholestasis from pancreatitis

Reduce or discontinue TPN if severe

Increased CO2

Overfeeding with carbohydrate calories; lung


disease

Reduce total calories or substitute fat


calories for some CHO calories

Pre-renal azotemia
Increased BUN

Excess amino acids; renal insufficiency,


dehydration

Reduce amino acids and nitrogen in TPN

Hyponatremia

Overhydration from TPN and IV fluids;


increased losses from urine or gut; inadequate sodium in TPN

Determine if there are increased losses;


increase Na in TPN and/or reduce fluids

Examination

147
SUP09

Answer each question by checking the correct answer online or filling the circle corresponding to the correct answer on the answer sheet. There is one best answer for each question. If you want a record of your
answers, photocopy the answer sheet or record your choices on another piece of paper. Do not detach the
examination from the book. This exam has 40 questions.

1. Enteral Nutrition should be considered:


a. when a patient has had inadequate intake for 1 to 2 days
b. in a patient with a complete small bowel obstruction
c. when an advanced directive is present and specifies no artificial nutrition support
d. in a patient with a small bowel resection along with TPN
e. 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, 510", 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

1991-2009 Nutrition Dimension/Gannett Education, Inc.

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

148

Exam (cont.)
SUP09

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

1991-2009 Nutrition Dimension/Gannett Education, Inc.

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

Exam (cont.)

149
SUP09

15. Your patient is diagnosed with alcoholic liver disease and has an ammonia level of 110. He is 42 years
old, 510", 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 cholecystitis. She is ventilator-dependent. Her needs are:
a. 1130 kcal
b. 1300 kcal
c. 2750 kcal
d. 1500 kcal

1991-2009 Nutrition Dimension/Gannett Education, Inc.

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

150

Exam (cont.)
SUP09

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, 510", 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

1991-2009 Nutrition Dimension/Gannett Education, Inc.

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

Exam (cont.)

151
SUP09

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

1991-2009 Nutrition Dimension/Gannett Education, Inc.

33. Your 54", 90 lb, 65-year-old female patient is ventilator-dependent after being hospitalized for exacerbation 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

152

Exam (cont.)
SUP09

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 transport 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

1991-2009 Nutrition Dimension/Gannett Education, Inc.

40. Only formulas containing essential amino acids should be used for the renal failure patient.
a. True
b. False