Guidelines for the Use of Parenteral and Enteral Nutrition

in Adult and Pediatric Patients

Section I: Introduction

The American Society for Parenteral and Enteral 1. The Guidelines must be factually up-to-date to
Nutrition (A.S.P.E.N.) is an organization comprised of reflect a current, evidence-based, best approach to
health care professionals representing the disciplines the practice of nutrition support.
of medicine, nursing, pharmacy, dietetics, and nutri- 2. The Guidelines must support the clinical and
tion science. The mission of A.S.P.E.N. is to serve as a professional activities of nutrition support practi-
preeminent, interdisciplinary, research-based, patient- tioners by articulating evidence-based recommen-
centered clinical nutrition society throughout the dations upon which to base personal and institu-
world. A.S.P.E.N. vigorously works to support quality tional practices and resource allocation.
patient care, education, and research in the fields of 3. The Guidelines should serve as a tool to help
nutrition and metabolic support in all health care set- guide policy makers, health care organizations,
tings. insurers, and nutrition support professionals to
Promulgation of safe and effective patient care by improve the systems and regulations under which
nutrition support practitioners is a critical role of the specialized nutrition support is administered.
A.S.P.E.N. organization. To this end, in 1993, the IPatients may be treated with specialized nutrition sup-
A.S.P.E.N. Board of Directors published &dquo;Guidelines Iport in any care setting, including hospitals, nursing
for the Use of Parenteral and Enteral Nutrition in Ihomes, rehabilitation facilities, and at home. For most
Adult and Pediatric Patients.&dquo; The guidelines were Ipatients, the duration of nutrition support therapy is
relatively short (less than 6 weeks); for others, depen-
created in accordance with Institute of Medicine rec-
Idence upon parenteral or enteral feeding may be life-
ommendations as &dquo;systematically developed state-
ments to assist practitioner and patient decisions long. These guidelines are intended to assist clinical
about appropriate health care for specific clinical cir- .
practitioners who provide specialized nutrition support
to patients in all care settings.
cumstances.&dquo;2 These clinical guidelines, designed for
use by health care professionals who provide nutrition

support services and their patients, offer clinical advice DEFINITIONS AND SUPPORTING
for managing adult and pediatric (including adoles- MATERIALS
cent) patients in inpatient and outpatient (ambulatory,
The A.S.P.E.N. Board of Diredtors has published a
home, and specialized care) settings. The utility of the series of related documents. These include:
Guidelines is attested to by the frequent citation of this
document in peer-reviewed publications and their fre- Definition of Terms Used in A.S.P.E.N. Guidelines
and Standards. JPEN 19(1):l, 1995
quent use by A.S.P.E.N. members and other nutrition Standards for Nutrition Support Hospitalized Pedi-
care professionals in clinical practice, academia, atric Patients. Nutr Clin Pract 11:217-228, 1996
research, and industry. They guide personal and pro-
fessional clinical activities, they are helpful as educa- Standards for Nutrition Support Hospitalized Pa-
tional tools, and they influence institutional practices tients. Nutr Clin Pract 10(6):208-219, 1995
and resource allocation. Standards for Nutrition Support for Residents of
In the Spring of 1999, the A.S.P.E.N. Board of Direc- Long-Term Care Facilities. Nutr Clin Pract 12:
tors established the A.S.P.E.N. Clinical Guidelines 284-293, 1997
Task Force to revise the 1993 Clinical Guidelines. Standards for Home Nutrition Support. Nutr Clin
Three objectives for the revised document were identi- Pract 14:151-162, 1999
fied. These objectives determined the process, format, Standards for Nutrition Support Pharmacists. Nutr
and content of this updated version: Clin Pract 14:275-281, 1999
Standards of Practice for Nutrition Support Dieti-
tians. Nutr Clin Pract 15:53-59, 2000
Standards of Practice for Nutrition Support Nurses.
Nutr Clin Pract 16(1):56-62, 2001
Correspondence and reprint requests: American Society for Par-
enteral and Enteral Nutrition, 8630 Fenton Street, Suite 412, Silver Standards of Practice for Nutrition Support Physi-
Spring, MD 20910-3805. cians. Nutr Clin Pract 11:235-240, 1996

1SA
2SA

The Science and Practice of Nutrition Support: A advice for managing adult and pediatric patients in the
Case Based Core Curriculum. American Society hospital or home. The guidelines are organized into the
for Parenteral and Enteral Nutrition and Kendall following sections:
Hunt Publishing Company, Dubuque, IA, 2001 1. Sections concerning issues generic to SNS in most
The A.S.P.E.N. Nutrition Support Practice Manual. or all patients (eg, nutrition assessment, nutrient

American Society for Parenteral and Enteral requirements), subdivided into Adult and Pediat-
ric discussions.
Nutrition, Silver Spring, MD, 1998
Clinical Pathways and Algorithms for Delivery of 2. Disease-specific sections for Adults.
Parenteral and Enteral Nutrition Support in 3. Disease-specific sections for Pediatrics.
Adults. American Society for Parenteral and With this 2002 revision, an attempt has been made,
when possible, to have the Adult and Pediatric sections
Enteral Nutrition, Silver Spring, MD, 1998
look and feel the same. Each section begins with a
Safe Practices for Parenteral Nutrition Formula-
tions. JPEN 22:49-66, 1998 Background that presents general information neces-
sary to understand the relevant physiologic and clini-
Here are listed terms that frequently appear within cal issues. This is followed by a presentation of Evi-
this Guidelines document and have specific meanings: dence that summarizes the applicable clinical studies
Clinical guidelines: Systematically developed state- that can be used to guide clinical practice. Next comes
ments to assist practitioner and patient decisions a Special Issues or Considerations subheading where
about appropriate health care for specific clinical cir- further evidence is presented about specialized, new,
cumstances.2 or controversial topics. The Practice Guidelines are
Nutrition screening: A process to identify an individ- then clearly stated in an active manner (eg, SNS
ual who is malnourished or who is at risk for malnu- should be administered ...), and annotated with a
trition to determine if a detailed nutrition assessment Strength of Evidence classification (see below). Finally,
is indicated. each section is referenced. Space limitations prevented
Nutrition assessment: A comprehensive approach to exhaustive referencing. Therefore, liberal use is made
defining nutrition status that uses medical, nutrition, in the references of review articles, summary state-
and medication histories; physical examination; ments, and meta-analyses that do contain references to
anthropometric measurements; and laboratory data. A the primary sources.
formal nutrition assessment should provide all of the Careful reading of the guideline statements with
information necessary to develop an appropriate nutri- their associated strength of evidence classifications
tion care plan. Because of the inextricable relationship should highlight those clinical situations where there
are strong data to support practice recommendations.
between malnutrition and severity of illness and the
fact that tools of nutrition assessment reflect both Absence of data, however, does not necessarily mean
that interventions are harmful or contraindicated. In
nutrition status and severity of underlying disease, an
situations where evidence based recommendations
assessed state of malnutrition or presence of specific
cannot be made because of a lack of relevant clinical
indicators of malnutrition in fact refers to the conse-
studies, clinicians must still make the best possible
quences of a combination of an underlying illness and decisions for their patients. Those areas where guide-
associated nutritional changes and deficits. lines are classified as being based on class C data
Nutrition care plan: A formal statement of the nutri- (formulated using expert opinion and editorial consen-
tion goals and interventions prescribed for an individ- sus) reflect an attempt to make the best recommenda-
ual using the data obtained from a nutrition assess- tions possible within the context of the available data
ment. The plan, formulated by an interdisciplinary and expert clinical experience. These class C guidelines
process, should include statements of nutrition goals identify an agenda for critical, clinical research to more
and monitoring parameters, the most appropriate firmly establish SNS as an evidence-based specialty.
route of administration of specialized nutrition support A thread running throughout many of the disease-
(oral, enteral, and/or parenteral) method of nutrition specific guidelines is the rationale for choosing enteral
access, anticipated duration of therapy, and training over parenteral SNS or alternatively parenteral over
and counseling goals and methods. enteral when a decision to use SNS has been made. The
Pediatric: Patients <17 years old, including prema- A.S.P.E.N. Board of Directors and the A.S.P.E.N. Clin-
ture newborns, neonates, infants, toddlers, children, ical Guidelines Task Force struggled with this crucial
and adc lescents. issue. The generic data relevant to this decision are
Specialized nutrition support (SNS): Provision of presented in the section entitled &dquo;Indications for
nutrients orally, enterally, or parenterally with thera- Administration of Specialized Nutrition Support.&dquo;
peutic intent. This includes, but is not limited to, pro- In some specific clinical situations (eg, critical care,
vision of total enteral or parenteral nutrition support trauma), data support the use of enteral over paren-
and provision of therapeutic nutrients to maintain teral nutrition because of improved outcomes and
and/or restore optimal nutrition status and health. reduced complication rates. A critical review of the
literature, however, offers little guidance in other
areas. Nevertheless, because of data suggesting a
HOW TO USE THESE GUIDELINES
lower cost for enteral nutrition (EN) than parenteral
These clinical guidelines, designed for health care nutrition (PN) and because of general consensus that
professionals who provide SNS services, offer clinical the gut should be used when possible, these guidelines
 3SA

are biased toward recommending EN when feasible not produce disease in otherwise healthy humans,
and reserving PN for those patients in whom the gut is whereas essential nutrients must be provided to both
not functional, enteral access is not possible, or the risk healthy and ill people. Patients with advanced malnu-
of EN-related complications (eg, aspiration) is unac- trition or who are at risk for becoming severely mal-
ceptably high. nourished must be fed to prevent death by starvation.
Another fundamental issue that influences many of Some of the guideline statements that follow in this
the discussions and recommendations in the Guide- document were developed on the basis of expert opin-
lines is the relationship between nutrition assessment, ion and editorial consensus (class C data) because of
nutrition status, malnutrition, and severity of disease. the ethical dilemma of conducting prospective random-
It can be argued that a formal nutrition assessment ized trials involving patients at risk for starvation.
does not define the presence and extent of malnutrition
per se, but instead identifies the metabolic conse- DEVELOPMENT OF THE GUIDELINES
quences of an underlying disease state as defined by
parameters that are also deranged in a state of pure The 2002 A.S.P.E.N. &dquo;Guidelines for the Use of Par-
starvation. Therefore, when a nutrition assessment is enteral and Enteral Nutrition in Adult and Pediatric
performed on an ill patient, the results reflect meta- Patients&dquo; were developed in response to the need to
bolic consequences of both undernutrition and the factually update the 1993 Guidelines in light of new
underlying disease. In this document, the terms mal- evidence. This opportunity was also used to improve
nutrition and nutrition risk are used to identify clinical the Guidelines suitability to change institutional and
situations in which the parameters of the nutri- clinical practices and resource allocation and to influ-
tion assessment (eg, weight loss, temporal wasting, ence policy leaders, health care organizations, insur-
hypoalbuminemia, etc) are abnormal as a result of the ers, and SNS professionals. Although there are excep-
intermingled effects of both undernutrition and the tions, such as the Clinical Efficacy Assessment Project
underlying disease. In this context, the goals of SNS of the American College of Physicians, most medical-
are to both treat malnutrition and to support the practice guidelines in the United States are now devel-
patient nutritionally and metabolically to prevent fur- oped by professional medical and other health care
ther physiologic deterioration while primary disease organizations having expertise in particular special-
directed therapy is being administered. ties. The advantage of this approach is that profession-
The 2002 Guidelines update the original A.S.P.E.N. als who are familiar with the literature and the prac-
Clinical Guidelines first published nine years ago. To tice of health care in specific subspecialties prepare the
avoid a future gap in the timeliness of the guidelines, guidelines. These individuals presumably have greater
the A.S.P.E.N. Board of Directors is committed to con- knowledge and more experience with the particular
tinuously review them and update them on a rotating service or procedure. The disadvantage of this
cycle. approach is that professional specialists may make
biased judgments in the course of developing medical-
STRENGTH OF EVIDENCE
practice guidelines that affect their own practice.
The strength of the evidence supporting each guide- A.S.P.E.N. considered the advantages and disadvan-
line statement has been coded using a modified version tages and concluded that guidelines could be prepared
of the method used by the Agency for Healthcare objectively by experts in our Society. Care has been
Research and Quality (AHRQ), US Department of taken throughout the guidelines development process
Health and Human Services. After review of the refer- to assure objectivity as best as possible.
ences cited, the section authors and the Clinical Guide- In the Spring of 1999, the A.S.P.E.N. Board of Direc-
lines Task Force used the AHRQ criteria to classify the tors established the Clinical Guidelines Task Force
strength of the evidence supporting each guideline (CGTF). The members of the task force are as follows:
statement. The evidence supporting each statement is
classified as follows:
A There is good research-based evidence to support
the guideline (prospective, randomized trials).
B There is fair research-based evidence to support
the guideline (well-designe4 studies without ran-
domization).
C The guideline is based on expert opinion and
editorial consensus.
The preference of the AHRQ to rely primarily on
prospective randomized clinical trials as the basis for
establishment of practice guidelines is appropriate
because therapies that are accepted and widely used
may subsequently be found lacking when such trials
are conducted.3 However, a major distinction between

therapeutic trials of the efficacy of a drug or procedure

and the feeding of nutrients known to be essential to
the maintenance of human health and survival must The task force members were carefully selected for
be made. Withholding a drug or invasive procedure will their experience, integrity, and knowledge of SNS.
4SA

Their backgrounds span all of the SNS disciplines responsibility for actual writing of the components of
(physicians, dietitians, nurses, and pharmacists) and the Guidelines. The CGTF members selected section
the areas of expertise embodied within the guidelines. authors and supervised the authors efforts. The
Their generous donation of time and expertise made authors were selected for their detailed knowledge and
completion of this document possible. The CGTF &dquo;met&dquo; experience in a chosen niche. These authors deserve
frequently between September 1999 and August 2001 the credit for reviewing the primary literature, synthe-
by conference call, e-mail, and (on two occasions) for sizing and summarizing it, and formulating the guide-
intense 36-hour face-to-face discussions, review, and line statements. Without their detailed knowledge of
editing. The process was initiated by reviewing and the literature and current best practice, the document
revising the table of contents from the 1993 Guidelines. could not have been completed. The authors and the
After approval of this new table of contents by the contributions for which they are credited are listed
A.S.P.E.N. Board of Directors, it was used to divide up below:
SECTION I: INTRODUCTION 5SA
6SA

When the authors drafts were completed, they were Notice: These A.S.P.E.N. Clinical Guidelines are
reviewed by the section editors (the members of the general statements. They are based upon general con-
CGTF), edited and/or rewritten, and then reviewed clusions of health professionals who, in developing
twice by the members of the CGTF as a group. The such guidelines, have balanced potential benefits to be
entire document was then re-edited by the CGTF derived from a particular mode of medical therapy
Chair. This four-times-edited draft was submitted to against certain risks inherent with such therapy. How-
the A.S.P.E.N. Board of Directors and more than 180 ever, the professional judgment of the attending health
experts in the field of nutrition support (including professional is the primary component of quality med-
experts and organizations outside of A.S.P.E.N.) for ical care. The underlying judgment regarding the pro-
content, format, and style review. These reviewers priety of any specific procedure must be made by the
were also specifically asked to check each guideline
statement for appropriateness, accuracy, and strength attending health professional in light of all of the cir-
cumstances presented by the individual patient and
of evidence. This review phase stimulated a final cycle
the needs and resources particular to the locality.
of editing by the CGTF and the CGTF Chair. The final
document was then approved by the A.S.P.E.N. Board These guidelines are not a substitute for the exercise of
of Directors and submitted to the Journal or Parenteral such judgment by the health professional, but rather
are a tool to be used by the health professional in the
and Enteral Nutrition for publication.
The members of the Clinical Guidelines Task Force, exercise of such judgment. These guidelines are volun-
the A.S.P.E.N. Board of Directors, and the section tary and should not be deemed inclusive of all proper
authors feel that this document represents the current methods of care, or exclusive of methods of care rea-
state of the art in provision of specialized nutrition sonably directed toward obtaining the same results.
support to adult and pediatric patients and provides an
evidence-based rationale for the recommendations. We
also hope that these Guidelines help highlight impor- REFERENCES
tant areas for future clinical and translational research 1. A.S.P.E.N: Board of Directors. Guidelines for the Use of Paren-
so that practitioners of nutrition support may provide teral and Enteral Nutrition in Adult and Pediatric Patients.
even better care for patients in the future. The Chair, JPEN 17:1SA-52SA, 1993
2. Committee to Advise Public Health Service on Clinical Practice
Co-Chair, and members of the Clinical Guidelines Task
Force and the A.S.P.E.N. Board of Directors express guidelines (Institute of Medicine). Clinical Practice Guidelines:
Directions fora New Program. National Academy Press, Wash-
their deep gratitude to all of the volunteers who con- ington, DC, 1990, p 58
tributed their time and expertise to make this docu- 3. Pocock SJ, Elbourne DR: Randomized trials or observational trib-
ment possible. ulations? New Engl J Med 342:1907-1909, 2000
 Section .II: Nutrition Care Process

The process of nutrition care may be broken down tion support. Figure 2 presents an algorithm that may
into a series of steps with feedback loops. These include be used to determine whether the optimal route of
nutrition screening, formal nutrition assessment, for- nutrition support is enteral or parenteral in a specific
mulation of a nutrition care plan, implementation of clinical situation. In general, it is assumed that enteral
the plan, patient monitoring, reassessment of the care support is preferable to parenteral support because
plan and reevaluation of the care setting, and then enteral support is more cost-effective. The data that
either reformulation of the care plan or termination of support this assumption are presented elsewhere in
therapy. These Guidelines suggest how each of these the document.
steps may be carried out to optimize clinical outcomes
and cost-effectiveness. Frequent reference to Figure 1
while reviewing the guidelines can help orient the user REFERENCES
to where within the overall plan of nutrition care spe-
cific guidelines fit. 1. A.S.P.E.N: Board of Directors: Standards for nutrition support:
Hospitalized patients. Nutr Clin Pract 10:208-218, 1995
Integral to the process of nutrition care and the 2. A.S.P.E.N: Board of Directors: Clinical Pathways and Algorithms
administration of specialized nutrition support is the for Delivery of Parenteral and Enteral Nutrition Support in
decision of route of administration of specialized nutri- Adults. A.S.P.E.N., Silver Spring, MD, 1998, p 5

I - I

FIG. 1. The nutrition care process (Taken From the A.S.P.E.N. Standards for Nutrition Support: Hospitalized Patients).

7SA
8SA

FIG. 2. Route of Administration of Specialized Nutrition Support2 (Taken from the A.S.P.E.N. Clinical Pathways and Algorithms for Delivery
of Parenteral and Enteral Nutrition Support in Adults).
 Section III: Nutrition Assessment-Adults

NUTRITION SCREENING Although few data are available from clinical stud-
Background ies, it makes sense that an effective nutrition screening
can be used to efficiently identify those patients that
Malnutrition is defined as any disorder of nutrition may benefit from a more extensive formal nutrition
status, including disorders resulting from adeficiency assessment. It may be particularly important to
of nutrient intake, impaired nutrient metabolism, or
over-nutrition. The consequences of malnutrition are aggressively screen elderly patients, because the
related to premorbid condition of the patient, the elderly may experience eating or swallowing difficul-
extent and of time nutrient intake is inade- ties, adverse drug-nutrient interactions, alcohol abuse,
length depression, reduced appetite, functional disabilities,
quate, and the concurrent presence of other diseases or taste and smell, and/or effects of polyphar-
illnesses. Nutrient depletion is associated with impaired
7
increased mortality and morbidity. Wound healing is macy.7
delayed, complication rates are increased, and an Practice Guidelines
.

increased rate of rehospitalization occurs in the pres-

ence of malnutrition.3 Malnutrition is a common occur- , Screening y
rence in hospitalized patients, with an incidence of
30-55%.4 Malnourished hospitalized patients have 1. A nutritionscreening incorporating objective data
been shown to have increased lengths of stay, with such height, weight, weight change, primary
as
associated increased costs of care. 5,6 Factors indicative diagnosis, and presence of comorbidities should
of malnutrition include: involuntary loss or gain of be a component of the initial evaluation of all
>_10% of usual body weight within 6 months, or ~5% of patients in ambulatory, hospital, home, or alter-
usual body weight in 1 month; body weight of 20% over nate site care settings. (C)
or under ideal body weight, especially in the presence 2. The health care organization should determine
of chronic disease or increased metabolic require- who will perform the screen and the elements to
ments ; and inadequate nutrition intake including an be included in the screen. (C)
1
impaired ability to ingest or absorb food adequately. 3. A procedure for periodic nutrition re-screening
Nutrition screening identifies individuals who are should be implemented. (C)
malnourished or who are at risk for malnutrition. The
purpose of the nutrition screening is to determine if a REFERENCES
more detailed nutrition assessment is necessary. 7,8
Nutrition screening is a dynamic process to identify 1. American Society for Parenteral and Enteral Nutrition Board of
Directors: Definition of terms used in A.S.P.E.N. guidelines and
changes in a patients condition that effect nutritional standards. JPEN 19:1-2, 1995
status.9 The nutrition screen identifies risk factors that 2. Ireton-Jones C, Hasse J: Comprehensive nutritional assessment:
place a patient at nutrition1 risk and that may lead to The dietitians contribution to the team effort. Nutrition 8:75-
nutrition related problems. 81, 1992
3. F: Nutritional screening and assessment in home care.
Ottery
Infusion September:36-45, 1996
Evidence 4. Shopbell JM, Hopkins B, Shronts EP: Nutrition screening and
assessment. IN The Science and Practice of Nutrition Support.
Subjective and objec+ive data can facilitate early Gottschlich MM (ed). Kendall/Hunt, Dubuque, IA, 2001, pp 107-
intervention and assist initiation of a formal nutrition 140
assessment. These data may be obtained easily, 5. Robinson G, Goldstein M, Levine GM: Impact of nutritional
status on DRG length of stay. JPEN 11:49-52, 1987
quickly, and efficiently.10 Objective data such as 6. Green MS, Rubinstein E, Amit P: Estimating the effects of nos-
height, weight, weight change, primary diagnosis, and ocomial infections on the length of hospitalization. J Infect Dis
presence of comorbidities can be used in nutrition 145:667-672, 1982
screening to indicate malnutrition or risk of malnutri- 7. ADAs Definition for nutrition screening and assessment. J Am
tion,~ Adult nutrition screening tools designed for use Diet Assoc 94:838-839, 1994
8. Nutrition Interventions Manual for Professionals Caring for
by staff nurses have been tested for validity and repro- Older Americans: Project of the American Academy of Family
ducibilityll and evaluated for ease of use, cost-effec- Physicians, The American Dietetic Association, and National
tiveness, and for validity, reliability, sensitivity, and Council on Aging. Washington, DC: Nutrition Screening Initia-
specificity. 12 tive, 1994

9SA
10SA

9. Barrocas A, Belcher D, Champagne C, et al: Nutrition assess- The

body mass index (BMI) accounts for differences
ment practical approaches. Clin Geriatr Med 11:675-713, 1995
in body composition by defining the level of adiposity
10. Guidelines for initial nutrition screening. IN Suggested Guide-
lines of Nutrition and Metabolic Management of Adult Patients according to the relationship of weight to height and
Receiving Nutrition Support. Winkler MF, Lysen L (eds). The eliminates the dependence on frame size. BMI is a
American Dietetic Association, Chicago, 1993 useful assessment tool because it has a low correlation
11. Kovacevich DS, Boney AR, Braunschweig CL, et al: Nutrition with height and high correlation with independent
risk classification: A reproducible and valid tool for nurses. Nutr
measures of body fat for adults (including the elderly).
Clin Pract 12:20-25, 1997
12. Arrowsmith H: A critical evaluation of the use of nutrition A BMI of 14 to 15 kg/M2 is associated with significant
screening tools by nurses. Br J Nurs 12:1483-1490, 1999 mortality, less than 18.5 kg/m2 is considered under-
weight, greater than 25 kg/m2 connotes overweight,
and a BMI greater than 30 kg/m2 indicates obesity.5>6
NUTRITION ASSESSMENT Patient history and physical examination are
Background required for an adequate nutrition assessment. The
intensity of the assessment should match the severity
Nutrition assessment is &dquo;a comprehensive approach of illness and degree of suspected malnutrition for the
to defining nutrition status that uses medical, nutri- patient. The patient history should focus on weight
tion, and medication histories; physical examination; (ideal, usual, and current weight, and recent weight
anthropometric measurements; and laboratory data. loss), changes in eating habits and gastrointestinal
Further, it includes the organization and evaluation of function, the nature and severity of the underlying
information to declare a professional judgment.&dquo; Eval- disease, and any unusual personal dietary habits or
uation of nutrition status consists of two components: restrictions. The physical assessment can include the
nutrition assessment and metabolic assessment.2 general appearance of the patient, noting the presence
Nutrition assessment utilizes static measurements of of edema, ascites, cachexia, obesity, skin changes, dry
body compartments and examines the alterations mucous membranes, petechiae or ecchymoses, poorly
caused by undernutrition. Metabolic assessment healing wounds, and glossitis, stomatitis, or cheilosis.
includes the analysis of the structure and function of Additionally, the patients musculoskeletal system
organ systems, of altered metabolism as it relates to should be inspected and palpated, recognizing asym-
the loss of lean body mass or other body compartments, metry may occur with a preexisting neurologic disorder
and of the metabolic response to nutrition intervention such as stroke and that the size of muscles are exercise
(whether beneficial or harmful). The goals of a formal dependent. The temporalis muscles, deltoids, supra-
nutrition assessment are to identify patients who are scapular and infrascapular muscles, the bulk and tone
malnourished or who are at risk for malnutrition; to of the biceps, triceps, and quadriceps, and the interos-
collect the information necessary to create a nutrition seus muscles of the hands should be the areas of spe-
care plan; and to monitor the adequacy of nutrition cial attention.7 The clinician can often easily identify
therapy. loss of subcutaneous fat and muscle wasting in
There is an inextricable relationship between nutri- patients with severe underlying disease or those who
tion status and severity of illness. Severely ill patients, are bedridden. The physical assessment may also help
no matter what assessment tools are used, will be identify specific nutrient deficiencies. It should be
identified as being &dquo;malnourished.&dquo; Whether this focused on body areas with noticeable changes, such as
assessment in fact truly indicates malnutrition (a state hair-bearing areas, the oral mucosa, gravity-depen-
induced by nutrient deficiency that may be improved dent areas, and peripheral sensation in the hands and
solely by administration of nutrients) or is merely a feet. However, the clinical signs and symptoms of most
reflection of the severity of the metabolic derange- nutrient deficiencies are not manifest until an
ments caused by the underlying illness is arguable. advanced state of deficiency develops. If the signs and
Likely it reflects a combination of both malnutrition symptoms of a deficiency exist, it must be correlated
and the presence of an underlying disease process. with the patients history and laboratory data to estab-
When thought of in this context, the use of nutrition lish a deficiency diagnosis.
assessment tools to identify patients who are malnour- Serum proteins levels correlate with nutrition status
ished or at nutrition risk does not imply that nutrition and severity of illness.3,4,8 The most often analyzed
support alone will reverse the problem. Rather, in the visceral proteins are serum albumin, transferrin, and
setting of malnutrition or nutrition risk, nutrition sup- prealbumin.9 Studies have shown that hypoalbumin-5
port is essential so that if the medical treatment is emia is associated with poor clinical outcomes.5
appropriate and effective, nutrients are available to Hypoalbuminemia is not a normal result of aging.
prevent undernutrition and to facilitate disease Serum albumin level has been shown to be an indepen-

directed therapy and promote recovery. 3,4 Because of dent risk factor for mortality of all causes in older

the relationship between malnutrition and severity of personas. 1,9 Although albumin levels may have prognos-
illness and the fact that tools of nutrition assessment tic value, they have been found to be poor indicators of
reflect both nutrition status and severity of underlying .

the adequacy of nutrition support.9 Serum transferrin

disease, an assessed state of malnutrition or the pres- .

has a short half-life (8.8 days) and a relatively small

ence of specific indicators of malnutrition in fact refers~ body pool so it may more accurately reflect acute pro-
to the consequences of a combination of both an under- .
tein depletion and replenishment.9 Transferrin has not
lying illness and associated nutritional changes and1 been studied extensively in relation to nutrition status.
deficits. . Serial and frequent measurements of prealbumin
 11SA

(half-life of 2 to 3 days) may help assess nutrition I3NI, the PINI, and the NRI all reliably predict mor-
status changes in response to therapy.99 t)idity in perioperative patients. The only clinical
Indirect calorimetry and body composition analysis rnethod that has been validated as reproducible and

using a multitude of techniques have been suggested that evaluates nutrition status (and severity of illness)
for clinical use to quantitatively measure energy needs t)y encompassing patient history and physical param-
and assess nutrition status. Although these tech- E~ters is the subjective global assessment (SGA).13,14 It

niques, especially indirect calorimetry, may be helpful inay be used in a variety of clinical settings. With the
in settings where nutrition requirements are difficult E3GA, data obtained from the patients history and
to estimate or when complications of over- or under- Iphysical examination are subjectively weighted to clas-
feeding are suspected, their routine use cannot be E3ify the patient as well nourished, moderately mal-
advocated. They are expensive and technically de- ilOurished, or severely malnourished. The SGA has

manding, and methodologic biases may introduce 1)een found to be a good predictor of complications in
errors in estimates obtained using these &dquo;quantitative&dquo; Ipatients undergoing gastrointestinal surgery, liver
tools. None of these techniques has been demonstrated t;ransplantation, and dialysis.5 The use of the SGA in
to effectively predict clinical outcome or improve the (critically ill patients has not been formally evaluated
effectiveness of administration of SNS. 4,10 iand future research in this area is needed. The use of
Multifactorial prognostic indices have been devel- I3GA is more specific than sensitive and may miss some
oped that utilize objective measures of nutrition status. ]patients with mild degrees of malnutrition.o
The Prognostic Nutrition Index (PNI) uses serum albu-
min and transferrin levels, triceps skin fold measure- Practice Guidelines
.

ments, and delayed hypersensitivity skin test reactiv- Nutrition Assessment

ity to predict the risk of operative morbidity and
mortality in relation to nutrition status.ll The Prog- 1. A formal nutrition assessment should be carried
nostic Inflammatory and Nutritional Index (PINI) uses out in any patient, independent of the care set-
markers of the inflammatory response (alpha 1 acid
ting, who is identified by a nutrition screen as
glycoprotein and C-reactive protein) in combination nutritionally at risk. (C)
with nutrition assessment parameters (albumin and 2. In the absence of an outcomes validated approach
prealbumin) to predict infectious complications and to nutrition assessment, a combination of clinical
death.8 The, Nutritional Risk Index (NRI), used in the
Veterans Administration Cooperative Group study of
(history and physical exam) and biochemical
parameters should be used to assess the presence
preoperative parenteral nutrition, successfully strati- of malnutrition. (C)
fies operative morbidity and mortality using serum 3. A written summary should be created and made
albumin and the ratio of current weight to usual available to the patients care providers which
weight.l2 includes the following: The objective and subjec-
The nutrition care plan is the final component of the tive data collected for the nutrition assessment;
nutrition assessment. The care plan is used to organize the explicit nutrition risk stratification; and the
the information obtained in the assessment and &dquo;to
declare a professional judgment Many aspects of
specific recommendations to be incorporated into
the nutrition care plan (protein, calorie, and
patient care such as consultation, treatments, medica- micronutrient requirements, route of administra-
tions, patient assessment and monitoring, education, tion, and treatment goals and monitoring param-
and activity level are integrated into the nutrition care eters). (C)
plan and coordinated with the overall care plan. The
nutrition care plan should include nutrition goals and
the route of administration of nutrition support. Goals REFERENCES
of nutrition care/intervention are stated. Because 1. ADAs definition for nutrition screening and assessment. J Am
nutrition status is dynamic, nutrition goals may be Diet Assoc 94:838-839, 1994
2. Guidelines for initial nutrition screening. IN Suggested Guide-
long term and/or short term. Goals should be set uti- lines of Nutrition and Metabolic Management of Adult Patients
lizing the clinical information as well as patient and/or Receiving Nutrition Support. Winkler MF, Lysen L (eds). The
caregiver wishes. In some cases, the nutrition care plan American Dietetic Association, Chicago, 1993
may not include a nutrition support regimen when the 3. Kotler DP. Cachexia. Ann Intern Med 133:622-634, 2000
nutrition goal is palliative care. Nutrition goals should 4. Trujillo EB, Chertow GM, Jacobs DO: Metabolic assessment. IN
Parenteral Nutrition. Rombeau JL, Rolandelli RH (eds). WB
be measurable to evaluate the adequacy of the care
Saunders, Philadelphia, 2001, pp 80-108
plan. Monitoring of the effect of the nutrition interven- 5. Charney P: Nutrition assessment in the 1990s, where are we
tion should be performed at regular intervals as now? Nutr Clin Pract 10:131-139, 1995
denned in the nutrition care plan. 6. NHLBI Obesity Education Initiative Expert Panel on the Iden-
tification, Evaluation, and Treatment of Overweight and Obesity
in Adults. Clinical guidelines on the identification, evaluation,
Evidence and treatment of overweight and obesity in adults&mdash;The evi-
dence report. Obes Res 6(Suppl 2):51S-209S, 1998
Ideally, there should be data from clinical trials that 7. Jeejeebhoy KN: Bulk or bounce: The object of nutritional sup-
address the hypothesis, &dquo;Formal, appropriate nutrition port. JPEN 12:539-549, 1988
8. Shopbell JM, Hopkins B, Shronts EP: Nutrition screening and
assessment results in the implementation of nutrition assessment. IN The Science and Practice of Nutrition Support.
interventions that improve patient outcomes.&dquo; Unfor- Gottschlich MM (ed). Kendall/Hunt, Dubuque, IA, 2001 pp 107-
tunately, no such studies exist. As noted above, the 140
12SA

9. Ireton-Jones C, Hasse J: Comprehensive nutritional assessment: 12. The Veterans Affairs Total Parenteral Nutrition Cooperative
The dietitians contribution to the team effort. Nutrition 8:75-81, Study Group: Perioperative total parenteral nutrition in surgical
1992 patients. N Engl J Med 325:525-532, 1991
10. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in 13. Baker JP, Detsky AS, Wesson DE, et al: Nutritional assessment:
clinical practice: Review of published data and recommendations A comparison of clinical judgment and objective measurements.
for future research directions. JPEN 21:133-156, 1997 N Engl J Med 306:969-972, 1982
11. Mullen, J, Buzby G, Waldman T, et al: Prediction of operative 14. Detsky AS, McLaughlin JR, Baker JP, et al: What is subjec-
morbidity and mortality by preoperative nutritional assessment. tive global assessment of nutritional status? JPEN 11:8-13,
Surg Forum 30:80-82, 1979 1987
 Section IV: Nutrition Assessment-Pediatrics

MALNUTRITION AND ITS CONSEQUENCES Evidence

Background Primary malnutrition is a common cause of morbid-
Malnutrition is a pathologic state of varying severity ity and mortality in the developing countries of the
world where 40% of children under 5 years of
nearly
with clinical features caused by deficiency, excess, or
age are affected.2 Malnutrition due
to the effects of
imbalance of essential nutrients. The cause may be acute or chronic disease has been described in 44% of
primary (involving the quantity or quality of food con- hospitalized children in the United States and is a
sumed) or secondary (involving alterations in nutrient frequently described problem in children with a variety
requirements, utilization, or excretion). of specific disease states in both the inpatient and
Historically, malnutrition in children has been outpatient settings. 3-7 Excessive intake of nutrients
defined using the terms marasmus and kwashiorkor. leading to obesity has increased significantly in the last
Marasmus develops after severe deprivation of calories 20 years, with the prevalence in children in the United
and is characterized by weight loss and wasting of fat States rising approximately 8%.g
and muscle tissue. Low weight-for-height and a The immediate and long-term consequences of mal-
reduced height-for age are commonly observed. In the nutrition in children have been described. For the child
child with kwashiorkor, protein deficits outweigh calo- with acute or chronic disease, poor nutrition status
rie deficits. Edema due to visceral protein depletion may have a negative effect on recovery or response to
occurs along with muscle wasting. Although some therapy.4,5,8 For the developing fetus and very young
degree of growth failure may be present, weight-for- infant, intrauterine and very early deprivation may
height may not be notably low secondary to retention of have life long consequences.9
fluid in the extravascular compartment. Irritability,
apathy, anorexia, and fatigue may be seen in both Special Considerations
marasmus and kwashiorkor. Children throughout their developmental cycle have
Currently, most forms of pediatric malnutrition a growth imperative that makes them especially vul-
are defined by the term protein-calorie malnutrition nerable to the impact of malnutrition. Children are
(PCM). PCM represents a state where features of additionally vulnerable because of their dependence on
both kwashiorkor and marasmus are present. In their adult caregivers to ensure that their nutrient
addition to growth impairment, physiologic alter- needs are met. The nutrition status of the mother
ations include electrolyte and micronutrient imbal- influences the growth and well being of the developing
ances and reduced levels of serum proteins and fetus.9 The socioeconomic and psychological well being
albumin. Gastrointestinal function may be altered of the family influences the supply of food available to
in children with protein-calorie malnutrition as the child. Malnutrition due to an inadequate or inap-
well as immune function with impairment of cell- propriate food supply may be a sign of child neglect or
mediated immunity, phagocyte function, and com- abuse. 10
plement systems. For the child with chronic or
acute disease, these effects may contribute to sub-
. ~ Guidelines
.

optimal response to medical and surgical therapy.

i i i, Its Consequences
In addition, cognitive and behavioral development
may be adversely affected. 1. Prevention and early detection of malnutrition in
Excess intake of nutrients may also present a health children throughout the developmental cycle
hazard and can be considered a state of malnutrition. should be integrated into all health care encoun-
Overfeeding may lead to obesity, which may be char- ters. (B)
acterized as weight for height above the 95th percentile 2. Prevention and detection strategies should be
for age or BMI greater than 30.0 kg/m2.1 The obese adapted to the clinical setting and the needs of the
child is at risk for a variety of health problems includ- pediatric patient. (C)
ing sleep apnea, hyperlipidemia, hepatic steatosis, and 3. A family centered approach should be used for
orthopedic problems. prevention and early detection of malnutrition to
13SA
14SA

address all the factors that may have an im- 1 ;ify pediatric ambulatory patients at high nutrition
pact on the adequate delivery of nutrients to the risk who require more formal, extensive nutrition
child. (C) , assessment. Importantly, although these regulations
nave been implemented by most hospitals in order to
REFERENCES comply with JCAHO standards, no evidence-based lit-
1. Torun B, Chew F: Protein-energy malnutrition. IN Modern erature exists to support these standards, nor has it
Nutrition in Health and Disease. Shils ME, Shike M, Olson J, et been shown that assessment within 24 hours of admis-
al (eds). Lippincott, Williams & Wilkins, Media, PA, 1999 sion actually has an impact on the outcome of adult or
2. deOnis M, Blossner M: WHO Global database on child growth
and malnutrition. WHO/NUT/97.4 Geneva, Switzerland: Pro- pediatric hospitalized patients. To accomplish nutri-
gramme of Nutrition. World Health Organization, 1997 tion screening within JCAHO guidelines, a health care
3. Hendricks KM, Duggan C, Gallagher L, et al: Malnutrition in organization may decide on the components of the
hospitalized pediatric patients. Current prevalence. Arch Pedi- screen and who will complete the screen. The organi-
atr Adolesc Med 149(10):1118-120, 1995
4. Sermet-Gaudelus I, Poisson-Salomon AS, Colomb V, et al: Sim- zation may choose to include the results of the screen
ple pediatric nutritional risk score to identify at risk of malnu- in the medical record or choose to document by excep-
trition. Am J Clin Nutr 72(1):64-70, 2000 tion, noting only the results of those screens that iden-
5. Reilly JJ, Weir J, McColl JH, et al: Prevalence of protein-energy
malnutrition at diagnosis in children with acute lymphoblastic tify malnutrition or nutrition risk, in the medical
leukemia. J Pediatr Gastroenterol Nutr 29:194-197, 1999 record .5,6 Because of the 24-hour, 7-day-a-week time
6. Cameron JW, Rosenthal A, Olson AD: Malnutrition in hospital- requirement for the initial nutrition screen, many
ized children with congenital heart disease. Arch Pediatr Adolesc organizations use staff nurses to complete the screen
Med 149:1098, 1995
7. Motil KJ, Phillips SM, Conkin CA: Nutritional assessment. IN
during the admission process. These screens are gen-
Pediatric Gastroenterology. Wylie R, Hyams JS (ed). Philadel- erally shorter in length than more in depth screens
phia, 1999 that include laboratory values, but have the advantage
8. Flegal KM, Troiano RR: Changes in the body mass index of that they can be done efficiently and in a timely fash-
adults and children in the US population. Int J Obesity 24: ion. Data are not available concerning the reliability
807-818, 2000 and reproducibility of nutrition screening performed by
9. Briassoulis G, Shekhar V, Thompson AE: Energy expenditure in
critically ill children. Crit Care Med 28: 1166-1172, 2000 staff nurses in this population.
10. Scrimshaw NS: The relation between fetal malnutrition and Periodic rescreening for patients who &dquo;passed&dquo; the
chronic disease in later life: Good nutrition and lifestyle matter initial nutrition screen should be performed. The
from womb to tomb. Br Med J 315:825-826, 1997
11. Dubowitz H: Child neglect: Guidance for pediatricians. Pediatr
patients condition may change and nutrition problems
Rev 21:111-116, 2000 develop.5
NUTRITION SCREENING-PEDIATRICS Evidence
Background Adult nutrition screening tools designed for use by
Pediatric patients have high nutrient needs for staff nurses have been tested for validity and reproduc-
growth and development and low nutrient reserves ibility~ and evaluated for ease of use, cost-effective-
when compared with adults. Malnutrition continues ness, and facilitation of an action plan.&dquo;
to be a problem among pediatric surgical patients, with
A pediatric screening tool has been evaluated and
the prevalence noted in 1995 to be 25% in a pediatric validated in the pediatric intensive care setting. This
screen identified patients at increased risk for adverse
tertiary care facility.2 Nutrition screening is the first outcomes.4 A pediatric risk score has been developed to
step in the nutrition care process: It allows identifica- be used within the first 48 hours of admission. The
tion of high risk individuals so that nutrition services
can be provided in a timely manner to those with the score, used to identify patients at risk for malnutrition,
3 includes the following: anthropometric measurements,
greatest need.3 food intake, the ability to eat and retain food, medical
There has been little research on pediatric nutrition
screening upon which to make evidence based practice condition, and symptoms interfering with feeding.9
recommendations. There is only one study that vali- Bessler10 has published a pediatric screening profile
dates a nutrition screening method for pediatric that uses weighted criteria including diagnosis, labo-
patients.4 Clinicians therefore have based their prac- ratory values, anthropometrics, diet, feeding ability,
tice upon guidelines described by the Joint Commis- and clinical status to dictate the next step in the nutri-
sion for Accreditation of Healthcare Organizations tion care process. This tool is used by dietetic techni-
cians to determine priority level and follow-up. An
(JCAHO). In lieu of evidence-based practice, these
requirements will be described. organization may use several different screens for their
Nutrition screening is the process of using charac- varied populations.
teristics known to be associated with nutrition prob-
lems to determine if individuals are malnourished or at practice Guidelines
.

risk for malnutrition.5 The screening process should be Nutrition Scre ning-Pediatrics
fast and efficient so that resources may subsequently
be allocated to those patients with current problems or 1. A nutrition screen, incorporating objective data
at risk. The JCAHO standard is that a nutrition screen such as height, weight, weight change, primary
be completed within 24 hours of admission, even on diagnosis, and presence of comorbidities should
weekends and holidays.5 Screening is also used to iden- be a component of the initial evaluation of all
 15SA

in ambulatory, hospital, home,

pediatric patients time frame as defined by the hospital. A preadmission
alternate site care settings. (C)
or assessment may be done if completed no more than 30
2. The health care organization should determine lays before admission or readmission. The report
an
the data elements to be included in the screening nust be included in the patients record and any sig-
tool and who will perform the screen. (C) zificant changes in the patients condition documented
1
3. A procedure for periodic nutrition re-screening at the time of admission.
should be established. (C) A qualified clinician with nutrition expertise should
perform the nutrition assessment, using input from
REFERENCES other members of the health care team. The following
1. Marian, M: Pediatric nutrition support. Nutr Clin Pract 8:171- components should be considered as part of the assess-
175, 1993 ment :
2. Hendricks, KM, Duggan, C, Gallagher, I, et al: Malnutrition in . Adequacy of previous and current nutrient intakeB
hospitalized pediatric patients: Current prevalence. Arch Pedi- . Current enteral diet or parenteral fluid prescrip-
atric Adolesc Med 149:1118, 1995
3. Klotz KA, Wessel LL, Hennies G: Goals of nutrition support and tion and the number of days with nothing per
nutrition assessment. The A.S.P.E.N. Nutrition Support Practice mouth 1.
Manual. A.S.P.E.N., Silver Springs, MD, 1998, pp 23-23 . Feeding behavior and feeding skill development2;
4. Mezoff A, Gamm L, Konek S, et al: Validation of a nutritional . Financial resources for food2;
screen in children with respiratory synctial virus admitted to an
. Food intolerance or allergies;
intensive care unit. Pediatrics 97:543-546, 1996
5. Joint Commission for Accreditation of Healthcare Organizations: . Growth evaluation using current anthropometric
Comprehensive Accreditation Manual for Hospitals. Oakbrook measurements and growth history according to
Terrace, IL, JCAHO, 2000 standards, sections: GL-1, TX-4, PE appropriate growth charts 1,2;
1.7.1, PE 1.3.1 . Medications that may affect nutrient statusB
6. Krasker GD, Balogen LB: JCAHO Standards: Development and
relevance to dietetics practice. J Am Diet Assoc 95:240-243, . Medical history including conditions that alter
1995 ingestion, digestion, absorption, or use of nutri-
7. Kovacevich DS, Boney AR, Braunschweig CL, et al: Nutrition ents;
risk classification: A reproducible and valid tool for nurses. Nutr . Nutritional implications of laboratory tests~;
Clin Pract 12:20-25, 1997
8. Arrowsmith H: A critical evaluation of the use of nutrition . Physical examination including manifestations of
screening tools by nurses. Br J Nursing 12:1483-1490, 1999 nutrient deficiencies and excess and assessment
9. Sermet-Gaudelus I, Poisson-Salomon AS, Colomb V, et al: Sim- of development and activity level2;
ple pediatric nutritional risk score to identify children at risk of . Religious, cultural, ethnic, and personal food pref-
malnutrition. Am J Clin Nutr 72:64-70, 2000
10. Bessler S: Nutritional assessment. IN Handbook of Pediatric erencesi; and
Nutrition. Samour PQ, Helm KK, Lang CE (eds). Aspen Publish- . The family viewpoint regarding nutrition and
ers, Gaithersburg, MD, 1999, p 19 feeding.22
The nutrition assessment can be viewed as an ongo-
3
NUTRITION ASSESSMENT-PEDIATRICS ing process, particularly in the acute care setting.3
Clinical circumstances and medical or surgical man-
Background agement may change rapidly, altering the nutrition
Nutrition assessment is the second stage of the assessment. Some practitioners use a nutrition acuity
nutrition care process. Nutrition screening identifies rating to capture the intensity of the nutrition care
patients who require a comprehensive nutrition plan and describe the timing of assessments.4
assessment. The nutrition assessment describes the Feeding skill level may be impossible to assess in the
current nutrition status of the infant, child, or adoles- acute setting. In the recuperative phase of treatment it
cent and facilitates the development of a nutrition care may be the focus of the assessment, determining the
plan. feeding approach for the nutrition care plan. All of the
There is little research in the area of pediatric nutri- components of the comprehensive assessment should
tion assessment upon which to formulate evidence- be evaluated to properly understand the nutrition sta-
based practice guidelines. Clinicians are therefore tus of the child within their family setting.
obliged to follow the regulations set forth by the
JCAHO, despite there being no outcomes-based data to Evidence
support these guidelines.
The nutrition assessment is defined by JCAHO as a The comprehensive nutrition assessment is used to
comprehensive process for defining an individuals describe acute protein-calorie malnutrition (PCM). The
nutrition status using medical, nutrition, and medica- presence of PCM correlates with increased surgical
tion intake histories, physical examination, anthropo- morbidity and mortality. Its prevalence is high in pedi-
metric measurements, and laboratory data. As part of atric general surgical patientS5 and pediatric cardiac
the nutrition care process, the assessment is completed surgical patients.&dquo; The nutrition assessment can be
and updated at specific intervals when warranted by an important part of the surgical evaluation process
the patients needs or condition. The 2000 edition of the and demonstrates those perioperative patients at risk
JCAHO Comprehensive Manual for Hospitals does not for PCM.~6
require a written prescription or order for nutrition There are many comprehensive articles and texts
1
assessment. available to describe the nutrition assessment process
According to JCAHO, the initial assessment should for pediatrics. 2,7-17 The pediatric evaluation is very
be performed and documented within a reasonable different from the assessment of adults in that growth
16SA

and development are essential factors that must be .3. Mitchell MK: Nutrition Across the Life Span. WB Saunders,
assessed and monitored. A Cochrane database review Philadelphia, 1997, pp 28-48
14. Rickert V: Adolescent Nutrition: Assessment and Management.
recently examined the evidence for growth monitoring. Chapman and Hall, New York, NY, 1995
Despite worldwide attention on growth monitoring, 15. Samour PQ, Helm KK, Lang CE, eds. Handbook of Pediatric
there were only two studies available for review, both Nutrition. A.S.P.E.N., Gaithersburg, MD, 1999
from developing countries.i8 No conclusions can be 16. Williams CP, ed: Pediatric Manual of Clinical Dietetics. Ameri-
can Dietetic Association, Chicago, IL, 1998, pp 14-15
drawn. 17. Leleiko NS, Luder E, Fridman M, et al: Nutritional assessment
of pediatric patients admitted to an acute-care pediatric service
Practice Guidelines

utilizing anthropometric measurements. JPEN 10:166-168, 1986

Nutrition Assessment-Pediatrics 18. Panpanich R, Garner P: Growth monitoring in children.
Cochrane Database Syst Rev 2:CD001443, 2000

1. A formal nutrition assessment should be carried

out in any pediatric patient, independent of the CREATION OF A NUTRITION CARE PLAN-
care setting, who is identified by a nutrition PEDIATRICS
screen as nutritionally at risk.(C)
Background
2. The nutrition assessment should be patient spe-
cific and include evaluation of the medical course, The nutrition care plan serves as a template for
medication history, nutritional history, feeding nutrition therapy and should be integrated into the
skill level, analysis of typical and current diet, medical and surgical treatment care plans. The nutri-
tion care plan should address all supplemental nutri-
physical examination, anthropomorphic measure- ents and oral, enteral, and parenteral nutrition modal-
ments, and laboratory data. (C)
3. A written summary of the objective and subjective ities. It is developed to correct nutritional problems or
data collected for the nutrition assessment, of the reduce nutritional risks identified by the formal nutri-
tion assessment. It also serves as an outline of sequen-
explicit nutrition risk stratification, and of the
specific recommendations to be incorporated into tial, reasonable, and achievable interventions and
the nutrition care plan (protein, calorie, and counseling for the infant, child, or adolescent within a
micronutrient requirements, route of administra- given setting. A nutrition care plan is dynamic because
of the changes in clinical status and shifting needs of
tion, and treatment goals and monitoring param-
eters) should be created and made available to the growth and development that characterize pediatric
patients care providers. (C) patients.
4. Nutrition goals should be developed as a part of A care plan consists of a nutrition assessment, identi-
the nutrition care plan. (C) fication of nutrition problems and/or potential nutrition
5. The frequency of nutrition monitoring and re-as- risks, measurable goals or outcomes, education and inter-
sessment should be based on the patients clinical vention strategies, parameters for evaluating (monitor-
course and upon an objective nutrition acuity rat- ing) results, reassessment and modification of the care
ing. (C) plan as needed, and recommendations for follow-up
care. Interventions are developed to meet established
REFERENCES
goals. The appropriate modality of nutrition intervention
(oral, enteral, parenteral, or a combination) is considered
1. Joint Commission for Accreditation of Healthcare Organizations: first. Delivery site, method of administration, equipment,
Comprehensive Accreditation Manual for Hospitals. Oakbrook nutrient solution (composition and concentration), rate of
Terrace, IL, JCAHO, 2000, TX-4, GL, PE 1.2, PE 1.7 delivery, and need for any additional additives are then
2. Isaacs JC, Cialone J, Horsley JW, et al: Children with Special
Needs: A Community Pocket Guide. American Dietetic Associa- addressed. Monitoring parameters are chosen relative to
tion, Chicago, IL, 1997 the goals and timing of specific interventions. Frequency
3. Baxter JP: Problems of nutritional assessment in the acute set- of nutritional monitoring depends upon severity of clini-
ting. Proc Nutr Soc 58:39-46, 1999 cal condition, degree of malnutrition, level of metabolic
4. Williams CP, ed. Pediatric Manual of Clinical Dietetics. Ameri-
can Dietetic Association, Chicago, IL, 1998, pp 14-15
stress, and existing nutrient deficiencies (Table I). Mon-
5. Cooper A, Jakobowski D, Spiker J, et al: Nutritional assessment: itoring parameters provide information for the evalua-
An integral part of the preoperative pediatric surgical evalua- tion of care plan outcomes. If the evaluation reveals that
tion. J Pediatr Surg 16:554-556, 1981 goals are not being met or that new problems/risks have
6. Leite HP, Fisberg M, Novo NF, et al: Nutritional assessment and
surgical risk markers in children submitted to cardiac surgery.
arisen, the process repeats itself with reassessment and
Rev Paul Med 113:706-714, 1995 the modification of the care plan. The effectiveness of
7. Mascarenhas MR, Zemel B, Stallings VA: Nutritional assess- nutrition intervention is determined through periodic
ment in pediatrics. Nutrition 14:105-115, 1998 nutrition reassessment. Condition-specific and growth
8. Marian M: Pediatric nutrition support. Nutr Clin Pract 8:171- charts are integral components of any pediatric care plan.
175, 1993
9. Klotz KA, Wessel LL, Hennies G: Goals of nutrition support and
nutrition assessment. The A.S.P.E.N. Nutrition Support Practice Evidence
Manual. A.S.P.E.N., Silver Springs, MD, 1998, p 23.3
10. Groh-Wargo S, Thompson M, Cox JH: Nutritional Care for High Whether oral, enteral, parenteral nutrition is uti-
or
Risk Newborns, 3rd ed. Precept Press, Chicago, IL, 2000
11. Kessler D, Dawson P. Failure to Thrive and Pediatric Undernutri-
lized, the presence of malnutrition, level of
physiolog-
tion : A Transdisciplinary Approach. Brookes, Baltimore, MD, 1998
ical stress, and level of gastrointestinal function need
12. Kleinman RE, ed. Pediatric Nutrition Handbook, 4th ed. Amer- to be determined before setting goals. Calorie and pro-
ican Academy of Pediatrics, Elk Grove Village, IL, 1999 tein goals will vary depending upon the desired out-
 17SA

come, such as prevention of weight loss, minimal TABLE II

growth, normal growth velocity, or catch-up growth. Suggested monitoring during enteral nutrition support of infants
Monitoring parameters may include measured actual
nutrient delivery (calories and protein) compared with
measured or estimated needs (Tables I and II). Aber-
nathy al2 reported that adult patients fed by
et
nasoenteric tube received only 61% of their caloric
goals.
Children who are malnourished are at greater risk
for infections and metabolic problems. All moderately
to severely malnourished children should have serum
potassium, phosphorus, magnesium, and glucose levels
checked during the first week of refeeding because of
metabolic alterations seen in the nutritional recovery
syndrome. 3,4
Goals of nutrition care should be stated in measur-

TABLE I
Suggested care plan monitoring parameters and frequency
for pediatric patients

Adapted with permission: Davis A. Indications and techniques for

enteral feeds. IN Pediatric Enteral Nutrition. Baker SB, Baker RD
Jr, Davis A, ed. Aspen Publishers, Gaithersburg, MD, 1994.

able behavioral or quantitative terms and be directly

related to the effectiveness of nutrition interventions.0

Practice.Guidelines
Creation of a I I ,

I ~ I 1

1. Nutrition goals should include short-term and

long-term objectives. (C) .

2. A plan for monitoring the effect of nutrition inter-

ventions should be stated in the nutrition care
plan. (C)
REFERENCES
1. Nutritional care process. IN Krauses Food, Nutrition, and Diet
Therapy. Mahan LK, Escott-Stump S (eds). WB Saunders, Phila-
delphia, PA, 1996, p 403-423
2. Abernathy GB, Heizer WD, Holcombe BJ, et al: Efficacy of tube
feeding in supplying energy requirements of hospitalized
patients. JPEN 13:387-391, 1989
3. Solomon SM, Kirby DF: The refeeding syndrome: A review. JPEN
14:90-97, 1990
4. Mezoff AG, Gremse DA, Farrell MK: Hypophosphatemia in the
nutritional recovery syndrome. Am J Dis Child 143:1111, 1989
5. August DA: Outcomes research in nutrition support: background,
Frequency depends on clinical condition. methods, and practical applications. IN Practice-oriented Nutri-
*For metabolically unstable patients, need to check more frequently. tion Research. Ireton-Jones CS, Gottschlich MM, Bell SJ (eds).
1 For patients on parenteral nutrition. Aspen Publishers, Gaithersburg, MD, 1998, p 129-156
 Section V: Administration of Specialized Nutrition Support

INDICATIONS FOR SPECIALIZED include diffuse peritonitis, intestinal obstruction,

NUTRITION SUPPORT intractable vomiting, paralytic ileus, intractable diar-
Background rhea, and gastrointestinal ischemia.55 Advances in
administration of EN make its use possible in some
Specialized nutrition support (SNS) is defined as the patients with conditions previously felt to contraindi-
provision of nutrients orally, enterally, or parenterally cate its use (eg, acute pancreatitis and high-output
with therapeutic intent. Enteral nutrition (EN) in- enterocutaneous fistulae).
volves the nonvolitional delivery of nutrients by tube
PN is an invasive therapy with inherent risks. Its
into the gastrointestinal tract. Parenteral nutrition
purpose is to provide nutrition for individuals without
(PN) is the administration of nutrients intravenously. GI function.6 The use of PN in specific dis-
For individuals who cannot, should not, or will not eat adequate
ease conditions is discussed in detail in other sections
adequately and in whom the benefits of improved of this document.
nutrition outweigh the risks, SNS may be imple-
mented. Patients who are malnourished or at signifi- A major controversy in the field of nutrition support
concerns the relative indications for the use of PN
cant risk for becoming malnourished should receive
versus EN. Proposed advantages of EN include
SNS. The administration of SNS is never an emer-
reduced cost, better maintenance of gut integrity,
gency ; it should not be initiated until the patient is
reduced infection, and decreased hospital length of stay.
hemodynamically stable. A distinction between nutri- It has been suggested that critically ill patients who
tion support as primary therapy for a disease versus its
value as an adjunct to primary therapy is essential. do not receive enteral nutrients may experience trans-
SNS is used to treat malnutrition when present and to location of intestinal flora and associated endotoxin
avoid the development of malnutrition resulting from release, which can activate inflammatory pathways. It
insufficient energy and nutrient intake in the face of is proposed that the resultant systemic activation con-
increased energy needs. Only in relatively uncommon tributes to the etiology, progression, and morbid-
circumstances is SNS used to treat specific disease ity/mortality of multisystem organ failure. However,
manifestations (eg, altered protein intake in patients there are few human data to substantiate this .7 Provi-
with renal failure or hepatic encephalopathy). This sion of enteral nutrients appears to help maintain
section reviews general issues generic to the decision to mucosal structure and function of the intestine.8 A
initiate SNS. Consult guideline statements in the met- number of trials have found reduced septic complica-
abolic and disease-specific sections regarding specific tions in abdominal trauma patients given EN when
indications for the use of EN and PN in individual compared with PN.9,10 Decreased rates of infection
in enterally fed burn patients have been noted in
patients with specific metabolic conditions or diseases. two studies, 11,12 and comparable results have been
achieved in comparisons of PN and EN administered to
Evidence
patients with severe head injury. 13-15
Canned, liquid meal replacement beverages are widely Sufficient randomized, prospective, controlled trials
available commercially. These products are used to sup- with carefully matched patients receiving EN and PN are
plement the nutrient intake of individuals who are not available to conduct a meta-analysis comparing
unable to ingest adequate nutrients in the form of a enteral and parenteral interventions across a wide vari-
standard oral diet. Two small studies suggest that inges- ety of illnesses.16 Therefore, no definitive conclusions
tion of these beverages may have a role in improving the about the superiority of EN over PN can be made in many
nutrition status of homebound elderly persons. 1,2 They disease states. 17 Many studies show an improved ability
have also been used soon after gastrointestinal and hip to meet nutrient goals with PN over EN, and there may
fracture surgery to improve nutritional parameters. 3,4 be some clinical situations where even with a functional
There are no data supporting routine use of commercial gut, it is not possible to administer adequate SNS other
canned, meal replacement beverages. than with PN. It must be observed, however, that nutri-
A functioning gastrointestinal tract is required for ent delivery is only an intermediate end point, and reli-
the use of EN. A functioning gastrointestinal tract is of ance on outcome data is preferable.
sufficient length and condition to allow adequate nutri- Costs, charges, and reimbursement for PN have all
ent absorption. Contraindications to enteral feeding been found to be higher than those for EN by numerous

18SA
 19SA

investigators.18-20 There are no studies that show oral 4. SNS should be initiated in patients with inade-
diets or EN to be more expensive than PN. However, it quate oral intake for 7 to 14 days, or in those
must also be acknowledged that true and accurate cost patients in whom inadequate oral intake is
data (as opposed to charge based estimates) are hard to expected over a 7- to 14-day period. (B)
come by. Furthermore, it is very difficult to calculate true
REFERENCES
global costs (including complications, additional x-rays,
monitoring, etc) of these therapies. Nevertheless, from a 1. Lipschitz DA, Mitchell CO, Steele RW, et al: Nutritional evalu-
financial perspective, oral diets and EN are likely less ation and supplementation of elderly subjects participating in a
"meals on wheels" program. JPEN 9:343-347, 1985
costly than PN. In situations where there are no specific 2. Gray-Donald K, Payette H, Boutier V: Randomized clinical trial of
data demonstrating improved outcomes with PN over nutritional supplementation shows little effect on functional status
EN, EN therefore seems preferable on a cost basis. among free-living frail elderly. J Nutr 125(12):2965-2971, 1995
Another controversial issue is the optimal timing of 3. Delmi M, Rapin C-H, Bengoa J-M, et al: Dietary supplementa-
tion in elderly patients with fractured neck of the femur. Lancet
initiation of SNS. Initiation of enteral feedings early in 335:1013-1016, 1990
the course of illness has been recommended to attenuate 4. Keele AM, Bray MJ, Emery PW, et al: Two phase randomized
the stress response and improve feeding tolerance. controlled clinical trial of postoperative oral dietary supplements
in surgical patients. Gut 40:393-399, 1997
Although there are reports of enteral feeding being well 5. A.S.P.E.N: Board of Directors. Guidelines for the use of paren-
tolerated when initiated within 6 to 12 hours after teral and enteral nutrition in adult and pediatric patients. JPEN
injury,21-23 these data suggest feasibility but not neces- 17(Suppl):1SA-52SA, 1993
sarily benefit. Many protocols exist for enteral feeding 6. Shils ME, Brown RO. Parenteral nutrition. IN Modern Nutrition
advancement, but these are largely untested. There in Health and Disease, 9th ed. Shils ME, Olson JA, Shike M,
Ross AC (eds). Williams and Wilkins, Baltimore MD, 1999, p 1658
appears to be no benefit to elaborate regimens for slow 7. Lipman TO: Bacterial translocation and enteral nutrition in
initiation of enteral feeding,24 and newer studies show humans: An outsider looking in. JPEN 19:156-165, 1995
full feedings can usually be tolerated within 2 to 3 days of 8. Hernandez G, Velasco N, Wainstein C, et al: Gut mucosal atro-
formula initiation.21-23 EN is generally considered safe, phy after a short enteral fasting period in critically ill patients.
but gastrointestinal, metabolic, and respiratory compli- J Crit Care 14:73-77, 1999
9. Moore FA, Feliciano DV, Andrassy RJ, et al: Early enteral feed-
cations have been documented. Inappropriate formula
ing compared with parenteral, reduces postoperative complica-
advancement or feeding interruptions may result in tions. The results of a meta-analysis. Ann Surg 216:172-183, 1992
underfeeding.25 A reduced incidence of metabolic abnor- 10. Kudsk KA, Croce MA, Fabian TC, et al: Enteral versus paren-
malities and other improved outcomes of EN have been teral feeding: effects on septic morbidity following penetrating
trauma. Ann Surg 215:503-513, 1992
demonstrated when tube-fed patients are managed by an
11. Gottschlich MM, Jenkins M, Warden GD, et al: Differential
interdisciplinary team. 26-28 At least one study docu- effects of three enteral dietary regimens on selected outcome
mented the cost-effectiveness of this approach. 28 variables in burn patients. JPEN 14:225-236, 1990
The number of days to wait before initiating PN is a 12. Garrell DR, Razi M, Lariviere F, et al: Improved clinical status
and length of care with low fat nutrition support in burn
complex, frequently asked question. There are no pro-
spective, randomized, clinical trials that specifically patients. JPEN 19:482-491, 1995
13. Norton JA, Ott LG, McClain C, et al: Intolerance to enteral
address this issue. In many studies of the use of PN, feeding in the brain-injured patient. J Neurosurg 68:62-66, 1988
the majority of patients are able to eat orally within 6 14. Grahm TW, Zadrozny DB, Harrington T: The benefits of early
to 8 days; it is unlikely that these patients benefit from jejunal hyperalimentation in the head-injured patient. Neuro-
such short-duration PN. This is likely true even in surgery 25:729-735, 1989
15. Borzotta AP, Pennins J, Papasadero B, et al: Enteral versus
malnourished patients.29-31 It is also likely that
parenteral nutrition after severe closed head injury. J Trauma
patients who do not eat or receive SNS for more than 37:459-468, 1994
10 to 14 days after hospital admission or after surgery 16. Braunschweic C, Levy P, Sheean P, et al: Enteral versus paren-
do have worse clinical outcomes, longer hospital stays, teral nutrition: A meta analysis. Am J Clin Nutr 74:534-542,
2001
and higher costs of care. 8,29 Unfortunately, it is diffi-
17. Lipman TO: Grains or veins: Is enteral nutrition really better
cult to identify these patients prospectively. On the than parenteral nutrition? A look at the evidence. JPEN 22:167-
basis of these data, it does seem reasonable to initiate 182, 1998
SNS in patients with inadequate oral intake for 7 to 14 18. Adams S, Dellinger P, Wertz MJ, et al: Enteral versus paren-
teral nutritional support following laparotomy for trauma: A
days or in those patients in whom inadequate oral randomized prospective trial. J Trauma 26:882-891, 1986
intake is expected over a 7- to 14-day period. 19. Kotler DP, Fogleman L, Tierney A: Comparison of total paren-
teral nutrition and an oral, semielemental diet on body compo-
Practice Guidelines
.
sition, physical function, and nutrition-related costs in patients
with malabsorption due to acquired immunodeficiency syn-
t t I I Specialized t
drome. JPEN 22:120-126, 1998
t Support 20. Senkel M, Mumme A, Eickhoff U, et al: Early postoperative
enteral immunonutrition: Clinical outcome and cost-comparison
1. SNS should be used in patients who cannot meet analysis in surgical patients. Crit Care Med 25:1489-1496, 1997
21. Braga M, Gianotti L, Vignali A, et al: Artificial nutrition after
their nutrient requirements by oral intake. (B) major abdominal surgery: Impact of route of administration and
2. When SNS is required, EN should generally be composition of the diet. Crit Care Med 26:24-30, 1998
used in preference to PN. (B) 22. Gianotti L, Braga M, Vignali A, et al: Effect of route of delivery
3. When SNS is indicated, PN should be used when and formulation of postoperative nutritional support in patients
the gastrointestinal tract is not functional or can- undergoing major operations for malignant neoplasms. Arch
Surg 132:1222-1230, 1997
not be accessed and in patients who cannot be 23. Rees RG, Keohane PP, Grimble GK, et al: Tolerance of elemental
adequately nourished by oral diets or EN. (B) diet without starter regimen. Br Med J 290:1868-1869, 1985
 20SA

24. McClave SA, Sexton LK, Spain DA, et al: Enteral tube feeding in
the intensive care unit: Factors impeding adequate delivery. Crit
temporary impairment of gastric emptying, psycholog-
ical and metabolic disorders such as severe cardiac,
Care Med 27:1252-1256, 1999
25. Brown RO, Carlson SD, Cowan GS, et al: Enteral nutritional pulmonary, and renal disease are not covered for HPN.
support management in a university teaching hospital: team vs. To be covered, Medicare also requires that the need for
nonteam. JPEN 11:52-56. 1987 HPN be &dquo;permanent&dquo; (expected duration of therapy
26. Powers DA, Brown RO, Cowan GS, et al: Nutritional support
team vs. nonteam management of enteral nutritional support in
greater than 90 days). Many other payers require that
a veterans administration medical center teaching hospital.
similar standards be met for HPN. The total number of
JPEN 10:635-638, 1986 patients on HSNS is unknown. The Health Care
27. Hassell JT, Games AD, Shaffer B, et al: Nutrition support team Finance Administration has published data on paren-
management of enterally fed patients in a community hospital is teral and enteral nutrition use based on workload sta-
cost-beneficial. J Am Diet Assoc 94:993-998, 1994 tistics from Blue Cross and Blue Shield of South Caro-
28. Sandstrom R, Drott C, Hyltander A, et al: The effect of postop-
erative intravenous feeding (TPN) on outcome following major lina, one of two fiscal intermediaries for Medicare,
surgery evaluated in a randomized study. Ann Surg 217:185- between 1986 and 1993. Blue Cross and Blue Shield of
195, 1993 South Carolina managed 75% of the HSNS covered
29. Holter AR, Fischer JE: The effects of perioperative hyperalimen-
tation on complications in patients with carcinoma and weight
during the time of this survey. By adjusting this survey
loss. J Surg Res 23:31-34, 1977
for the number of patients not covered by this payer, it
30. Sako K, Lore JM, Kaufman S, et al: Parenteral hyperalimenta- was estimated that there were 40,000 patients on HPN
tion in surgical patients with head and neck cancer: a random- and 152,000 on HEN in 1992 . 1,3 HSNS data for non-
ized study. J Surg Oncol 16:391-402, 1981 Medicare patients has never been made public because
31. Brennan MF, Pisters PW, Posner M, et al: A prospective ran- home care providers and payers consider this informa-
domized trial of total parenteral nutrition after major pancreatic
resection for malignancy. Ann Surg 220:436-444, 1994 tion to be proprietary. In addition, a registry of
patients on HSNS (North American Home Parenteral
HOME SPECIALIZED NUTRITION SUPPORT and Enteral Nutrition Patient Registry), which had
Background provided useful information on these patients, was dis-
continued in 1993.
The indications for home specialized nutrition sup-
port (HSNS) are similar to those for the use of special- Evidence
ized nutrition in the hospital setting. Home enteral
Based on data from the North American Home Par-
nutrition (HEN) is used in patients requiring SNS
enteral and Enteral Nutrition Patient Registry, the
when the gastrointestinal tract is functional. HEN is
survival rate and rehabilitation of HSNS patients is
commonly used for swallowing disorders associated highest in the pediatric age group (0 to 18 years) and
with strokes, neuromuscular illness, head and neck
lowest in those greater than 65 years of age.4 Con-
cancers, gastroparesis, and mild to moderate malab-
sorption. 1,2 Home parenteral nutrition (HPN) is versely, therapy-related complications are highest in
the pediatric age group. The primary diagnosis for
reserved for patients who are unable to maintain an
which HSNS is required is a predictor of outcome.
adequate nutrition status when fed via the gastroin- Patients with inflammatory bowel disease have the
testinal tract. Common indications for HPN include
inflammatory bowel disease, nonterminal cancer, isch- highest 5-year survival rate, approximately 90%.2
Patients who start HSNS when they are under 40
emic bowel, radiation enteritis, motility disorders of
the bowel, bowel obstruction, high-output intestinal or years of age are also more likely to do well, with a
5-year survival rate greater than 80%.2 Complication
pancreatic fistulae, celiac disease, hyperemesis gravi- rates and cost of treatment are higher for HSNS
darium, and protein-losing enteropathy. 1,2 Although patients who are opiate and sedative dependent to
combined enteral and parenteral therapy is used in the
control pain.5 A majority of the complications that
hospital setting, it is rarely used in the home because occur are related to the underlying disease for which
this approach increases the complexity of care, and it is
the therapy is required. However, HSNS itself is asso-
rarely covered by third-party payers (particularly ciated with serious complications. These include cath-
Medicare and Medicaid).
eter sepsis, metabolic abnormalities, organ dysfunc-
Because of the expense of HEN and HPN, reimburse-
ment issues may delineate and limit the options avail- tion, and technical problems associated with feeding
device placement. The use of clinical pathways for HSNS
able to individual patients. HSNS is reimbursed under
Medicare Part B (prosthetic device benefit provision) patients has been reported to facilitate more cost-enec-
tive care and to improve communication between home
when specific conditions are satisfied (see below).
care clinicians and the patients physician.6
These therapies may also be covered by state Medicaid
programs, private insurance carriers, managed care
payers, and other insurance entities. Medicare
Special Considerations
requires documentation of severe steatorrhea, malab- Some studies of the HSNS population have
sorption, short bowel syndrome, intestinal motility dis- addressed quality of life issues. Many HSNS patients
order or obstruction, or exacerbation of inflammatory are not aware that a national support group, the OLEY
bowel disease for HPN. Documentation includes one or Foundation, and other advocacy or support groups
more of the following: operative reports, x-ray studies, exist. HSNS is perceived by patients to have anega-
discharge summaries, fecal fat tests, and small bowel tive impact on their quality of life. Despite the fact that
motility studies. Under certain circumstances malnu- it is life saving for patients who have lost GI function,
trition must be documented. Swallowing disorders, the technological and psychological burdens of HPN
 21SA

are significant. In a study of HPN patients in Den- 2. When HSNS is required, HEN is the preferred
mark, patients reported reduced strength for physical route of administration when feasible. (B)
activity, feelings of depression and anger, loss of inde- 3. When HSNS is indicated, HPN should be used
pendence, and reduced social interaction.8 Patients in when the gastrointestinal tract is not functional
the United States have reported problems with loss of and in patients who cannot be adequately sup-
friends, loss of employment, and depression.9 Support- ported with HEN. (B)
ive interventions for HSNS patients should include
financial evaluation and (when needed) psychosocial REFERENCES
initiatives to improve self-esteem, manage depression,
1. Howard L, Ament M, Fleming R, et al: Current use and clinical
and enhance coping skills. outcome of home parenteral and enteral n nutrition therapies in
The cost of HSNS is substantial. Based on Medicare the United States. Gastroenterology 109:355-365, 1995
charges, HPN has been estimated to cost $55,193 2. Scolapio JS, Fleming CR, Kelly DG, et al: Survival of home
30,596 annually, and HEN has been estimated to cost parenteral nutrition-treated patients: 20 years of experience at
the Mayo Clinic. Mayo Clin Proc 74:217-222, 1999
$9605 9237 annually.10 Rehospitalizations, which cost 3. Dickerson RN, Brown RO: Parenteral and enteral nutrition in
up to $140,220 per year for HPN patients and $39,204 the home and chronic care settings. Am J Managed Care 4 :445-
per year for HEN patients, occur an average of 0.52 to 455, 1998
1.10 times per year for HPN and 0 to 0.50 times 4. Howard L, Malone M: Clinical outcome of geriatric patients in
patients
per year for HEN patients. Monitoring of therapy is
the United States receiving home parenteral and enteral nutri-
tion. Am J Clin Nutr 66:1364-1370, 1997
important to prevent complications and to institute early 5. Richards DM, Scott NA, Shaffer JL, et al: Opiate and sedative
intervention, but the cost of care to providers is also dependence predicts a poor outcome for patients receiving home
substantial. Industry providers have not published infor- parenteral nutrition. JPEN 21:336-338, 1997
mation on costs; however, the annual costs of case man- 6. Ireton-Jones C, Orr M, Hennessy K: Clinical pathways in home
nutrition support. J Am Diet Assoc 97:1003-1007, 1997
agement to a hospital nutrition support team has been 7. Smith CE, Curtas S: Research data: source of information for
estimated at $2070 per patient.&dquo; patient education materials. Nutrition 15:180-181, 1999
8. Jeppesen PB, Langholz E, Mortensen PB: Quality of life in
Practice guidelines
.
patients receiving home parenteral nutrition. Gut 44:844-852,
1999
Home Specialized Nutrition Support
,

9. Smith CE: Quality of life in long-term total parenteral nutrition

patients and their family caregivers. JPEN 17:501-506, 1993
1. Home SNS should be used in patients who cannot 10. Reddy P, Malone M: Cost and analysis of home parenteral and
enteral nutrition. JPEN 22:302-310, 1998
meet their nutrient requirements by oral intake
11. Curtas S, Hariri R, Steiger E: Case management in home total
and who are able to receive therapy outside of an parenteral nutrition: a cost-identification analysis. JPEN
acute care setting. (B) 20:113-119, 1996
 Section VI: Normal Requirements-Adults

Background ranges for enteral and parenteral nutrients provided

(Tables I through III) are considered acceptable refer-
The nutrient requirements for a group of otherwise
ence points to meet individual patients estimated
normal adults unable to take adequate substrate
through the oral route from foods, and needing SNS, requirements. A dosing weight needs to be determined
for each patient (ideally based on body cell mass or lean
should not differ from those consuming a usual diet.
However, SNS is rarely given to &dquo;otherwise normal tissue, because actual body weight does 7
not account for
variations in water or fat content).7
adults,&dquo; and the dosing of required nutrients may differ
with the route of administration and the formulation Although energy is not itself a nutrient, it is provided
for by the administration of macronutrients. Although
provided-given issues of bioavailability, physiologic there is no &dquo;standard&dquo; EN or PN formulation for a
regulatory mechanisms, and physicochemical charac- &dquo;normal&dquo; adult requiring SNS, surveys reveal that
teristics of enteral or parenteral products. The nutri-
tional requirements for adults who need SNS should be patients frequently receive standard formulas that
based on the results of the formal individualized nutri- provide excess energy.7 Current energy allowances by
the Food and Nutrition Board 8 and the World Health
tion assessment. The requirements for each nutrient
may vary with nutrition status, disease, organ func-
Organization9 may overestimate or underestimate
tion, metabolic condition, medication use, and duration requirements for many individuals, given the variabil-
of nutrition support. Unfortunately, there are few stud- ity both in energy expenditure and its measurement.
The requirement for energy, in kilocalories (or kilo-
ies that have critically evaluated the influence of nutri-
ent dosing via SNS on body composition or function. joules), is patient specific. Calories should be adminis-
tered in an amount adequate to meet basal energy
Requirements are based on available information. expenditures and provide for a level of physical activity
to maintain a healthy body mass index. Basal energy
Evidence expenditure can vary with disease state. In the absence
of usual food selection and regulation of food intake,
Nutrient requirements for EN can reasonably be
based on the Food and Nutrition Board, Dietary Ref- identifying energy needs during nutrition support
erence Intakes (DRIs). 1-4 A requirement here is
requires indirect measurement or estimation of expen-
ditures. Predictive equations to estimate energy
defined as the lowest continuing intake level of a nutri-
ent that maintains a specified indicator of adequacy. 1-4 requirements in healthy adults may be valuable.10
This estimated amount should fall within a range of 20
These nutrient standards are based on data generated
to 35 kcal/kg (85-145 kJ/kg) daily. While providing the
from epidemiologic, depletion-repletion, and clinical
calories to meet energy needs, the daily dose of carbo-
studies, using appropriate indicators of nutrient ade- hydrates and lipids should not exceed 7 and 2.5 g/kg
quacy, including clinical and functional outcome
markers.l-4 The inherent limitation to the application per day, respectively, to minimize adverse metabolic
of the DRIs, or more specifically the Recommended consequences .5 Some data support the use of a maxi-
mum of lipid 1 g/kg/d intravenously, especially in crit-
Dietary Allowance (RDA)/Adequate Intake (AI) levels, ically ill patients. 11,12 The only recommendation
is that they are designed to be met from a usual diet
for healthy individuals to prevent deficiencies and, regarding specific fatty acids is that 1% to 2% of daily
where the data exist, to minimize the risk from
nutrition-related chronic disease and developmental TABLE I
disorders.l-4 Although they take into account individ- Daily electrolyte requirements 4,8t
ual variability, they are not intended for use in people
with acute or chronic disease. The RDA/AI values
should be used as a guide for planning individual nutri-
ent intake level. 1-4 The uppermost RDA/AI value of
each nutrient can serve as a reference point for SNS
in nonpregnant/nonlactating adults. Previously pub-
lished practice guidelines for parenteral nutrition for-
mulationS5 can also provide a basis for prescribing
6
parenterally administered nutrients.6 The dosing
22SA
 23SA

energy requirements should be derived from linoleic TABLE III

acid (to6) and about 0.5% of energy from a-linolenic Daily trace element requirement1.3.8t
acid (m3) to prevent essential fatty acid deficiency.
Guidelines for a few fatty acids in health have been
suggested, as has a ratio for w6:w3 fatty acids.l3
Protein needs cannot be determined solely from fac-
torial and nitrogen balance data, but require amino
acid turnover data and, ideally, data on metabolic and
functional status to reflect proteins roles. The current
recommendations for protein are based predominantly
on
nitrogen balance data, but not on optimal metabolic
balance or metabolic function.8,9 More recent data sup- tTables give general ranges for safe administration of nutrients in
port levels of about 186 mg/kg per day of essential generally healthy people. Nutrient prescriptions must be individu-
amino acids to make up 25% to 30% of protein intakes. 14 alized for each patient and clinical situation.
Adequate energy substrate must be provided along RDA/AI levels. Dosing beyond the RDA/AI values near
with protein to assure its proper utilization. The use of
the tolerable upper intake level is not generally sup-
SNS has actually led to a re-evaluation of the role of
amino acids in health. Assessment of an individuals ported by experimental data for most patients requir-
protein status helps determine individual require- ing SNS. The dosing guidelines for parenteral vitamins
and trace elements should be considered as approxi-
ments. For the unstressed adult patient with adequate
mations of need.~16 The parenteral vitamin recommen-
organ function requiring SNS, 0.8 g/kg per day may be dations were intended to meet the needs of patients
adequate, but requirements may rise with metabolic with increased requirements and should be given daily
demands to levels of about 2 g/kg per day (or, rarely,
in patients with limited oral intake. Until the antici-
even higher). Protein requirements based on fat-free
mass may decrease with age.5 Optimal intake of spe-
pated reformulation of parenteral multivitamin prod-
ucts to include vitamin K (as well as additional thia-
cific amino acids from the diet for health maintenance
or improvement are being investigated, but the data
min, pyridoxine, folate, and vitamin C), vitamin K
should be administered in addition to the vitamin
available at this time do not allow for general recom-
K-free multivitamin products currently used.l7 Micro-
mendations for SNS beyond specific metabolic condi-
nutrients present as contaminants in parenteral prod-
tions.
ucts should also be taken into consideration. 18
Based on an appropriate assessment, water require-
ments are individualized to fluid balance and solute Although fiber, as defined by a variety of character-
istics (viscosity, water dispersability, fermentability,
load. Alterations in fluid and electrolyte needs are
managed in a patient-specific manner, taking into bulk, and binding properties), is an important compo-
nent of the diet with benefit on colonic function, specific
account disturbances of volume, concentration, and/or
composition. The fluid requirement for adults is gener- dosing recommendations cannot be made for enteral
nutrition at this time.
ally met with volumes of 30 to 40 mL/kg per day, or at
1 to 1.5 mL/kcal expended. 5,8 Enteral electrolyte doses
follow RDA/AI reference values. The standard dosing
Practice Guidelines
.

Normal
t Requirements-Adults
t

ranges for parenteral electrolytes assumes normal

organ function, without abnormal losses. Electrolyte
content of parenteral nutrient stock solutions should 1. Determination of nutrient requirements should
be taken into consideration. be individualized, based on assessment of body
Vitamins and trace elements are essential nutrients composition and function, and fall within accept-
that act as coenzymes and cofactors involved in metab- able ranges, while taking physiologic and patho-
olism. For EN, recommendations are based on the physiologic conditions into account. (B)
REFERENCES
TABLE II
vitamin requirementsl-4,sf 1. Institute of Medicine, Food and Nutrition Board: Dietary refer-
Daily
ence intakes: calcium, phosphorus, magnesium, vitamin D, and
fluoride. National Academy Press, Washington, DC, 1997
2. Institute of Medicine, Food and Nutrition Board: Dietary refer-
ence intakes: thiamin, riboflavin, niacin, vitamin B6, folate, vita-
min B12, pantothenic acid, biotin, and choline. National Acad-
emy Press, Washington, DC, 1998
3. Institute of Medicine, Food and Nutrition Board: Dietary refer-
ence intakes: vitamin C, vitamin E, selenium, and carotenoids.
National Academy Press, Washington, DC, 2000
4. Institute of Medicine, Food and Nutrition Board: Dietary refer-
ence intakes: Vitamin A, vitamin K, arsenic, boron, chromium,
copper, iodine, iron, manganese, molybdenum, nickel, silicon,
vanadium, and zinc. National Academy Press, Washington, DC,
2001
5. National Advisory Group on Standards and Practice Guidelines
for Parenteral Nutrition: Safe Practices for parenteral nutrition
formulations. JPEN 22:49-66, 1998
24SA

6. American Medical Association Department of Foods and Nutri- 13. Kris-Etherton PM, Taylor DS, Yu-Poth S, et al: Polyunsaturated
tion, 1975: Multivitamin preparations for parenteral use: a state- fatty acids in the food chain in the United States. Am J Clin Nutr
ment by the nutrition advisory group. JPEN 3:258-262, 1979 71(Suppl):179S-188S, 2000
7. Schloerb PR: Electronic parenteral and enteral nutrition. JPEN 14. Young VR, Borgonha S: Adult human amino acid requirements.
24:23-29, 2000 Curr Opin Clin Nutr Metab Care 2:39-45, 1999
8. National Research Council: Recommended dietary allowances, 15. Millward DJ, Fereday A, Gibson N, et al: Aging, protein
10th ed. National Academy Press, Washington, DC, 1998
9. WHO (World Health Organization): Energy and protein require-
requirements, and protein turnover. Am J Clin Nutr 66:774-
ments : Report of a joint FAO/WHO/UNU expert consultation.
786, 1997
16. American Medical Association Department of Foods and Nutri-
Technical Report Series 724. WHO: Geneva, 1985
tion : Guidelines for essential trace element preparations for
10. Vinken AG, Bathalon GP, Sawaya AL, et al: Equations for pre-
dicting the energy requirements of healthy adults aged 18-81 y. parenteral use. A statement by an expert panel. JAMA 241:
Am J Clin Nutr 69:920-926, 1999 2051-2054, 1979
11. Nussbaum MS, Fischer JE: Parenteral nutrition. IN Nutrition in 17. Food and Drug Administration. Parenteral Multivitamin Prod-
Critical Care. Zaloga GP (ed). Mosby-Year Book, St Louis, 1994, ucts ; Drugs for Human Use; Drug Efficacy Study Implementa-
pp 371-397 tion; Amendment: Federal Register April 20, 2000. Vol 65, num-
12. Battistella FD, Widergren JT, Anderson JT, et al: A prospective, ber 77: 21200-21201
randomized trial of intravenous fat emulsion administration in 18. Pluhator-Murton MM, Fedorak RN, Audette RJ, et al: Trace
trauma victims requiring total parenteral nutrition. J Trauma element contamination of total parenteral nutrition. JPEN
43:52-60, 1997 23:222-232, 1999
 Section VII: Normal Requirements-Pediatrics

INTRODUCTION possible energy requirements should be based on mea-

surements of expenditure rather than intake.&dquo;4 Heird
This section is divided into two separate sections:
et al5 have estimated that a 1-kg infant has only a
fluid and energy needs and substrate requirements.
The latter area includes protein, carbohydrate, and 4-day nutritional reserve, and a full-term infant may
live for no more than month without nutrition. In
a
lipid requirements. Although fluid and energy are not general, infants require calories if fed enterally
more
nutrients, they clearly play a critical role in the nutri- rather than parenterally.6 Methods to estimate the
tional care of infants and children. Additionally, the
energy needs of infants and older children are well
requirements are quite specific for various ages of chil- described.7 Energy requirements before adolescence
dren and disease states, as delineated below. Finally,
appear to differ between sexes, with lower energy
many disease states have specific energy, fluid, and needs in girls because of lower activity states.8 Adoles-
substrate requirements or restrictions.
cence increases energy requirements. Bitar et al9
This section discusses nutritional requirements pre-
showed that energy needs in adolescence vary with
dominately for the healthy child. Subsequent individ- gender, body composition, and even the season. Admin-
ual sections will highlight specific needs for individual
istration of nutrition support will alter energy needs.
disease states.
Special Considerations
ENERGY
Although each individual section will deal with spe-
Background cific disease states, there are some important energy
The energy needs and reserves of infants and chil- considerations that should be mentioned here.
dren are quite unique and have been reviewed by sev- Unlike increased substrate utilization observed in
eral authors. Energy in a child is required for both adult surgical patients, substrate utilization has not
maintenance of body metabolism as well as for growth. been shown to increase substantially in neonates fol-
Estimated energy needs of an infant and older child are lowing surgery. In fact, previous estimates of early
shown in Table I. Caloric requirements in an infant postoperative energy requirements apparently over-
state needs. Administration of calories at 50% above
may be calculated in a variety of ways, including a
modification of the Harris-Benedict equation, which REE levels to perioperative neonates leads to signifi-
has been designed for use in younger children and cant overfeeding.10
infants. 2,3 Energy requirements for most pediatric Johann-Liang et al11 showed that energy intake, but
not energy expenditure, in HIV-infected children was
patients can also be calculated based on standard
nomograms (eg, Recommended Daily Allowance [RDA] significantly reduced compared with age- and gender-
matched controls. This suggests that there may be a
tables) or by indirect calorimetry.
benefit to increasing energy delivery to HIV-infected
Evidence children who are growth impaired; however, studies
are needed to confirm this.11,12
Energy requirements vary with age. Because of the
great variability of energy needs, the World Health . ,
Organization Expert Consultation on Energy and Pro- energy
tein Requirements have recommended that &dquo;whenever
1. Energy needs in infants and children should be
estimated using standard formulas or nomograms
TABLE I and then adjusted according to the clinical course
Estimated energy needs
of the child. (B)
2. Energy requirements should be adjusted depend-
ing on the route of SNS administration. (B)
3. Energy needs for patients undergoing surgical
procedures should be based on indirect calorime-
try or adjusted down from standard formulas to
avoid overfeeding. (B)

25SA
26SA

REFERENCES taken into account and should be replaced milliliter for

1. Wells JC: Energy metabolism in infants and children. Nutrition milliliter. Acute weight loss almost always reflects
14:817, 1998 fluid loss; any acute weight deficit should be added to
2. Baker J, Detsky A, Wesson D: Nutritional assessment: A com- fluid requirements. When there are additional fluid
parison of clinical judgment and objective measurements. N Engl losses (for instance from an ileostomy or biliary drain),
J Med 306:969, 1982
3. Caldwell MD, Kennedy-Caldwell C: Normal Nutritional require- this fluid should also be replaced on a daily basis. Fever
ments. Surg Clin North Am 61:491, 1981 increases insensible water loss via respiration and via
4. Anonymous: World Health Organization. Energy and protein the skin. For each degree of temperature above 38C,
requirements. Report of a joint F AO/WHOIUNU Expert Consul- insensible water loss is increased by 5 mL/kg per 24
tation. Geneva: World Health Organization WHO Technical
hours.33
Report Series No. 724, 1985
5. Heird W, Driscoll J, Schullinger J: Intravenous alimentation in Electrolyte requirements. In an otherwise healthy child,
pediatric patients. J Pediatr 80:351, 1972 essentially all electrolyte loss occurs via the urine. There-
6. Reichman B, Chessex P, Putet G, et al: Diet, fat accretion, and fore, recommendations for electrolyte requirements come
growth in premature infants. N Engl J Med 305:1495, 1981 from measurements of sodium, potassium, and chloride
7. Anonymous: National Academy of Sciences. Recommended
losses in healthy children. As with fluids,
Dietary Allowances. National Academy Press, Washington, DC, urinary
1989, p 24 unusual losses of electrolytes (diarrhea, stoma output,
8. Goran MI, Gower BA, Nagy TR, et al: Developmental changes in bums, exercise, diuretic therapy, renal abnormalities,
energy expenditure and physical activity in children: Evidence etc) need to be considered. Electrolyte requirements may
for a decline in physical activity in girls before puberty. Pediat-
rics 101:887, 1998 be summarized: sodium, 3 mEq/kg per day; potas-
9. Bitar A, Fellmann N, Vernet J, et al: Variations and determi- sium, 2 mEq/kg per day; chloride, 5 mEq/kg per day.2
nants of energy expenditure as measured by whole-body indirect Calcium. Because children synthesize new bone, they
calorimetry during puberty and adolescence. AJCN 69:1209, should be in continual
1999 positive calcium balance. The
10. Letton RW, Chwals WJ, Jamie A, et al: Early postoperative American Academy of Pediatrics, Committee on Nutri-
alterations in infant energy use increase the risk of overfeeding. tion recently updated their policy on calcium.4 The
J Pediatr Surg 30:988, 1995 Committee followed the recommendations for calcium
11. Johann-Liang R, ONeill L, Cervia J, et al: Energy balance, viral intake of the National Academy of Sciences: 0 to 6
burden, insulin-like growth factor-1, interleukin-6 and growth
impairment in children infected with human immunodeficiency months, 210 mg/d; 6 months to 1 year, 270 mg/d; 1 to 3
virus. AIDS 14:683, 2000 years, 500 mg/d; 4 to 8 years, 800 mg/d; and 9 to 18
12. Henderson RA, Talusan K, Hutton N, et al: Resting energy years, 1300 mg/d.5 Administration of parenteral cal-
expenditure and body composition in children with HIV infec- cium is often limited by its solubility.
tion. J Acquir Immune Defic Syndr 19:150, 1998
Fluid and electrolyte therapy in the neonate is dif-
ferent than in the older pediatric patient. Shifts in fluid
FLUID AND ELECTROLYTES and electrolytes from one compartment to another
occur normally as the baby adjusts to extrauterine life.
Background The aim of therapy is not to maintain balance, but to
Fluid requirements. The standard method of calculat- allow these shifts to occur while not letting them
ing fluid requirements for pediatrics was described in become exaggerated. The full-term newborn can lose
an article published in 1957. Fluid requirements are up to 10% body weight during the first week of life, and
related to caloric expenditure, and caloric expenditure the preterm infant can lose up to 20%. It can be diffi-
is determined by a simple formula using body weight: cult to decide when this weight loss is appropriate and
100 kcal/kg for an infant 3 to 10 kg when it becomes dangerous. The usual measures of
1000 kcal + 50 kcal/kg for every kg over 10 kg for a kidney function such as creatinine and BUN are not
child 10 to 20 kg helpful in the immediate postpartum period. They
1500 kcal + 20 kcal/kg for every kg over 20 kg for a largely reflect clearance by the placenta and the
child over 20 kg mother.6
Approximately 40 mL/100 kcal per 24 hours replaces
insensible losses and 60 mL/100 kcal replaces urinary
Evidence
losses. Serendipiuously, 100 mL/100 kcal or 1 mL/kcal
per 24 hours is needed to replace fluid losses.2 Adjust- Evidence concerning fluid and electrolyte needs in
ments are made for pathologic situations (fever, stress, infants comes from relatively few well-performed stud-
etc). This method of calculating fluid requirements is ies. Alteration of total body water has been shown to be
in very close agreement with several other methods affected by the nutrition status of the child. In normal
based on formulas, body surface area, basal calories infants on PN, a decline in both total body water and
plus activity calories, and age. With the development of extracellular fluid volume has been noted despite ade-
parenteral nutrition and of oral rehydration therapy, quate weight gain. 15 This suggests that weight gain is
this method of calculating basal fluid needs remains due to actual tissue accretion and not just an increase
valid and is used as the basis for fluid calculations. in body fluid. In support of adequate electrolyte deliv-
Enteral and parenteral fluid requirements are essen- ery to infants, strong evidence suggests that patients
tially the same. In the absence of diarrhea, stool losses evidence failure to thrive if they develop sodium deple-
are minimal, implying that almost all of the ingested tion. Sacher et al 16 have shown that the depletion of
fluid is absorbed. However, if diarrhea is present, fluid total body sodium in infants with obligate electrolyte
loss can increase dramatically. Diarrhea should be losses from a small bowel stoma results in a plateau in
 27SA

weight gain. Subsequent repletion of electrolytes TABLE I

results in resumption of growth. Estimates of protein requirements for healthy pediatric patients

Practice Guidelines
.

tt i electrolytes

1. Fluid needs vary with the age and weight of the

child and should be adjusted accordingly. (B)
2. Water and electrolyte requirements should be
adjusted in pediatric patients undergoing surgical
procedures or who have on-going losses from sto-
mas or other sites. (B)
requirements are more difficult to define in the child
than in the adult, data exist for guidelines to be artic-
REFERENCES
ulated for premature neonates, full-term neonates, and
1. Gamble JL. Chemical Anatomy. Physiology and Pathology of children. The ideal dietary amino acid composition for
Extracellular Fluid. Cambridge, Harvard University Press, 1964 these groups, however, remains controversial.
2. Fiorotto ML, Klish WJ: Total body electrical conductivity mea-
surements in the neonate. Clin Perinatol 18:611-627, 1991
The protein needs of children may be assessed using
3. Ellis KJ, Shypailo RJ, Wong WW: Measurement of body water by multiple techniques. Methods include the analysis of
multi-frequency bi0electrical impedance spectroscopy in a mul- growth and body composition, nitrogen balance, stable
tiethnic pediatric population. Am J Clin Nutr 70:847-853, 1999 isotopic tracer techniques, and biochemical indices
4. Forbes GB: Growth of lean body mass in man. Growth 36:325-
such as plasma amino acid concentrations. In full-term
338, 1972
5. Boineau FG, Lewy JE: Estimation of parenteral fluid require- infants up to 6 months of age, protein requirements
ments. Pediatr Clin N Am 37:257-264, 1990 may also be estimated on the basis of the protein con-
6. Hill LL: Body composition, normal electrolyte concentrations, tent of human milk consumed by normal children.
and the maintenance of normal volume, tonicity, and acid-base
metabolism. Pediatr Clin N Am 37:241-256, 1990 Implicit in all of these methods is that energy require-
7. Stokes JB: Disorders of the epithelial sodium channel: Insights ments are met, as inadequate calorie administration
into the regulation of extracellular volume and blood pressure. will prevent protein anabolism.
Kidney Int 56:2318-2333, 1999
8. Bello-Reuss E, Colindres RE, Pastoriza-Munoz E, et al: Effects of
acute unilateral renal denervation in the rat. J Clin Invest Evidence
56:208-217, 1975
9. Holliday MA, Segar WE: The maintenance need for water in Immature humans have higher proportional protein
parenteral fluid therapy. Pediatrics 19:823-832, 1957 requirements. Low-birth-weight neonates need approx-
10. Chesney RW: Maintenance needs for water in parenteral fluid imately 2 to 4 g/kg per day of protein to maintain a
therapy. Pediatrics 102:399-400, 1998 growth rate similar to that in utero.1 Premature neo-
11. Mirkin G: Insensible weight loss in infants with fever. Pediatrics
nates show adequate growth rates and nitrogen reten-
30:279, 1962
12. Calcium requirements of infants, children and adolescents. Pol- tion at protein allotments of approximately 3.0 g/kg per
icy statement. Pediatrics 104:1152-1157, 1999 day.2 The administration of protein in a range higher
13. Institute of Medicine, Food and Nutrition Board: Dietary refer- than 4 g/kg per day may result in abnormal amino acid
ence intakes for calcium, phosphorus, magnesium, vitamin D,
and fluoride. National Academy Press, Washington DC, 1997 profiles.3 When protein 6 g/kg per day is given to low-
14. Lorenz JM: Assessing fluid and electrolyte status in the new- birth-weight neonates, untoward effects such as
born. National Academy of Clinical Biochemistry. Clin Chem azotemia, pyrexia, a higher rate of strabismus, and
43:205-210, 1997 lower IQ have been reported. 4,5 Reviews suggest that
15. Coran AG, Drongowski RA, Wesley JR: Changes in total body the quantities of protein (or amino acids) needed for
water and extracellular fluid volume in infants receiving total
low birth weight or premature neonates approximate 3
parenteral nutrition. J Pediatr Surg 19:771, 1984
16. Sacher P, Hirsig J, Gresser J, et al: The importance of oral to 4 g/kg per day.6,7 The requirements of extremely low-
sodium replacement in ileostomy patients. Prog Pediatr Surg birth-weight neonates are less well understood, but
24:226, 1989 these patients have high rates of proteolysis and
attaining adequate growth remains difficult.8
PROTEIN REQUIREMENTS Well-established guidelines exist for the provision of
Background protein to full-term neonates.91 These estimates
range from 2 to 3 g/kg per day. Although this range
The protein requirements of neonates and children appears adequate for most neonates, those who are crit-
vary according to age (Table I). Optimal protein nutri- ically ill remain in profound negative protein balance
tion in this population is dependent on both the quan- despite provision of apparently adequate protein.ll In
tity of protein as well as its quality (amino acid com- well children from age 1 to 10 years, the recommended
position). Adequate energy substrate must be provided dietary allowance for protein remains relatively static,
along with protein to assure its proper utilization. The decreasing slowly from 1.2 to 1.0 g/kg per day.9 During
amount of protein necessary for neonates and children adolescence, boys have a slightly higher recommended
is higher than in adults when expressed in proportion dietary allowance than girls (0.9 and 0.8 g/kg per day,
to body weight. Neonates also potentially differ quali- respectively).9,o Common clinical practice is to give hos-
tatively from adults because of their limited capacity pitalized children, who are presumed to be under meta-
to synthesize certain amino acids. Although protein bolic stress, 1.5 g/kg per day of protein.7 Those children
28SA

who are manifesting catch-up growth may also require CARBOHYDRATES

increased quantities of protein.
The optimal amino acid composition (protein quality)
Background
of pediatric diets has not been established. For full- Carbohydrates are a major component of both EN
term neonates to infants 12 months of age, breast milk and PN. Carbohydrates can be provided in one of three
affords a guide to ideal amino acid allotment. Histidine different ways: Monosaccharides (glucose and fruc-
has been shown to be a conditionally essential amino tose), disaccharides (lactose, sucrose, and maltose);
acid in neonates up to age 6 months, and growth is and complex carbohydrates (starches). Because the
compromised in its absence. 12 Cysteine has been sug- body is capable of forming sugars from both lipids as
gested as possibly conditionally essential in low-birth- well as amino acids, there is no essential amount of
weight neonates because of the low activity of the carbohydrate needed. However, carbohydrates are
enzyme cystathionase (which converts methionine to required1 to prevent breakdown of somatic protein
cysteine).13 Both cysteine and its metabolite taurine sources
are found in high concentrations in human milk, but
are absent in commercial parenteral amino acid formu- Evidence
lations. Although newer stable isotopic techniques are Much of the evidence for the use of carbohydrates is
aiding to further define neonatal amino acid synthesis, empiric. Standards have been established by the Amer-
histidine remains the only amino acid that, at present, ican Academy of Pediatrics and have a generally sound
must be considered conditionally essential in the basis. A recent review has further defined the upper
newborn. and lower boundaries of appropriate carbohydrate
intake in relation to age.2 The primary enteral carbo-
Practice Guidelines
.

hydrate delivered to neonates and young infants is

Protein Requirements lactose. Preterm infants may be unable to digest cer-
tain carbohydrates, particularly lactose, because of
1. Protein requirements should be adjusted accord- inadequate intestinal lactase activity. Thus, in small
ing to the age of the child. (B) preterm infants, formulas that have a 50/50 3mixture of
2. Histidine is a conditionally essential amino acid lactose and glucose polymers are indicated.3
for neonates and infants up to 6 months of age Although somewhat empiric, stable infants should
and should be specifically supplemented. (B) receive approximately 40% to 45% of their total caloric
intake as carbohydrate. Parenteral nutrition for the
REFERENCES neonate should begin administering approximately 6
to 8 mg/kg per minute of dextrose to maintain adequate
1. Zlotkin SH, Bryan MH, Anderson GH: Intravenous nitrogen and
serum glucose levels. Lesser amounts of glucose in a
energy intakes required to duplicate in utero nitrogen accretion
in prematurely born human neonates. J Pediatr 99:115-120, young neonate will lead to hypoglycemia because of
1981 inadequate hepatic production of glucose. Older neo-
2. Kashyap S, Schulze KF, Forsyth M, et al: Growth, nutrient nates tolerate greater loads of glucose, provided it is
retention, and metabolic response in low birthweight infants fed administered through a central venous catheter (10 to
varying intakes of protein and energy. J Pediatr 113:713-721,
1988 14 mg/kg per minute). Glucose intolerance in the pre-
3. Benevenga NJ, Steele RD: Adverse effects of excessive consump- mature infant is not uncommon and is not only mani-
tion of amino acids. Annu Rev Nutr 4:157-161, 1984 fested by hyperglycemia, but also quite commonly by
4. Goldman HI, Fredenthal R, Holland B, et al: Clinical effects of
two different levels of protein intake on low birth weight infants. hypertriglyceridemia.
J Pediatr 74:881-889, 1969
5. Goldman HI, Liebman OB, Fredenthal R, et al: Effects of early Special Considerations
dietary protein intake on low-birth-weight infants: Evaluation at
3 years of age. J Pediatr 78:126-129, 1971 Hyperglycemia is a major adverse effect of carbohy-
6. Heird WC, Kashyap S, Gomez MR: Protein intake and energy drate administration in the immediate postoperative
requirements of the infant. Semin Perinatol 15:438-448, 1991 period. This problem is due to a decrease in insulin
7. Shew SB, Jaksic T: The metabolic needs of critically ill children concentration and possibly due to an increase in glu-
and neonates. Semin Pediatr Surg 8:131-139, 1999
8. Kalhan SC, Iben S: Protein metabolism in the extremely low- coneogenesis .4,5 Hyperglycemic states resolve much
birth weight infant. Clin Perinatol 27:23-56, 2000 more quickly in neonates compared with adult postop-
9. Food and Nutrition Board, National Research Council: Recom- erative patients. Glucose levels were found to be two
mended dietary allowances, 10th ed. National Academy Press, times preoperative values after major surgery in neo-
Washington, DC, 1989 nates and returned to baseline levels after 12 hours.6
10. Committee on Nutrition, American Academy of Pediatrics: Pedi-
atric nutrition handbook, 4th ed. American Academy of Pediat- Postsurgical hyperglycemia appears to be due to ele-
rics, Elk Grove Village, IL, 1996 vated levels of catecholamines.7 Postoperative hyper-
11. Keshan TH, Miller RG, Jahoor F, et al: Stable isotopic quanti- glycemia also appears to be associated with increased
tation of protein metabolism and energy expenditure in neonates
on and post extracorporeal life support. J Pediatr Surg 32:958-
production of both lactate and pyruvate.
963, 1997
12. Snyderman SE: The protein and amino acid requirements of the Practice Guidelines
premature infant. IN Visser HKA, Toreistra JA (eds). Nutrica Carbohydrates
Symposium: Metabolic Processes in the Fetus and Newborn
Infant. Stenfert Kroese, Leiden, Netherlands, 1971, pp 128-143
13. Sturman JA, Gaull GE, Raiha NCR: Absence of cystathionase in 1. Carbohydrates should comprise 40% to 50% of the
human fetal liver: Is cysteine essential? Science 169:74&mdash;76, 1970 caloric intake in infants and children. (C)
 29SA

2. Small amounts of carbohydrates should be used lipoprotein profiles, and increase intake of potentially
in infants and children who are not otherwise harmful trans-fatty acids as saturated fats are
receiving nutrition support to suppress protein replaced by polyunsaturated fats.2 It appears that the
catabolism. (B) amount of total fat ingested/administered may not be
3. In infants who are lactose tolerant, lactose should as critical a risk factor as the type of fat. Furthermore,
be the predominate enteral carbohydrate admin- evidence is building that specific dietary fatty acids
istered in the first 3 years of life. (B) may not only decrease the risk or severity of a number
4. Preterm infants should receive a formula that of chronic diseases, but may also play a role in therapy
has a 50/50 mixture of lactose and glucose poly- of specific diseases.3 This section will principally focus
mers. (B) on the evidence and recommendations for lipid require-
5. For the neonate, carbohydrate delivery in PN ments in full-term healthy infants and children.
should begin at approximately 6 to 8 mg/kg per
minute of dextrose and be advanced, as tolerated
Evidence
to a goal of 10 to 14 mg/kg per minute. (B)
6. Carbohydrate administration should be closely In the United States, multiple organizations such as
monitored and adjusted in the postoperative the US Department of Agriculture, the Department of
period in neonates and children to avoid hyper- Health and Human Services Dietary Guidelines for
glycemia. (B) Americans, the American and Heart Association, and
the National Heart, Lung, and Blood Institute have
REFERENCES recommended a &dquo;moderate-fat diet&dquo; consisting of <30%
1. Kien L: Carbohydrates. IN Tsang RC, Lucas A, Vauy R (eds). energy from total fat and < 10% from saturated fat for
Nutritional Needs of the Preterm Infant, Scientific Basis and everyone over the age of 2 years, with a gradual tran-
Practical Guidelines. Williams & Wilkins, Baltimore, 1993, pp 47 sition from an unrestricted to a moderate-fat diet
2. Kalhan SC, Kilic I: Carbohydrate as nutrient in the infant and
child: Range of acceptable intake. Eur J Clin Nutr 53(Suppl
occurring between 2 and 5-6 years.4-6 However, the
results of clinical studies examining the energy and
1):594, 1999 nutrient adequacy of moderate-fat restricted diets for
3. American Academy of Pediatrics: CoN: Practical significance of
lactose intolerance in children. Pediatrics 86(Suppl):643, 1990 children have been inconsistent.4
4. Wilmore D: Glucose metabolism following severe injury. Nutrient needs in general, and lipid needs in partic-
J Trauma 21:705, 1981
5. Watters J, Bessey P, Dinarello C: Both inflammatory and endo-
ular, are high in the first year of life, and dietary
crine mediators stimulate host response to sepsis. Arch Surg
recommendations are well delineated. Fat intake
121:179, 1986 should be unrestricted in the infant diet. Lipid needs in
6. Elphick M, Wilkinson A: The effects of starvation and surgical the second year of life, as most infants transition from
injury on the plasma levels of glucose, free fatty acids, and neutral predominantly breast milk/formula based diets to
lipids in newborn babies suffering from various congenital anom- adult-style diets, have not been clearly defined. Most
alies. Pediatr Res 15:313, 1981
7. Anand K, Sippell W, Schofield N: Does halothane anaesthesia information suggests that fats in this age group not be
decrease the metabolic and endocrine stress response of newborn restricted.7 A recent longitudinal study of growth and
infants undergoing operation? Br Med J 296:668, 1988 infant nutrition conducted in the US found that the
intake of some key nutrients during the period of
LIPIDS dietary transition between 12 and 18 months of life
was insufficient in infants on a low-fat diet.8 In con-
Background trast, recent data presented from the Special Turku
Considerable controversy exists regarding the coronary Risk factor Intervention Project (STRIP), an
requirements for fat intake in children. As the debate ongoing longitudinal cohort study of more than 1000
about lipid recommendations has raged over the past children in Finland, reported that a low saturated fat
two decades, the prevalence of obesity in children in and cholesterol diet begun before the age of 1 year
the United States has increased alarmingly. Almost resulted in lower LDL cholesterol and unchanged HDL
one quarter of US children are now overweight or cholesterol, with no adverse effects on growth, devel-
obese, an increase of over 20% in the past decade. 1,2 opment (to age 5-6 years), or overall nutrient intake.9
There is concern that this change will translate into The differences between these two studies and others
increased adult obesity and associated comorbidities is probably related to study design and/or cultural
such as hyperlipidemia, hypertension, and type II dia- issues in that the Finnish children received frequent
betes. As research data began pointing to a direct cor- follow-up and dietary assessment, whereas popula-
relation between dietary fat and risk factors for cardio- tions in the US are frequently &dquo;free living.&dquo;
vascular disease, advice to the public at large, Beyond age 2 years, recommendations from many
including children, was to reduce total fat, saturated organizations concur that there should be a slow tran-
fat, and cholesterol intake. sition from unrestricted dietary fat to a goal of <30%
However, children, especially in the first several total fat and <10% saturated fat as a percentage of
years of life, have nutrient requirements that differ total energy intake. However, the details of this tran-
markedly from those of adults. Concerns have been sition continue to be a point of debate. The American
voiced that lowering fat intake in the growing child Academy of Pediatrics has agreed with USDA/HHS
might result in decreased supply of omega-6 and guidelines, recommending that the transition between
omega-3 essential fatty acids, have adverse effects on unrestricted dietary fat and a moderate-fat diet occur
normal growth and development, lead to adverse by the age of 5 years.7 A recent cross-sectional study of
30SA

2802 US children 4 to 8 years old reported that spon- (moderate fat) diet (less than 30% of total energy
taneous consumption of diets with approximately 30% from fats and less than 10% from saturated
energy from fat did not significantly increase the risk fats). (B)
for nutritional inadequacy, and high-fat diets did not
consistently protect against inadequacy.4 Other inves- REFERENCES
tigators, however, have echoed the recommendations 1. Ogden C, Troiano RP, Briefel R, et al: Prevalence of overweight
made in the Canadian Dietary Guidelines, suggesting among preschool children in the United States, 1971 through
that the transition from high- to moderate-fat diets 1994. Pediatrics 99:el-el3, 1997
2. Deckelbaum RJ, Williams CL: Fat intake in children: Is there
occur over the longer time frame of linear growth (ado-
need for revised recommendations? J Pediatr 136(1):7-9, 2000
lescence).lO,l1 The rationale for prolonging the transi- 3. Deckelbaum RJ, Calder PC: Lipids in health and disease: Quan-
tion from a high- to a moderate-fat diet has been to tity, quality, and more. Curr Opin Nutr Metabol 3(2):93-94, 2000
minimize the potential for adverse effects on growth, 4. Ballew C, Kuester S, Serdula M, et al: Nutrient intakes and
dietary patterns of young children by dietary fat intakes. J Pedi-
development, lipoprotein profiles, and immunologic atr 136(2):181-187, 2000
function that might occur with a more rapid transi- 5. Report of the Dietary Guidelines Advisory Committee for the
tion.2 The most definitive statement regarding this 2000 Dietary Guidelines for Americans (in progress)
6. US Dept of Health and Human Services and US Dept of Agri-
approach is by Rask-Nissila et al. 13 This randomized, culture : Nutrition and Your Health: Dietary Guidelines for
controlled study showed that 5-year-old children raised
Americans, 4th ed. US Dept of Health and Human Services and
since infancy on a low-fat, low-cholesterol diet had US Dept of Agriculture, Washington, DC, 402-519, 1995
equivalent neurologic development while having lower 7. American Academy of Pediatrics Committee on Nutrition State-
serum cholesterol levels compared with those receiving ment or: "Cholesterol in Childhood." Pediatrics101:145-147,
control diets. 1998
8. Picciano MF, Smiciklas-Wright H, Birch LL, et al: Nutritional
To date, the data seem to indicate that emphasizing
guidance is needed during dietary transition in early childhood.
fat-modified diets by encouraging consumption of low- Pediatrics 106(1):109-114, 2000
fat dairy products, fruits, vegetables, and grains does 9. Lagstrom H, Seppanen R, Jokinen E, et al: Influence of dietary
not compromise childrens nutrition status, growth, fat on the nutrient intake and growth of children from 1 to 5 y of
and development. 12 It may be most important to age: The Special Turku Coronary Risk Factor Intervention
Project. Am J Clin Nutr 69:516-23, 1999
emphasize avoidance of excess total caloric intake and 10. Olson RE: The folly of restricting fat in the diet of children. Nutr
promotion of increased physical activity, rather than Today 30:234-245, 1995
making changes in very specific recommendations 11. Joint Working Group of the Canadian Pediatric Society and
Health Canada. Nutrition recommendations update&mdash;Dietary
regarding fat intake in children.2 fat and children. Ministry of Supply and Services. Publications
Similar to adults receiving SNS, it is recommended Distribution, Health Canada, Ottawa, Ontario, Canada, 1993
that 1% to 2% of energy should be derived from linoleic 12. Johnson R: Can children follow a fat-modified diet and have
acid (<jo6) and about 0.5% of energy from a-linolenic adequate nutrient intakes essential for optimal growth and
acid (co3) to prevent essential fatty acid deficiency.&dquo; development? J Pediatr 136(2):143-145, 2000
13. Rask-Nissila L, Jokinen E, Terho P, et al: Neurological develop-
ment in 5-year old children receiving a low-saturated fat, low-
cholesterol diet since infancy: A randomized controlled trial.
Special Considerations JAMA 284:993, 2000
Characteristic findings in infants suffering from 14. Uauy R, Hoffman DR: Essential fat requirements of preterm
infants. AJCN 71:245S-250S, 2000
trauma or undergoing surgery are increases in circu-
15. Anand K, Brown M, Causon R, et al: Can the human neonate
lating fatty acids, ketone bodies, and glycero1.15 These mount an endocrine and metabolic response to surgery? J Pedi-
changes are indicative of lipolysis and ketogenesis. atr Surg 20:41, 1985
These products appear to be a major source of energy 16. Wolfe R, Herndon D, Peters E: Regulation of lipolysis in severely
after surgery. In fact, it is estimated that some 75% to burned children. Ann Surg 206:214, 1987
17. Anand K, Sippell M, Aynsley-Green A: Randomized trial of fen-
90% of postoperative energy requirements come from
tanyl anesthesia in preterm babies undergoing surgery: Effects
fat metabolism, with the remainder coming from pro- on the stress response. Lancet 1:243, 1987
tein stores. It appears that these changes are driven by
a release of catecholamines starting intraoperatively. 16
MICRONUTRIENT REQUIREMENTS
A reversal of these changes has been demonstrated
with the administration of halothane anesthesia, Vitamins
because halothane can suppress the catecholamine
17 Background. As complex organic substances, vitamins
response. are considered essential contributors to human growth
and health. The essentiality of vitamins dictates a
Practices . sustained exogenous intake (with perhaps the excep-
Lipids . - tion of vitamin D) in order to avoid deficiency. Classi-
fied by solubility, the lipid-soluble vitamins A, D, E,
1. Full term infants up to 1 year of age should be and K have the potential for storage and therefore the
allowed an unrestricted fat intake. (A.) potential for toxicity. The water-soluble vitamins
2. Children between 1 and 2 years of age should ascorbic acid and the B-complex vitamins are consid-
have very limited or no restrictions on fat ered relatively nontoxic and are excreted when admin-
intake (B) istered in excess.
3. Between age 2 and 5 to 6 years, children should Evidence. Both lipid- and water-soluble vitamins
transition from a high-fat diet to a fat-modified should be provided in PN solutions. The subcommittee
 31SA

on Pediatric Parenteral Nutrient Requirements of the TABLE II

Committee on Clinical Practice Issues of The American Daily trace element requirement-infants
Society for Clinical Nutrition published guidelines in
1988 outlining recommendations for vitamins in PN
solutions for term infants and children (Table 1).
Owing to limited product selection, the choice of mul-
tivitamin preparations differs for children less than
and greater than 11 years of age. For children greater
than 11 years, vitamin K should be provided in con-
junction with a multivitamin package at a dose of 200 important nutrient. Cobalt, chromium, copper, iodine,
.Lg/d.2 In addition to routine vitamin K supplementa- manganese, molybdenum, selenium, and zinc are all
tion, specific products may require supplemental dos- considered to be essential micronutrients for of
support
ing with other vitamins. normal human metabolic processes (Table II).
Carnitine, synthesized from methionine and protein Evidence. Routine addition of zinc, copper, selenium,
bound lysine, is the requisite transporter of long chain chromium, and manganese to PN solutions is recom-
fatty acids across the inner mitochondrial membrane mended to avoid deficiency.5 Although not a conven-
for (3-oxidation. Carnitine can be obtained through the tional addition, molybdenum supplementation may be
diet, exogenous supplementation, and endogenous bio- appropriate in long term TPN therapy.6 The 1988 sub-
synthesis. Now a standard addition to many enteral committee recommendations identify trace element
formulas, carnitine may become conditionally essential requirements in the term infant and child for zinc,
in the neonate on long term PN secondary to limited copper, selenium, chromium, manganese and molybde-
biosynthetic capability and immature conservation num.2 Intakes for preterm infants are also suggested.
mechanisms.3 Carnitine supplementation should be The type of nutrition support (breast milk, enteral
provided once a deficiency has been confirmed. formula or PN) can influence the trace element status
Special considerations. Vitamin supplementation rec- of the patient and should be considered when deter-
ommendations are provided below for stable pediatric mining supplementation or analyzing levels., 8
patients and do not account for conditions of catabolic Special considerations. The provision of balanced
stress, ventilatory support, or organ dysfunction. The nutrients will prevent both deficiency and toxicity.
1988 subcommittee recommendations also include sug- Trace element contamination must be considered when
gested intakes for preterm infants. To avoid potential determining element supplementation. Blood concen-
toxicity related to impaired metabolism, multivitamin trations of copper, chromium and manganese may
preparations administered to the preterm infant become elevated because of contamination of TPN solu-
should be formulated without propylene glycol or poly- tions by these metals. 2,9-12 In addition, specific disease
sorbate, which may be found in adult formulations.2 states will necessitate adjustments in the elements
provided. Copper and manganese should be adminis-
Trace Elements tered cautiously, if at all, in patients with impaired
biliary excretion or cholestatic liver disease.7,13-15
Background. Trace elements generally function as Because of renal excretion of these elements, dosage
prosthetic groups of enzymes. Zinc, copper, chromium reduction for selenium, molybdenum, and chromium
and manganese are all in the first transition series of should be evaluated in patients with renal dysfunc-
metals in the periodic table, and therefore, have many tion.2,5 Additional zinc supplementation is necessary in
physical and chemical properties in common. Sele- conditions of increased losses, such as diar-
nium, chemically classified as a nonmetal, is an equally rhea or excessive ileostomy drainage.2 persistent
Recently, Williams et al13 reported on new recom-
mendations for dietary fiber by the American Academy
TABLE I of Pediatrics Committee on Nutrition. For children
Daily vitamin requirement-infants2~3 older than 2 years of age, they recommend a minimum
of 5 g/d of dietary fiber and children over 5 years of age
should consume 10 g/d of dietary fiber.16
The widespread occurrence of iron deficiency anemia
before the 1970s resulted in a 1976 statement by the
American Academy of Pediatrics (AAP) Committee on
Nutrition entitled &dquo;Iron Supplementation for Infants.&dquo;
Updated in 1989, and again in 1999, the AAP state-
ment recommends using iron-fortified formula (4 to 12
mg/L of iron) from birth to 12 months in the absence of
exclusive breast feeding. 17 Guidelines for parenteral
supplementation using iron dextran are less clear and
differ among the child and the term and preterm infant
in conjunction with the total estimated duration of PN
therapy. Additionally, iron replacement for docu-
mented deficiency and iron supplementation to main-
tain iron balance or meet fetal accretion rates are
32SA

dosed differently. Compatibility problems due to pre- requirements in low-birth-weight infants receiving parenteral
and enteral nutrition. JPEN 23(3):155-159, 1999
cipitation of iron phosphate and trivalent-induced 7. Krachler M, Rossipal E, Micetic-Turk D: Concentrations of trace
instability of lipid emulsions must also be considered elements in sera of newborns, young infants, and adults. Biol
before iron supplementation using PN solutions. 18 Trace Element Res 68(2):121-135, 1999
8. Aquilio E, Spagnoli R, Seri S, et al: Trace element content in
Practice Guidelines human milk during lactation of preterm newborns. Biol Trace
Micronutrient requirements Element Res 51(1):63-70, 1996
9. Frankel DA: Supplementation of trace elements in parenteral
nutrition: Rationale and recommendations. Nutr Res 13:583-
1. Vitamins and trace elements should be compo- 596, 1993
nents of all PN solutions and enteral formulas. (A) 10. Moukarzel AA, Song MK, Buchman AL, et al: Excessive chro-
2. Vitamin and trace element levels should be mon- mium intake in children receiving total parenteral nutrition.
itored periodically during long-term PN adminis- Lancet 339:385-388, 1992
11. Bougle D, Bureau F, Deschrevel G, et al: Chromium and paren-
tration. (C)
teral nutrition in children. J Pediatr Gastro Nutr 17:72-74, 1993
12. Kurkus J, Alcock NW, Shiles ME: Manganese content of large
REFERENCES volume parenteral solutions and of nutrient additives. JPEN
1. Linder MC: Nutrition and metabolism of vitamins. IN Nutri- 8:254-257, 1984
tional Biochemistry and Metabolism with Clinical Applications, 13. Reynolds AP, Kiely E, Meadows N: Manganese in long term
Linder MC (ed). Elsevier Science, New York, 1985, pp 69-131 pediatric parenteral nutrition. Arch Dis Child 71:527, 1994
2. Greene HL, Hambidge M, Schanler R, et al: Guidelines for the 14. Fell JME, Reynolds AP, Meadows N, et al: Manganese toxicity in
use of vitamins, trace elements, calcium, magnesium, and phos- children receiving long-term parenteral nutrition. Lancet 347-
phorus in infants and children receiving total parenteral nutri- 1218, 1996
tion : report of the Subcommittee on Pediatric Parenteral Nutri- 15. Kafritsa Y, Fell J, Long S, et al: Long term outcome of brain
ent Requirements from the Committee on Clinical Practice manganese deposition in patients on home parenteral nutrition.
Issues of The American Society for Clinical Nutrition. Am J Clin Arch Dis Child 79(3):263-265, 1998
Nutr 48:1324-1342, 1988 16. Williams CL, Bollella M, Wynder EL: A new recommendation for
3. Borum PR: Carnitine in neonatal nutrition. J Child Neurol dietary fiber in childhood. Pediatrics 96:985, 1995
10(Suppl 2):2S25-2S31, 1995 17. Anonymous: Iron fortification of infant formulas. American
4. Szwanek M, Khalidi N, Wesley JR: Trace elements and paren- Academy of Pediatrics Committee on Nutrition. Pediatrics 104:
teral nutrition. Nutr Suppl Ser 7:8-14, 1987 119-123, 1999
5. Leung FY: Trace elements in parenteral micronutrition. Clin 18. Allwood MC, Martin H, Greenwood M, et al: Precipitation of
Biochem 28(6):561-566, 1995 trace elements in parenteral nutrition mixtures. Clin Nutr
6. Friel JK, MacDonald AC, Mercer CN, et al: Molybdenum 17:223, 1998
 Section VIII: Access for Administration of Nutrition Support

ENTERAL ACCESS Eighty percent of tubes were in the stomach or duode-

Background num, 19% in the esophagus, and 1% in the pleural
space.2 Because of the possibility of false positives and
Enteral nutrition is indicated for patients with a the potential for tube malposition in the tracheobron-
functional gastrointestinal tract whose oral nutrient chial tree,
intake is insufficient to meet estimated needs. Selec- the tube
radiographic confirmation of the position of
tip is recommended. 19,21-22
tion of the proper enteral access device is based on the tubes may predispose to nasopharyn-
Nasally placed
patients gastrointestinal anatomy and function, antic- geal ulcers, nasal septum necrosis, sinusitis, otitis,
ipated duration of enteral nutrition, and the potential hoarseness, and vocal cord paralysis .21 Small-bore
for aspiration. The nasoenteric tube is the most com-
tubes made from polyurethane or silicone, in
monly used method of enteral access because it can be feeding
sizes from 5F to 12F, are soft, smooth, and more flex-
inserted into the stomach, duodenum, or the jejunum.
These tubes are indicated for short-term (less than 4 ible than the stiff, large-bore nasogastric tubes
weeks) use because they have low complication rates, designed for decompression and gastric drainage.
are relatively inexpensive, and easy to place. They may These small tubes provide improved patient comfort
also be used for interim access before placement of a and decrease the risk of nasal-tissue necrosis.
Patients requiring long-term EN should receive
long-term device. Tube enterostomies are indicated more
when long-term (greater than 30 days) feeding is antic- permanent access. Gastrostomy is the most com-
mon method for long-term access because it eliminates
ipated or when obstruction makes nasal intubation
nasal irritation, psychosocial stress of having a tube in
impossible. the nose, and requirement for an infusion pump (intra-
Evidence gastric feedings may be administered as a bolus in
patients who tolerate it). Gastric tubes, because of
Access to the gastrointestinal tract can be attained their large diameter, can also be used for gastric
at the bedside, endoscopically, under fluoroscopic or decompression, pH monitoring, and medication deliv-
ultrasound guidance, or operatively. Bedside place- ery. Insertion can be performed surgically (with lapa-
ment of an enteric (postpyloric) tube involves advanc- rotomy or laparoscopy) or nonoperatively. Nonopera-
ing the tube into the stomach and allowing it to tive placement of gastric feeding tubes (percutaneous
migrate independently into the small bowel. Recent endoscopic gastrostomy [PEG]) or with fluoroscopic
studies report success rates approaching 90% if pH guidance) is favored because it can be performed with-
monitoring is used. 2,3 Positioning patients in the right out general anesthesia and allows feedings to be
lateral decubitus position has not been demonstrated administered soon after placement.24-27 A meta-anal-
to increase spontaneous tube migration into the small ysis of over 5000 cases found higher rates of successful
bowel. Prokinetic agents given before, but not after, tube placement for radiologic gastrostomy than for
tube insertion may facilitate tube passage into the PEG, a lower complication rate than with PEG or sur-
small bowel.5 Use of weighted tubes, pH sensors, mag- gery, and lower 30-day procedure-related mortality.18
nets, and bioelectrical detection devices to facilitate Jejunostomies can be placed at the time of laparot-
tube placement can be of help to confirm tube omy in patients in whom access to the small bowel is
location.6-12 Fluoroscopic, sonographic, and endoscopic desired. PEG tubes with a jejunal extension or direct
guidance are often used to achieve transpyloric tube percutaneous endoscopic placement provide additional
placement when blind methods fail. These techniques options for obtaining access to the jejunum when
have an 85 to 95% success rate for initial tube place- simultaneous gastric decompression is desired.28
ment.l3-ls However, these tubes frequently dislodge or These tubes have a high rate of mechanical dysfunction
migrate back into the stomach, necessitating repeat and dislodgment and are not advocated for long-term
tube insertion and increased costs.19 use.29 A skin level or low-profile device placed through
Tube placement can be confirmed by air insufflation, a mature gastrostomy offers long-term EN patients a
auscultation, aspiration of gastric or small bowel con- less obtrusive gastric tube. Preplacement marking for

tents, or radiographically. In one study, the location of optimal gastrostomy and jejunostomy tube site loca-
the feeding tube tip on 100 consecutive radiographs tions is recommended to decrease of
,

complications.
obtained within 4 hours of placement was analyzed. therapy and to promote patient self-care. Complica-

33SA
34SA

tions associated with tube enterostomies include per- Ewery 4 hours during continuous feedings and before
foration, hemorrhage, wound infection, bowel obstruc- mid after intermittent feedings and medications.44 Flu-
tion, bowel necrosis, and stomal leakage. Tube i ds with an acidic pH such as cranberry juice can
migration may lead to erosion of the exit site and Iprecipitate protein and cause tube clogging.45 When
leakage of gastric or intestinal contents onto the sur- iwater fails to declog feedings tubes, use of papain,
rounding skin. (-ombinations of activated pancreatic enzymes and
There is considerable controversy regarding the pre- Esodium bicarbonate mixed with water, or declogging
ferred site for EN delivery. Gastric feedings require (levices has been successful. 41
intact gag and cough reflexes and adequate gastric
emptying. Small bowel access is indicated in clinical special Considerations

,

conditions in which tracheal aspiration, reflux esoph-

agitis, gastroparesis, gastric outlet obstruction, or pre- A significant discrepancy is often seen between pre-
vious gastric surgery precludes gastric feedings, or f3cribed and delivered calories; that is, the volume of
when early postoperative feeding after major abdomi- iLube feeding received, expressed as a ercentage of the
nal procedures is planned. Prevention of aspiration;oal intake is often less than 100%. Reasons for
entails identification of high-risk patients, elevation of iinadequate tube feeding include slow advancement of
the head of the bed, careful monitoring of tube feeding imfusion rates, interruptions of feedings due to tube
delivery and patient tolerance, and adequate airway (iisplacement or gastric residuals, withholding of feed-
management. Studies have not consistently demon- iings for operative and diagnostic procedures, medica-
strated a benefit of small bowel feedings over gastric 1tion administration, physician underprescription, and
feedings to prevent aspiration.31-36 However, lack of an ]routine nursing procedures .42,48,50 EN protocols allow
accepted definition of clinically significant aspiration ;istandardized management of tube feedings and also
makes interpretation of these studies difficult. The ]help educate practitioners on the importance and mon-
physical presence of a nasogastric tube across the iitoring of outcomes. Several studies have demon-
lower esophageal sphincter probably impairs sphincter istrated that tube feeding delivery is improved with EN
function and promotes reflux of gastric contents.37 ]protocols.51-53
Pharmacologic intervention with antireflux agents has
been used to decrease the risk of gastric reflux, but it .
has not been shown to decrease the frequency of noso- Enteral Access
comial pneumonia or affect the mortality rate of criti-
cally ill patients receiving EN.38 1. Decisions regarding access for EN should be made
Gastric residuals are frequently used to monitor
considering the effectiveness of gastric emptying,
safety and effectiveness of tube feedings. Gastric motil- gastrointestinal anatomy, and aspiration risk. (B)
ity is affected by disease, mechanical obstruction, and 2. Nasoenteric tube placement should initially be
medications (including paralytic agents). There is no
attempted using a spontaneous or other bedside
agreement regarding the acceptable volume of gastric placement technique; if this is unsuccessful,
residual for monitoring tube feedings.39,40 The level of or endoscopic guidance should be
residual volume of concern in the critically ill patient fluoroscopic
used. (A)
appears to be 200 mL with a nasogastric tube located 3. Radiographic confirmation of the feeding tube tip
in the antrum or fundus or 100 mL for surgical or
position should be obtained after placement of a
endoscopic gastrostomy tubes located on the anterior nasogastric or nasoenteric access tube. (B)
gastric wall .41 McClave et a141 compared gastric resid- 4. Gastric residuals should be checked frequently
uals in critically ill patients, stable gastrostomy-fed when feedings are initiated and feedings should
patients, and normal healthy volunteers. They found be held if residual volumes exceed 200 mL on two
that there was a peak in residual volumes early in the successive assessments. (A)
study, with a subsequent reduction in those volumes 5. Feeding tubes should routinely be flushed with 20
over time. Lin and Van Critter, 40 using a computer
to 30 mL of warm water every 4 hours during
simulated model, found that gastric residual volumes continuous feedings and before and after inter-
after tube feeding reach a plateau similar to that found mittent feedings and medication administra-
in the postprandial stomach. It is probably prudent to
tion. (A)
check gastric residuals every 4 to 5 hours when initi- 6. Standardized protocols for enteral nutrition
ating feedings until a plateau of less than 50 mL has ordering, administration, and monitoring should
been achieved.4o42 One high residual volume should be utilized. (B)
not prompt stopping the feeding but instead to monitor
for signs and symptoms of intolerance.43 Patients with
persistently elevated gastric residual volumes may REFERENCES
benefit from a tube placed beyond the ligament of 1. American Gastroenterological Association Technical Review on
Treitz. Tube Feeding for Enteral Nutrition. Gastroenterology 108:1282-
All feeding tubes are subject to mechanical compli- 1301, 1995
2. Cohen LD, Alexander DJ, Catto J, et al: Spontaneous transpy-
cations, especially clogging. Clogging is caused by vis- loric migration of a ballooned nasojejunal tube: a randomized
cous formulas, inappropriate medication administra-
controlled trial. JPEN 24:240-243, 2000
tion, formula residue, and inadequate flushing. Tubes 3. Zaloga GP: Bedside method for placing small bowel feeding tubes
should be flushed with at least 20 to 30 mL warm water in critically ill patients. Chest 100:1643-1646, 1991
 35SA

4. Marian M, Rappaport W, Cunningham D, et al: The failure of 29. Shapiro T, Minard G, Kudsk KA: Transgastric jejunal feeding
conventional methods to promote spontaneous transpyloric feed- tubes in critically ill patients. Nutr Clin Pract 12:164-167, 1997
ing tube passage and the safety of intragastric feeding in the 30. Hanlon MD: Pre-placement marking for optimal gastrostomy
critically ill ventilated patient. Surg Gynecol Obstet 176:475- and jejunostomy tube site locations to decrease complications
479, 1993 and promote self care. Nutr Clin Pract 13:167-171, 1998
5. Kittinger JW, Sandler RS, Heizer WD: Efficacy of metoclopra- 31. Lazarus BA, Murphy JB, Culpepper L: Aspiration associated
mide as an adjunct to duodenal placement of small-bore feeding with long-term gastric versus jejunal feeding: A critical analysis
tubes: a randomized, placebo-controlled, double-blind study. of the literature. Arch Phys Med Rehab 71:46-53, 1990
JPEN 11:33-37, 1987 32. Montecalvo MA, Steger KA, Farber HW, et al: Nutritional out-
6. Thurlow PM: Bedside enteral feeding tube placement into duo- come and pneumonia in critical care patients randomized to
denum and jejunum. JPEN 10:104-105, 1986 gastric versus jejunal tube feedings. Crit Care Med 20:1377-
7. Gabriel SA, Ackerman RJ, Castresana MR: A new technique for 1387, 1992
placement of nasoenteral feeding tubes using external magnetic 33. Strong RM, Condon SC, Solinger MR, et al: Equal aspiration
guidance. Crit Care Med 25:641-645, 1997 rates for postpylorus and intragastric-placed small bore nasoen-
8. Davis TJ, Sun D, Dalton ML: A modified technique for bedside teric feeding tubes: A randomized, prospective study. JPEN
placement of nasoduodenal feeding tubes. J Am Coll Surgeons 16:59-63, 1992
178:407-409, 1994 34. Fox KA, Mularski KA, Sarfati MR: Aspiration pneumonia fol-
9. Salasidis R, Fleiszere, Johnston R: Air insufflation technique of lowing surgically placed feeding tubes. Am J Surg 170:564-567,
enteral tube insertion: A randomized, controlled trail. Crit Care 1995
Med 26:1036-1039, 1998 35. Methany N, Eisenberg P, Spies M: Aspiration pneumonia in
10. Cresci G, Grace M, Park M, et al: Accurate and timely blind patients fed through nasoenteral tubes. Heart Lung 15:256-261,
bedside placement of post-pyloric feeding tubes using an electro- 1986
magnetic navigation device. Nutr Clin Pract 14:101, 1999 36. Mullen H, Roubenoff RA, Roubenoff R: Risk of pulmonary aspi-
11. Lord LM, Weiser-Maimone A, Pulhamus M, et al: Comparison of ration among patients receiving enteral nutrition support. JPEN
weighted vs. unweighted enteral feeding tubes for efficacy of 16:160-164, 1992
transpyloric intubation. JPEN 17:271-273, 1993 37. Saxe JM, Ledgermwood MD, Lucas CE, et al: Lower esophageal
12. Ahmed W, Levy H, Kudsk K, et al: The rates of spontaneous
transpyloric passage of three enteral feeding tubes. Nutr Clin sphincter dysfunction precludes safe gastric feeding after head
Pract 14:107-110, 1999 injury. J Trauma 37:581-584, 1994
13. Minard G: Enteral access. Nutr Clin Pract 9:172-182, 1994 38. Yavagal DR, Karnad DR, Oak JL: Metoclopramide for prevent-
14. Gutierrez ED, Balfe DM: Fluoroscopically guided nasoenteric ing pneumonia in critically ill patients receiving enteral tube
feeding tube placement: Results of a 1-year study. Radiology feeding: A randomized controlled trial. Crit Care Med 28:1408-
178:759-762, 1991 1411, 2000
15. Patrick PG, Marulendra S, Kirby DF, et al: Endoscopic nasogas- 39. Heyland D, Cook, DJ, Winder B, et al: Enteral nutrition in the
tric-jejunal feeding tube placement in critically ill patients. Gas- critically ill patient: A prospective survey. Crit Care Med
trointest Endosc 45:72-76, 1997 23:1055-1060, 1995
16. Bosco JJ, Gordon F, Zelig M, et al: A reliable method for the 40. Lin HC, VanCritters GW: Stopping enteral feeding for arbitrary
endoscopic placement of a nasoenteric feeding tube. Gastrointest gastric residual volumes may not be physiologically sound:
Endosc 40:740-743, 1994 results of a computer simulated model. JPEN 21:280-289, 1997
17. Hernandez-Soocorro CR, Marin J, Ruiz-Santana S, et al: Bedside 41. McClave SA, Snider HL, Lowen CC, et al: Use of residual vol-
sonographic-guided versus blind nasoenteric feeding tube place- umes as a marker for enteral feeding intolerance: Prospective
ment in critically ill patients. Crit Care Med 1996, 24:1690-1694 blinded comparison with physical examination and radiographic
18. Wollman B, DAgostino HB, Walus-Wigle JR, et al: Radiologic,
findings. JPEN 16:99-105, 1992
endoscopic, and surgical gastrostomy: An institutional evalua- 42. McClave SA, Sexton LA, Spain DA, et al: Enteral tube feeding in
tion and meta-analysis of the literature. Radiology 197:699-704,
the intensive care unit. Factors impeding adequate delivery. Crit
1995
Care Med 27:1252-1256, 1999
19. Chen MY, Ott DJ, Gelfand DW: Nonfluoroscopic, postpyloric
43. Murphy LM, Bickford V: Gastric residuals in tube feeding: How
feeding tube placement: Number and cost of plain films for much is too much? Nutr Clin Pract 14:304-306, 1999
determining position. Nutr Clin Pract 15:40-44, 2000 44. Scanlan M, Frisch S: Nasoduodenal feeding tubes: Prevention of
20. Benya R, Langer S, Mobarhan S: Flexible nasogastric feeding
tube tip malposition immediately after placement. JPEN 108- occlusion. J Neurosci Nurs 24:250-259, 1992
109, 1990 VOLUME 45. Methany N, Eisenberg P, McSweeney M: Effect of feeding tube
21. Welch SK, Hanlon MD, Waits M, et al: Comparison of four properties and three irrigants on clogging rates. Nurs Res
bedside indicators used to predict duodenal feeding tube place- 37:165-169, 1998
ment with radiography. JPEN 18:525-530, 1994 46. Frankel EH, Enow NB, Jackson KC, etal: Methods of restoring
22. Bankier AA, Wiesmayr MN, Henk C, et al: Radiographic detec- patency to occluded feeding tubes. Nutr Clin Pract 13:129-131,
tion of intrabronchial malpositions of nasogastric tubes and sub- 1998
sequent complications in intensive care unit patients. Intensive 47. Petnicki PJ: Cost savings and improved patient care with use of
Care Med 23:406-410, 19,97 a flush enteral feeding pump. Nutr Clin Pract (Suppl) 1998,
23. Sofferman RA, Haisch CE, Kirchner JA, et al: The nasogastric 13:S39-41
tube syndrome. Laryngoscope 100:962-968, 1990 48. Echevarria CG, Winkler MF: Enteral feeding challenges in crit-
24. Baskin WN, Johansen JF: An improved approach to the delivery ically ill patients. Top Clin Nutr 16:37-42, 2000
of enteral nutrition in the intensive care unit. Gastrointest 49. Woodcock N, Zeigler D, Palmer MD, et al: Enteral versus par-
Endosc 42:161-165, 1995 enteral nutrition: A pragmatic study. Nutrition 17:1-12, 2001
25. Larson DE, Burton DD, Schroeder KW, et al: Percutaneous 50. Stechmiller J, Treolar DM, Derrico D, et al: Interruption of
endoscopic gastrostomy: Indications, success, complications and enteral feedings in head injured patients. J Neurosci Nurs
mortality in 314 consecutive patients. Gastroenterology 93:48- 26:224-229, 1994
52, 1987 51. Chapman G, Curtas S, Meguid M: Standardized enteral orders
26. Grant JP: Comparison of percutaneous endoscopic gastrostomy attain caloric goals sooner: A prospective study. JPEN 16:149&mdash;
with Stamm gastostomy. Ann Surg 207:598-603, 1988 151, 1992
27. Apelgren KN, Zambos J: Is percutaneous better than open gas- 52. Adams S, Batson S: A study of problems association with the
trostomy? : A clinical study in one surgical department. Am Surg delivery of enteral feedings in critically ill patients in five ICUs
55:596-600, 1989 in the UK. Intensive Care Med 23:261-266, 1997
28. Shike M, Latkany L, Gerdes H, et al: Direct percutaneous endo- 53. Spain DA, McClave SA, Sexton LK, et al: Infusion protocol
scopic jejunostomies for enteral feeding. Nutr Clin Pract improves delivery of enteral tube feeding in the critical care unit.
12(Suppl):S38-S42, 1997 JPEN 23:288-292, 1999
36SA

PARENTERAL ACCESS upper extremity vein is used for access by interven-

tional radiology using fluoroscopic guidance.11
Background Catheter-related infections and mechanical compli-
Parenteral nutrition administration requires central cations can occur after placement of a CVC. Catheter-
venous access in order to provide nutrients at greater related sepsis occurs in 5 to 8 per 1000 patient days
concentrations than is possible through peripheral and is associated with morbidity, mortality, and
veins. PN is appropriate when SNS is indicated and a increased medical COStS,12-15 Guidelines for the man-
contraindication to the use of EN is present or EN is agement of intravascular catheter-related infections
not tolerated. Selection of the most appropriate paren- have been jointly prepared by the Infectious Diseases
teral access device is based on the patients vascular Society of America, the American College of Critical
access history, venous anatomy, coagulation status, Care Medicine and the Society of Healthcare Epidemi-
the anticipated duration of PN, the care setting (hos- ology of America, 16 and the Hospital Infection Control
pital versus other), and the nature of the underlying Practices Advisory Committee. 17 An evidence-based
disease. For hospitalized patients, temporary percuta- review on prevention of catheter infection during PN
neous central venous catheters are often most appro- has also been published.18 The treatment of catheter-
priate. For long-term therapy in a nonhospital setting, related sepsis involves catheter removal and appropri-
subcutaneously tunneled percutaneous catheters or ate antibiotic coverage although success in managing
implanted subcutaneous infusion ports are most com- catheter infection with antibiotics alone has been
monly used. When selecting a long-term access device, reported. 13 Prophylactic catheter exchange over a
consideration should be given to the patients activity guide wire has not been shown to decrease the risk of
level, body-image concerns, physical ability to care catheter-associated infection.19
for the catheter, cognitive function, and caregiver Several strategies have been investigated to
involvement. decrease the risk of catheter-associated sepsis. Use of
full-barrier precautions during catheter insertion
Evidence (mask, cap, sterile gloves, long-sleeve gowns, and sheet
drapes) reduces the incidence of catheter-related infec-
Percutaneously inserted catheters advanced into the tions compared with the use of only sterile gloves and
superior vena cava (SVC) are the route of choice for the small drapes alone.2 Skin preparation with chlorhexi-
delivery of PN. Catheters inserted through the femoral dine results in a lower incidence of microbial coloniza-
veins are associated with higher risk of venous throm- tion of catheters than with povidone iodine.21 Antibi-
bosis and catheter-related sepsis and are not recom- otic prophylaxis during catheter insertion has not been
mended for PN.~1 demonstrated to reduce the incidence of catheter-re-
Access to the SVC can be gained through the internal lated blood stream infection.22 Prophylactic use of anti-
jugular vein, the subclavian vein, or through periph- biotic ointment at the catheter exit site encourages
eral veins in the arm. Internal jugular vein catheters the development of resistant flora and should be
are associated with a higher rate of local hematoma avoided.13,14 No differences in catheter-associated
formation, arterial injury, and catheter-associated sepsis were detected in comparisons of transparent
blood stream infections than subclavian vein cathe- film dressings with gauze dressings. 13
ters. 2,3 Subclavian vein catheters are associated with a Reductions in catheter-associated sepsis have been
higher risk of pneumothorax during insertion than reported when the devices were cared for by specially
internal jugular vein catheters. 2,4 A prospective, ran- trained nurses and when catheter manipulation was
domized trial comparing 102 centrally inserted subcla- minimized. 13 The use of catheters for multiple thera-
vian catheters versus peripherally inserted central peutic and diagnostic purposes, the use of accessory
catheters (PICC) for PN demonstrated a significantly devices (manometers, pressure transducers, flush solu-
higher rate of thrombophlebitis, malposition on inser- tions, stopcocks and &dquo;piggy-back&dquo; infusion sets), and
tion, and difficulties during insertion with PICC lines the infusion of blood products or intravenous medica-
but no difference in overall rate of infection, dislodge- tions increases the risk of bacteremia.13,14 One large
ment, or line occlusion.5 These findings are consistent single institution review found that PN therapy was
with other reports comparing PICC and non-PICC the most important risk factor for developing sepsis.3
venous access in which an increased incidence of local Colonization of catheter hubs as well as the skin sur-
complications, leaking catheters, phlebitis, and malpo- rounding the insertion site are the source of most cath-
sition is noted.6-8 PICCs are used, however, with eter-related infections.l5 Greater catheter hub manip-
increasing frequency in many institutions. It is likely ulation increases the risk for contamination. Catheter
that increased experience with their use will lead to hubs and sampling ports should be disinfected before
decreased complication rates. they are accessed. 13 Early studies of needleless sys-
Catheter tip misplacement during insertion of CVCs tems demonstrated an association between the devel-
is not infrequent. The use of fluoroscopy during cathe- opment of infection, site care, and frequency of end-cap
ter insertion allows immediate repositioning of the changes. Risk factors associated with catheter-related
catheter tip into its correct location in the SVC.9 A blood stream infections included patients who were
chest radiograph should be obtained after the insertion allowed to shower and wet the exit site and weekly
procedure to document catheter placement and rule end-cap changes. The risk of blood stream infection
out a pneumothorax.l A postprocedure chest x-ray decreases with use of rigorous aseptic technique and
yields little benefit if the internal jugular vein or an when end-caps are replaced every 2 days.22,23 A pro-
 37SA

spective study investigating the microbial contamina- results from a prospective, randomized trial. Crit Care Med
tion of needleless connectors and standard entry port 23:52-59, 1995
2. Sznajder JI, Zveibil FR, Bitterman H, et al: Central vein cathe-
caps connected to the hubs of CVCs immediately after
terization, failure and complication rates by three percutaneous
insertion found no difference in contamination rates.24
approaches. Arch Intern Med 146:259-261, 1986
Central venous catheters impregnated with chlor- 3. Mermel L: Central venous catheter-related infections and their
hexidine and silver sulfadiazine or with minocycline prevention: Is there enough evidence to recommend tunneling
and rifampin are associated with a lower rate of for short-term use? Crit Care Med 26:1315-1316, 1998
blood stream infection than untreated catheters.&dquo;, 25 4. Macdonald S, Watt AJ, McNally D, et al: Comparison of technical
success and outcome of tunneled catheters inserted via the jug-
Because of the higher cost of these catheters it is prob-
ular and subclavian approaches. J Vasc Interv Radiol 11:225-
ably reasonable to restrict their use to institutions or 231, 2000
units with particularly high infection rates. 26,27 5. Cowl CT, Weinstock JV, Al-Jurf A, et al: Complications and cost
Clinically relevant catheter-related thrombosis is a associated with parenteral nutrition delivered to hospitalized
late complication of long-term use of CVCs. Occlusion patients through either subclavian or peripherally-inserted cen-
may occur because of the formation of a fibrin sleeve or tral catheters. Clin Nutr 19:237-243, 2000
thrombin sheath, or partial or total vascular mural 6. Duerksen DR, Papineau N, Siemens J, et al: Peripherally
inserted central catheters for parenteral nutrition: A comparison
thrombosis .2 Heparin-bonded catheters have been with centrally inserted catheters. JPEN 23:85-89, 1999
associated with a significant reduction in thrombosis.29 7. Smith JR, Friedell ML, Cheatham ML, et al: Peripherally
Prophylactic use of anticoagulants has been shown to inserted central catheters revisited. Am J Surg 176:208-211,
decrease the risk of catheter-associated venous throm- 1998
8. Ng PK, Ault MJ, Ellrodt AG, et al: Peripherally inserted central
bosis in patients with long-term catheters.3o catheters in general medicine. Mayo Clin Proc 72:225-233, 1997
The selection of a vascular access device for home PN 9. Pomp A, Caldwell MD Feitelson M: Seldinger technique for cen-
involves multiple issues including patient preferences, tral venous catheter insertions, a prospective study of 200 cases.
device characteristics, frequency of infusions, and Clin Nutr 6(Suppl):103, 1987
duration of therapy. Subcutaneously tunneled (Hick- 10. Miller JA, Singireddy S, Maldjian P, et al: A reevaluation of the
man or Broviac) catheters or implanted subcutaneous
radiographically detectable complications of percutaneous
venous access lines inserted by four subcutaneous approaches.
infusion ports are most commonly used for home PN Am Surg 65:125-130, 1999
administration. PICCs are increasingly being used 11. Cardi JG, West JH, Stavropoulos SW: Internal jugular and
because of the ease and economy of bedside placement. upper extremity central venous access in interventional radiol-
No one device has been shown to provide the lowest ogy: Is a post-procedure chest radiograph necessary? Am J
rate of complications with the greatest therapeutic
Roentgenol 174:363-366, 2000
12. Forchielli ML, Gura K, Anessi-Pessina E, et al: Success rates
benefit and ease of maintenance for all patients.31 and cost-effectiveness of antibiotic combinations for initial treat-
ment of central-venous-line infections during total parenteral
I Guidelines nutrition. JPEN 24:119-125, 2000
13. Mermel LA: Prevention of intravascular catheter-related infec-
Parenteral Access tions. Ann Intern Med 132:391-402, 2000
14. Gosbell IB: Central venous catheter related sepsis: epidemiol-
1. Parenteral nutrition should be delivered through ogy, pathogenesis, diagnosis, treatment and prevention. Int Care
World 11:54-59, 1994
a catheter located with its distal tip in the supe- 15. Sitges-Serra A, Girvent M: Catheter-related bloodstream infec-
rior vena cava or right atrium. (A) tions. World J Surg 23:589-595, 1999
2. A chest x-ray should be obtained after catheter 16. Mermel LA, Farr BM, Sherertz RJ, et al: Guidelines for the
insertion unless internal jugular or upper extrem- management of intravascular catheter-related infections. Clin
Infect Dis 32:1249-1272, 2001
ity IV access is obtained by interventional radiol- 17. Pearson ML: Guideline for prevention of intravascular device-
ogy techniques. (B) related infections. Part 1. Intravascular device-related infec-
3. Full-barrier precautions should be used during tions: an overview. The Hospital Infection Control Practices
the insertion of central lines. (B) Advisory Committee. Am J Infect Control 24:262-277, 1996
18. Attar A, Messing B: Evidence-based prevention of catheter infec-
4. Skin preparation before catheter insertion should
tion during parenteral nutrition. Curr Opin Clin Nutr Metab
be performed using chlorhexidine. (B) Care 4:211-218, 2001
5. Catheter hubs and sampling ports should be dis- 19. Cook D, Randolph A, Kernerman P, et al: Central venous cath-
infected before access for medication administra- eter replacement strategies: A systematic review of the litera-
tion and blood drawing. (C) ture. Crit Care Med 25:1417-1424, 1997
20. Raad II, Hohn DC, Gilbreath BJ, et al: Prevention of central
6. Central catheters should not be exchanged rou- venous catheter-related infections by using maximal sterile bar-
tinely over guide wires. (A) rier precautions during insertion. Infect Control Hosp Epidemiol
7. The use of antimicrobial-impregnated catheters is 15:231-238, 1994
recommended in high risk patients and high risk 21. Maki DG, Ringer M Alvarado CJ: Prospective randomized trial
of povidone iodine, alcohol, and chlorhexidine for prevention of
care settings. (B) infection associated with central venous and arterial catheters.
8. Low dose anticoagulant therapy should be used in Lancet 338:339-343, 1991
patients requiring long-term catheterization. (B) 22. Do AN, Ray BJ, Banerjee SN, et al: Bloodstream infection asso-
9. Specialized nursing teams should care for venous ciated with needleless device use and the importance of infec-
access devices in patients receiving PN. (B)
tion-control practices in the home health care setting. J Infect
Dis 179:442-448, 1999
23. Hanchett M, Kung LY: Do needleless intravenous systems
increase the risk of infection? J Intraven Nurs 22:117-121, 1999
REFERENCES
24. Seymour VM, Dhallu TS, Moss HA, et al: A prospective clinical
1. Trottier SJ, Veremakis C, OBrien J, et al: Femoral deep vein study to investigate the microbial contamination of a needless
thrombosis associated with central venous catheterization: connector. J Hosp Infect 45:165-168, 2000
38SA

25. Maki DG, Stolz SM, Wheeler S, et al: Prevention of central come monitoring using end points such as quality of
venous catheter-related bloodstream infection by use of an anti-

septic-impregnated catheter. A randomized, controlled trial. Ann

life, morbidity and mortality, length of hospital stay,
Intern Med 127:257-266, 1997 and cost is much more relevant. There have been
26. Darouiche RO, Raad II, Heard SO, et al: A comparison of two numerous clinical outcome studies of patients receiv-
antimicrobial-impregnated central venous catheters. Catheter ing SNS that utilize nutritional efficacy markers in
study group. N Engl J Med 340:1-8, 1999 their monitoring or reassessment protocols. These
27. Veenstra DL, Saint S, Sullivan SD: Cost-effectiveness of anti-
septic-impregnated central venous catheters for the prevention have included large, prospective randomized trials in
of catheter-related bloodstream infection. JAMA 282:554-560, trauma patients, 10-14 ICU patients,15,16 and perioper-
1999 ative patients. 17 Nitrogen balance, serum proteins, and
28. Arenas-Marquez H, Anaya-Prado R, Barrera-Zepeda LM, et al:
Complications of central venous catheters. Curr Opin Clin Nutr energy balance were most often used in these studies to
Metab Care 4:207-210, 2001 measure nutritional efficacy of the SNS.
29. Marin MG, Lee JC, Skurnick JH: Prevention of nosocomial blood Unfortunately, there are no studies available that
stream infections: Effectiveness of antimicrobrial-impregnated
heparin-bonded central venous catheters. Crit Care Med specifically investigate the effect of monitoring nutri-
28:3332-3338, 2000 tional efficacy of SNS on clinical outcomes (morbidity,
30. Bern MM, Lokich JJ, Wallach SR, et al: Very low doses of mortality, quality of life). That is, there are no studies
warfarin can prevent thrombosis in central venous catheters. A that demonstrate or refute the hypothesis that, &dquo;Clin-
randomized prospective trial. Ann Intern Med 112:423-428,
1990 ical monitoring of patients receiving SNS to assess
31. Orr ME: Vascular access device selection for parenteral nutri- nutritional effects of therapy improves patient out-
tion. Nutr Clin Pract 14:172-177, 1999 comes.&dquo; There are, however, some data suggesting a
relationship between nutrition efficacy monitoring and
MONITORING FOR EFFICACY improved cost-effectiveness. These studies include
three prospective trials. Two randomized trials inves-
Background tigated enhanced SNS versus standard SNS1819 in a
Considerable cost and serious complications are heterogeneous group of patients, and one study looked
associated with specialized nutrition support (SNS). at early EN versus no nutrition intervention in gastro-
Regular monitoring and meticulous care are necessary intestinal surgical patients.2 In all three studies,
to ensure successful outcomes. Monitoring patients nutrition efficacy was monitored and the incidence of
maintained on SNS is necessary to determine efficacy complications was an outcome that was measured. In
of specialized nutrition therapy; detect and prevent all three studies, the intervention groups had signifi-
complications; evaluate changes in clinical condition; cantly fewer complications and lower costs compared
and document clinical outcomes. These guidelines with standard therapy. In one study,18 nitrogen bal-
address monitoring by the health care team to deter- ance was also used as an outcome variable, and posi-
mine efficacy or adequacy of the nutrition therapy with tive nitrogen balance was associated with decreased
attention to specific end points. These endpoints should
costs as well.
be defined based on the patients disease, condition,
Monitored parameters should be compared to the
setting, and wishes.2>3
goals of the nutrition care plan and documented.21
Focused, serial nutrition status reassessment is impor-
Evidence tant. Specifically, nutrient content of SNS adminis-
Once it is determined that a patient will receive tered should be regularly compared with predicted
SNS, goals for the nutrition support should be set with energy and protein needs. Changes in clinical condition
specific markers and outcomes to be measured. These and activity level may require periodic recalculation of
goals may include maintenance or repletion of lean energy requirements. If the patient is not responding
body mass, reduction in morbidity and mortality, appropriately, indirect calorimetry may be used to
improvement in quality of life, or optimization of clin- guide changes in energy intake.22 The patient should
ical outcomes such as reduction of hospital length of be evaluated periodically to determine whether contin-
stay and cost. ued SNS therapy is needed. Readjustments of the
Many studies of patients receiving SNS have used nutrition prescription may be necessary if oral intake
surrogate markers of nutrition status as clinical out- has improved.23,24
comes. Energy balance, body composition analyses,
body weight measurements, anthropometry, serum Practice Guidelines
protein concentrations, protein balance, functional sta- Monitoring; for i
tus, focused physical examination, and growth velocity
(in pediatric patients) are all parameters that have
been used to assess nutrition status and efficacy of 1. Nutrition and outcome goals should be stated in
SNS.24-9 Nitrogen balance has often been used to the nutrition assessment prior to the initiation of
monitor the nutritional efficacy of SNS.47-9 Many of SNS. (C)
these parameters are influenced by ongoing illness or 2. Nutritional and outcome parameters should be
injury, and thus it may not clearly reflect changes in measured serially during SNS therapy. (B)
the individuals nutritional status. Nutritional status, 3. Periodic comparison of nutritional and outcome
however, is an intermediate marker; the ultimate goal measures with SNS goals should occur to monitor
of SNS is to improve clinical outcomes. Clinical out- efficacy of therapy. (C)
 39SA

REFERENCES 23. A.S.P.E.N: Board of Directors. Guidelines for the use of paren-
teral and enteral nutrition in adult and pediatric patients. JPEN
1. A.S.P.E.N Board of Directors: Standards of practice: Nutrition 17:1SA-52SA, 1993
support nurse. Nutr Clin Pract 16:56-62, 2001 24. A.S.P.E.N: Board of Directors. Clinical Pathways and Algo-
2. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in rithms for Delivery of Parenteral and Enteral Nutrition Support
clinical practice: Review of published data and recommendations in Adults. A.S.P.E.N., Silver Spring, MD, 1998
for future research directions. JPEN 21:133-156, 1997
3. A.S.P.E.N Board of Directors: Standards for nutrition support
physicians. Nutr Clin Pract 11:235-240, 1996 MONITORING FOR COMPLICATIONS
4. Church JM, Hill GL: Assessing the efficacy of intravenous nutri-
tion in general surgical patients: Dynamic nutritional assess-
Background
ment with plasma proteins. JPEN 11:135-139, 1987
5. Bernstein LH, Leukhardt-Fairfield CJ, Pleban W, et al: Useful-
Although SNS can be a useful and life-saving ther-
apy in a variety of settings, both EN and PN may cause
ness of data on albumin and prealbumin concentrations in deter-

mining effectiveness of nutritional support. Clin Chem 35(2): significant complications. These complications can be
271-274, 1989 minimized through diligent patient monitoring by
6. Sawicky CP, Nippo J, Winkler MF, et al: Adequate energy intake nutrition support professionals.
and improved prealbumin concentration as indicators of the
response to total parenteral nutrition. J Am Diet Assoc 92(10): Evidence
1266-1268,1992
7. Fletcher JP, Little JM, Guest PK: A comparison of serum trans-
ferrin and serum prealbumin as nutritional parameters. JPEN
The refeeding syndrome is a complication that may
11(2):144-147, 1987
arise during aggressive administration of SNS. 1,2
8. Starker PM, LaSala PA, Forse RA, et al: Response to total Although more commonly reported in association with
parenteral nutrition in the extremely malnourished patient. PN, the refeeding syndrome may also occur in the
JPEN 9(3):300-302, 1985 setting of EN and even oral feeding. The refeeding
9. Iapichino G, Radrizzani D, Solca M, et al: The main determi- syndrome can be life threatening if not treated
nants of nitrogen balance during total parenteral nutrition in
critically ill injured patients. Intensive Care Med 10(5):251-254,
promptly. At greatest risk for the syndrome are chron-
1984 ically, semistarved marasmic patients whose bodies
10. Moore EE, Jones TN: Benefits of immediate jejunostomy feeding have adapted largely to use of free fatty acids and
after major abdominal trauma: a prospective, randomized study. ketone bodies as energy sources. Rapid reintroduction
J Trauma 26:874-881, 1986 of large amounts of carbohydrate feedings can result in
11. Moore FA, Moore EE, Kudsk KA, et al: Clinical benefits of an
metabolic abnormalities, including hypophosphatemia,
immune-enhancing diet for early postinjury enteral feeding.
J Trauma 37(4):607-615, 1994 hypokalemia, and hypomagnesemia. In particular,
12. Kudsk KA, Croce MA, Fabian TC, et al: Enteral vs. parenteral hypophosphatemia has been considered a hallmark of
feeding: Effects on septic morbidity after blunt and penetrating the refeeding syndrome. Hypophosphatemia is associ-
abdominal trauma. Ann Surg 215(5):503-513, 1992 ated with the hematologic, neuromuscular, cardiac,
13. Bastow MD, Rawlings J, Allison SP: Benefits of supplementary
tube feeding after fractured neck of femur: A randomized con-
and respiratory dysfunction in severe cases. Another
trolled trial. British Med J 287:1589-1592, 1983 common sequelum of the refeeding syndrome is fluid
14. Taylor SJ, Fettes SB, Jewkes C, et al: Prospective, randomized, retention due to the antinatriuretic effect of increased
controlled trial to determine the effect of early enhanced enteral insulin concentrations. Sudden expansion of extracel-
nutrition on clinical outcome in mechanically ventilated patients
lular fluid can lead to cardiac decompensation in
suffering head injury. Crit Care Med 27(11):2594-2595, 1999
15. Bower RH, Cerra FB, Bershadsky B, et al: Early enteral admin- severely marasmic patients. Alternatively, administra-
istration of a formula (Impact) supplemented with arginine, tion of dextrose may cause significant hyperglycemia,
nucleotides, and fish oil in intensive care unit patients: Results which may in turn result in osmotic diuresis and de-
of a multicenter, prospective, randomized, clinical trial. Crit
Care Med 23(3):436-449, 1995
hydration. Close monitoring of serum phosphate,
16. Montecalvo MS, Steger KA, Farber HW, et al: Nutritional out- magnesium, potassium, and glucose are imperative
come and pneumonia in critical care patients randomized to when SNS is initiated, particularly in malnourished
gastric versus jejunal tube feedings. Crit Care Med 20(10):1377- patients.3
1387, 1992 Bothhyperglycemia and hypoglycemia are potential
17. VA Total Parenteral Nutrition Cooperative Study Group: Peri-
operative total parenteral nutrition in surgical patients. N Engl complications of SNS. In one study, the incidence of
J Med 325(8):525-532, 1991 hyperglycemia (defined as a blood glucose greater than
18. MacBurney M, Young LS, Ziegler TR, et al: A cost-evaluation of 200 mg/dL) during PN was 7% in patients given less
glutamine-supplemented parenteral nutrition in adult bone than or equal to 5 mg/kg per minute of dextrose,
marrow transplant patients. J Am Diet Assoc 94(11):1263-1266,
whereas 49% of patients receiving greater than 5
1994
19. Senkal M, Zumtobel V, Bauer KH, et al: Outcome and cost- mg/kg per minute of dextrose developed hyperglyce-
effectiveness of perioperative enteral immunonutrition in mia. In this study, patients with a history of diabetes
patients undergoing elective upper gastrointestinal tract sur- mellitus or glucose intolerance, patients receiving sys-
gery: A prospective randomized study. Arch Surg 134(12):1309- temic corticosteroids, and patients with sepsis or mul-
1316, 1999
tisystem organ failure were excluded; the incidence of
20. Hedberg AM, Lairson DR, Aday LA, et al: Economic implications
of an early postoperative enteral feeding protocol. J Am Diet hyperglycemia would be expected to be even higher in
Assoc 99(7): 802-807, 1999 these patients. The extreme scenario of hyperglycemia
21. A.S.P.E.N: Board of Directors: Standards for nutrition support: is hyperosmolar hyperglycemic state (hyperosmolar
Hospitalized patients. Nutr Clin Pract 10:208-219, 1995 nonketotic coma). Mortality has been quoted to be 0%
22. Skipper A, Millikan KW: Parenteral nutrition implementation
and management. IN Merritt RJ (ed). The A.S.P.E.N. Nutrition
in patients less than 50 years of age and 14% in those
more than 50 years of age.~ Harbingers of impending
Support Practice Manual. A.S.P.E.N., Silver Spring, MD, 1998,
pp 9.1-9.9 hyperosmolar hyperglycemic state include elevated
40SA

blood glucose and osmolality in the absence of ketones. lestasis typically occurs later (months or years) in the
Confusion, dizziness, lethargy, and other neurologic course of therapy. Hepatic steatosis is reversible with

signs may precede frank obtundation and coma. Peri- discontinuation of PN. The chronic, irreversible, chole-
odic clinical examinations and close monitoring of static liver disease sometimes seen with long-term PN
blood glucose and urine glucose can minimize these can lead to liver failure and death. Many potential
complications. etiologic factors for these liver abnormalities have been
Patients with pre-existing diabetes or significant postulated; the cause is generally multifactorial. Care-
physiologic stress may develop hyperglycemia upon ful monitoring of liver function tests can help to iden-
initiation of PN. Because hyperglycemia has been tify these problems early, when changes in PN pre-
shown to be associated with decreased measures of scription may allow resolution.
immune function and increased risk of infectious com- Metabolic bone disease, which may present with
plications, efforts to monitor and control blood glucose bone pain and fractures, occurs with unknown fre-
during SNS are prudent.66 quency in patients receiving PN.12 Early studies
Rebound hypoglycemia upon discontinuation of par- revealed an incidence of 29% or more in long-term
enteral nutrition has been reported, although this is an patients. Recent availability of rapid, reproducible and
extremely uncommon event. Some experts continue to relatively inexpensive techniques for measuring bone
recommend that, particularly for patients receiving density should help to recognize this complication
large amounts of insulin along with their PN, the PN early. Risk factors for development of metabolic bone
infusion rate be cut in half for the last two hours prior disease include chronic systemic glucocorticoid use,
to discontinuation. This approach can avoid the need short bowel syndrome, menopause, and positive family
for careful blood glucose monitoring during discontin- history of bone disease; patients with these and other
uation of PN. risk factors should be closely monitored. ~3
Acid-base abnormalities are commonly seen in the Vascular access sepsis in patients receiving PN is a
patient receiving SNS. In a quality assurance study common complication. There is no monitoring that can
from a busy nutrition support service based in a large be routinely performed to detect the development of
hospital, found carbon dioxide content was abnormal sepsis prospectively. Careful symptomatic and labora-
up to 13% of the time. In the same study, blood chloride tory monitoring (fever, constitutional symptoms, tech-
values were unacceptable between 1% and 7% of the nical complications with the vascular access device,
time.7 In most cases, severe abnormalities are not due hyperglycemia) can help recognize an episode of sepsis
to the nutrition regimen itself but rather to the early.
patients underlying condition. Many of the current Gastroesophageal reflux and pulmonary aspiration
commercially available intravenous amino acid solu- are potential complications of EN. Significant aspira-
tions contain large amounts of endogenous acetate, tion can lead to pneumonia and death in an already
which tend to be alkalinizing. Metabolic acid-base debilitated patient; aspiration is considered to be one of
abnormalities may at least partially be addressed by the most serious complications of EN. Although post-
manipulating the acetate and chloride content of the pyloric feedings are frequently preferred by clinicians
PN solution. Periodic monitoring of serum electrolytes over gastric feedings in patients with impaired gag
can avoid problems before they pose a danger to the reflex or neurologic compromise, hard evidence to sup-
patient. port that aspiration risk is decreased by postpyloric
Hypertriglyceridemia may occur in some patients tube placement is lacking.14,15 Two factors commonly
receiving intravenous fat emulsion; if unnoticed and quoted as putting a patient at risk for aspiration are
untreated, this may lead to the development of pancre- presence of a nasoenteric feeding tube and supine
atitis and altered pulmonary function. These compli- patient positioning. Lack of a truly reliable bedside
cations can be avoided by prudent monitoring of serum method for detection of aspiration makes study of this
triglyceride levels during the administration of fat- complication difficult. Increasing gastric residuals and
containing PN. vomiting are warning signs that aspiration may occur,
Excessive carbon dioxide production in patients although aspiration may be asymptomatic especially in
receiving SNS may lead to difficulty with ventila- an obtunded patient.

tory support and weaning. This complication occurs Gastrointestinal complications are common during
less commonly now than in the past with the use of EN. Depending on the definition used, the incidence of
less aggressive feeding regimens. Early literature diarrhea occurs in 21% to 72% of patients receiving
attributed the excess carbon dioxide production to EN.16 In this study, the frequency of overall enteral
overfeeding with dextrose calories.9 Subsequently it feeding patient days in which diarrhea occurred was
was found that reduced energy administration typ- 2% to 26%, again varying with the definition of diar-
ical of current PN and EN regimens does not cause rhea. 16 Severe diarrhea can lead to life-threatening
significant carbon dioxide overproduction.l A fluid and electrolyte abnormalities. Common causes of
warning sign of excessive carbon dioxide production diarrhea in this population include concomitant medi-
is an elevation in the respiratory quotient as mea- cations (eg, sorbitol-containing medications, prokinetic
sured by indirect calorimetry, (especially if this agents), underlying illness predisposing to malabsorp-
value exceeds unity). tion, and Clostridium difficile colitis. Tube feeding-
Hepatobiliary complications may arise during related causes may include enteral feeding formula
administration of PN.l1 The incidence is uncertain. content (eg, fiber or lactose content) and administra-
Steatosis or fatty liver may occur early, whereas cho- tion technique. Contamination of enteral feeding
 41SA

tubes, delivery sets, and formula with microbes can REFERENCES

occur. Studies have looked at the frequency and impor- 1. Solomon SM, Kirby DF: The refeeding syndrome: A review.
tance of such contamination. Issues investigated JPEN 14:90-97, 1990
2. Brooks MJ, Melnik G: The refeeding syndrome: An approach to
included the use of tap versus sterile water to recon-
stitute formulas or rinse tubing, whether enteral deliv- understanding its complications and preventing its occurrence.
Pharmacotherapy 15:713-726, 1995
ery sets, were rinsed and the length of time delivery 3. Marik P, Bedigian MK: Refeeding hypophosphatemia in criti-
sets were utilized. 17 There is no consensus on optimiz- cally ill patients in an intensive care unit: A prospective study.
Arch Surg 131:1043-1047, 1996
ing many of these variables. 4. Rosmarin DK, Wardlaw GM, Mirtallo J: Hyperglycemia associ-
ated with high, continuous infusion rates of total parenteral
Practice ,.. nutrition dextrose. Nutr Clin Pract 11:151-156, 1996
5. Kaminski MV Jr: A review of hypersomolar hyperglycemic non-
Monitoring; l i i i i ketonic dehydration (HHND): Etiology, pathophysiology and
prevention during intravenous hyperalienation. JPEN 2(5):690-
1. Malnourished patients at risk for refeeding syn- 698, 1978
6. McMahon MM, Rizza RA: Nutrition support in hospitalized
drome should have serum phosphorus, magne-
patients with diabetes mellitus. Mayo Clinic Proc 71:587-594,
sium, potassium and glucose levels monitored 1996
closely at initiation of SNS. (B) 7. Owens JP, Geibig CB, Mirtallo JM: Concurrent quality assur-
ance for a nutrition-support service. Am J Hosp Pharm 46:2469-
2. In patients with diabetes or risk factors for glu-
2476, 1989
cose intolerence, SNS should be initiated with a 8. Sacks GS: Is IV lipid emulsion safe in patients with hypertri-
low dextrose infusion rate and blood and urine glyceridemia? Adult patients. Nutr Clin Pract 12:120-123, 1997
9. Askanazi J, Nordenstrom J, Rosenbaum SH, et al: Nutrition for
glucose monitored closely. (C) the patient with respiratory failure. Anesthesiology 54:373, 1981
3. Blood glucose should be monitored frequently 10. Talpers SS, Romberger DJ, Bunce SB, et al: Nutritionally asso-
upon initiation of SNS, after any change in insu- ciated increased carbon dioxide production. Excess total calories
lin dose, and until measurements are stable. (B) vs. high proportion of carbohydrate calories. Chest 102:551-555,

4. Serum electrolytes (sodium, potassium, chloride, 1992

11. Quigley EMM, Marsh MN, Shaffer JL, et al: Hepatobiliary com-
and bicarbonate) should be monitored frequently
plications of total parenteral nutrition. Gastroenterology 104:
upon initiation of SNS until measurements are 286-301, 1993
stable. (B) 12. Jeejeebhoy KN: Metabolic bone disease and total parenteral
nutrition: A progress report. Am J Clin Nutr 67:186-187,
5. Patients receiving intravenous fat emulsion
1998
should have serum triglyceride levels monitored 13. Seidner DL, Licata A: Parenteral nutrition-associated metabolic
until stable and when changes are made in the bone disease: Pathophysiology, evaluation, and treatment. Nutr
amount of fat administered. (C) Clin Pract 15:163-170, 2000
14. Lazarus BA, Murphy JB, Culpepper L: Aspiration associated
6. Liver function tests should be monitored periodi- with long-term gastric versus jejunal feeding: A critical analysis
cally in patients receiving PN. (A) of the literature. Arch Phys Med Rehabil 71:46-53, 1990
7. Bone densitometry should be performed upon ini- 15. Elpern EH: Pulmonary aspiration in hospitalized adults. Nutr
Clin Pract 12:5-13, 1997
tiation of long-term SNS and periodically thereaf-
16. Bliss DZ, Guenter PA, Settle RG: Defining and reporting diar-
ter. (C) rhea in tube-fed patients-what a mess! Am J Clin Nutr 55:753&mdash;
8. Postpyloric placement of feeding tubes should be 759, 1992
considered in patients at high risk for aspiration 17. Eisenberg PG: Causes of diarrhea in tube-fed patients: A com-
who are receiving EN. (C) prehensive approach to diagnosis and management. Nutr Clin
Pract 8:119-123, 1993
 Section IX: Drug-Nutrient Interactions

DRUG-NUTRIENT INTERACTIONS tions should not be crushed for administration via a

Background feeding tube. Occasionally, patients with feeding
tubes may be able to swallow oral medications, avoid-
Medications are frequently prescribed for patients ing potential bioavailability and mechanical tube prob-
receiving SNS. Unrecognized interactions between lems.
drugs and nutrients may lead to unexpected, poor out- Medications may be added to PN formulations in an
comes.2 Some interactions may be acute in onset.33 effort to decrease fluid requirements, reduce the need
Other interactions may develop over years before they for Y-site injections, reduce the possibility of line con-
become evident (eg, osteoporosis). A drug nutrient tamination due to manipulation, and decrease labor
interaction involves the alteration of the kinetics or time required for drug administration. Although these
reasons may seem compelling, the physiochemical
dynamics of a drug or nutritional element or a compro-
mise in nutrition status as a result of the action or side complexity of PN formulations makes their interac-
effect of a drug. Both the kinetic (absorption, metabo- tions with parenteral medications a very challenging
lism, disposition, or elimination) and/or the dynamic compatibility dilemma. A recent publication on safe
effect (clinical/physiological) of a drug (eg, phenytoin) practices for PN formulations emphasizes the number
and complexity of problems that have been reported.9
or a nutritional element (eg, folic acid) may be altered
The most common factors influencing compatibility of
as a result of the interaction. Decreased tetracycline
PN formulations with drugs include the drug pH,
absorption caused by complex with dairy products is a solubility, concentration, light sensitivity, and spe-
well-known interaction. Reduced elimination of potas- cific formulation. 10 Published information regard-
sium by cyclosporine and spironolactone and retention
of lithium by a sodium-rich diet are also examples of ing drug-PN physical incompatibilities in these
instances is limited, and applying the available in-
drug-nutrient interactions of this type. formation to a given patients needs is difficult due
Direct physical contact between drug molecules and
to the variety of medication concentrations used
nutrition elements in either the delivery system (eg,
infusion tubing and/or bags) or during the compound- clinically.11,12
ing process is an interaction that takes place outside of Evidence
the body. These are the most commonly observed inter-
actions in nutrition support patients. They are charac- Schneider and Mirtallol found that over 75% of the
terized by a hydrolytic process involving the direct drugs administered to 600 patients receiving PN were
mixing of an EN formula and the vehicles used in oral capable of interfering with SNS. Drug-nutrient inter-
liquid medications (eg, syrup),5 physical incompatibil- actions result in derangements in fluid and electrolyte
ity between intravenously administered drugs and PN homeostasis, changes in vitamin status, and distur-
admixtures, or the addition of a drug into an infusion bances in acid-base balance. 13 Recognition of these
device containing intravenous lipid emulsion resulting drug-nutrient interactions may assist the clinician to
in the disruption of the emulsion.7 prevent metabolic complications and to achieve desired
In the absence of parenteral access and an inability therapeutic outcomes.
to take medications orally, the feeding tube invariably Alteration in sodium homeostasis is a common elec-
becomes a route for medication delivery. Medications trolyte disorder induced by medications. In one study,
are available in multiple dosage forms: solid (tablets, almost 20% of all hypernatremic episodes identified
capsules), and liquid (elixirs, syrups, suspensions, during hospitalization were related to EN and PN.14
solutions) enteral forms; and parenteral forms. Most Parenteral medications available as sodium salts and
solid dosage forms require manipulation for adminis- delivered in normal saline are factors that contribute
tration via enteral feeding tubes. Dosage forms of med- to hypernatremia. Drugs may stimulate
ications are developed to maintain the integrity of the inappropriate
secretion of antidiuretic hormone. Renal 15,1 and gas-
drug product and facilitate its bioavailability. Any trointestinal 13 losses of sodium are frequent causes of
manipulation of the tablet, capsule, or liquid may influ- hyponatremia.
ence drug bioavailability; this needs to be considered Hypophosphatemia occurs in 20% to 40% of patients
when delivering drug therapy by the enteral tube. For receiving SNS.17 Certain agents, such as some antacids
example, sustained release or enteric-coated prepara- or sucralfate, can bind phosphorus in the gastroin-

42SA
 43SA

testinal tract and decrease serum phosphate con- ;I37C) and pH values (formulation pH of 6.0 versus
centrations. Urinary phosphate excretion is increased ]physiologic pH of 7.4) than that of the solution.27
by corticosteroids and thiazide diuretics, sometimes The physical compatibility of 102 drugs with 2-in-l
necessitating phosphate supplementation. Insulin PN solutions in a manner that simulates y-site admin-
administration may also cause a shift of phosphate into istration has been evaluated.&dquo; It was found that 20
the intracellular space. ,
drugs (including commonly used drugs such as ampho-
Hyperglycemia is a common metabolic complication tericin B, acyclovir, sodium bicarbonate, and cipro-
of SNS. Management of this problem with insulin or floxacin) were
incompatible with the PN solutions,
dietary modification of glucose intake is a difficult chal- resulting in formation of precipitates, haziness, or dis-
lenge that can be complicated by medications that coloration. The physical compatibility of 106 drugs
interfere with pancreatic function (eg, cyclosporine A)
with 3-in-l PN admixtures in a manner simulating
or stimulate gluconeogenesis (eg, corticosteroids).1819
Continuous infusions of propofol can lead to adminis- y-site administration was also studied.l2 It was found
tration of significant calories and to hypertriglycer- that 23 drugs were incompatible with the admixtures
idemia. 20 either by formation of a precipitate or emulsion disrup-
Occlusion of the feeding tube is a frequent complica- tion with separation of oil and water phases. Many of
tion of EN. Administration of syrups, medications with the incompatibilities were observed immediately after
a low pH, or oleaginous liquid medications can disrupt mixing, which is different than observed with the
the stability of the EN formula and cause enteral tube 2-in-1 solutions. It is interesting to note that compati-
occlusion.5 Liquid medications may be preferred for bility differed for 3-in-l admixtures versus 2-in-1 solu-
patients with feeding tubes. However, gastrointestinal tions, emphasizing that compatibility in one formula-
intolerance has been observed with liquid medications tion does not predict compatibility in the other. It is
that are hyperosmolar,21 contain sorbitol, or contain also worth noting that many of these interactions and
other ingredients like polyethylene glycol.22 Limiting incompatibilities may be noted simply by careful
sorbitol intake is difficult since it is not a requirement inspection of the PN formulas for precipitates, discol-
for the manufacturer to list its presence on the medi- oration, haziness, or breaking of the emulsion.9
cation label.
Bioavailability of medications administered via
enteral feeding tubes is a concern. The EN formula Special Considerations
itself may influence medication bioavailability. The EN Drug-nutrient interactions involve a myriad of real
formula or a component can adversely effect the and potential problems in patients receiving SNS. So
absorption, metabolism or excretion of a medication; common are some that reporting their clinical conse-
this has been observed with phenytoin.2 All medica-
quences is not pursued. As such, this limits the evi-
tions given directly into the stomach, duodenum or dence needed to
develop comprehensive guidelines. For
jejunum require an appropriate fluid flush (water, nor- PN, each institution, whether providing acute or
mal saline) before and after each administration. Leff
chronic care, has different compounding methods.
and Roberts23 found that drug bioavailability improved
These institutional practices often vary from the meth-
when proper flushing techniques were used.
in published compatibility trials. The order of
Diarrhea is a frequent complication of EN. The inci- ods used
dence of this complication is increased in patients mixing of the components of PN may also differ and
affect compatibility. Incompatibilities are also more
receiving antibiotics. Guenter et a124 found that diar-
rhea occurred in 41% of enteral tube fed patients common at higher drug concentrations. Guidelines for
receiving antibiotics versus 3% in those that did not. In compounding and professional practices intended to
the antibiotic group with diarrhea, 50% of stool cul- foster consistent procedures and processes have been
tures were positive for Clostridium difficile toxin. published and should be followed. For co-administra-
This is a frequent complication that complicates the tion of medications with PN, the United States Phar-
use of EN. macopeia provides specific recommendations that
Physical incompatibilities in PN solutions may lead address not only compatibility but also efficacy.28
to patient death. This has occurred as a result of pul- Finally, long-term PN formula stability (>48 hours)
monary deposition of calcium phosphate precipitates.25 and compatibility data are sparse, especially in the
Intravenous administration of substantial amounts of home care environment, and are in need of further
large (>5 pLm) particles resulting from an incompati- research.
bility is dangerous and potentially life threatening and
must be considered when evaluating compatibility Practice Guidelines
.

issues with PN. It should also be noted that once a

/ . , interactions
precipitate has formed, it is highly unlikely it will
redissolve, especially calcium phosphate. 26 Further,
there may be pharmaceutical factors in the patient 1. Medication profiles of patients receiving SNS
environment that promote incompatibilities. For should be reviewed for potential effects on nutri-
example, excessive heat and light (direct sunlight) can tion and metabolic status. (B)
initiate incompatibilities. Incompatibilities have also 2. Medications co-administered with EN should be
been reported to occur when PN is administered to reviewed periodically for potential incompatibili-
patients with higher core temperatures (25C versus ties. (B)
44SA

3. When medications are administered via an 10. Anonymous: Parenteral admixture incompatibilities: An intro-
duction. Int J Pharm Compound 1:165-167, 1997
enteral feeding tube, the tube should be flushed 11. Trissel LA, Gilbert DL, Martinez JF, et al: Compatibility of
before and after each medication is adminis- parenteral nutrient solutions with selected drugs during simu-
tered. (B) lated Y-site administration. Am J Health-Syst Pharm 54:1295-
4. Liquid medication formulations should be used, 1300, 1997
12. Trissel LA, Gilbert DL, Martinez JF, et al: Compatibility of
when available, for administration via enteral medications with 3-in-1 parenteral nutrition admixtures. JPEN
feeding tubes. (C) 23:67-74, 1999
5. EN patients who develop diarrhea should be eval- 13. Driscoll DF: Drug-induced metabolic disorders and parenteral
uated for antibiotic-associated causes, including nutrition in the intensive care unit: a pharmaceutical and met-
abolic perspective. Drug Intell Clin Pharm 23:363-371, 1989
C. difficile. (B) 14. Snyder NA, Feigal DW, Arieff AI: Hypernatremia in elderly
6. Co-administration or admixture of medications patients: A heterogeneous, morbid, and iatrogenic entity. Ann
known to be incompatible with PN should be pre- Intern Med 107:309-319, 1987
vented. (A) 15. Nanji AA: Drug-induced electrolyte disorders. Drug Intell Clin
Pharm 17:175-185, 1983
7. In the absence of reliable information concerning 16. Sunyecz L, Mirtallo JM: Sodium imbalance in a patient receiving
compatibility of a specific drug with an SNS for- total parenteral nutrition. Clin Pharm 12:138-149, 1993
mula, the medication should be administered sep- 17. Sacks GS, Walker J, Dickerson RN, et al: Observations of
arately from the SNS. (B) hypophosphatemia and its management in nutrition support.
8. Each PN formulation compounded should be Nutr Clin Pract 9:105-108, 1994
18. Pandit MK, Burke J, Gustafson AB, et al: Drug-induced disor-
inspected for signs of gross particulate contami- ders of glucose tolerance. Ann Intern Med 118:529-539, 1993
nation, discoloration, particulate formation, and 19. Knapke CM, Owens JP, Mirtallo JM: Management of glucose
phase separation at the time of compounding and abnormalities in patients receiving total parenteral nutrition.
before administration. (B) Clin Pharm 8:136-144, 1989
20. Lowery TS, Dunlap AW, Brown RO, et al: Pharmocologic influ-
ence on nutrition support therapy: Use of propofol in a patient

REFERENCES receiving combined enteral and parenteral nutrition support.

Nutr Clin Pract 1996:147-149
1. Schneider PJ, Mirtallo JM: Medication profiles in TPN patients. 21. Dickerson RN, Melnik G: Osmolality of oral drug solutions and
Nutr Supp Serv 3:40-46, 1983 suspensions. Am J Hosp Pharm 45:832-834, 1988
2. Gauthier I, Malone M: Drug-food interactions in hospitalized 22. Lutomski DM, Gora ML, Wright SM, et al: Sorbitol content of
patients. Methods of prevention. Drug Saf 18(6):383-393, 1998 selected oral liquids. Ann Pharmacother 27:269-274, 1993
3. Bauer LA: Interference of oral phenytoin absorption by continu- 23. Leff RD, Roberts RJ: Enteral drug administration practices:
ous nasogastric feedings. Neurology 132(5):570-572, 1982 report of a preliminary survey. Pediatrics 81:549-551, 1988
4. Shane E, Rivas M, McMahon DJ, et al: Bone loss and turnover 24. Guenter PA, Settle G, Perlmutter S, et al: Tube feeding-related
after cardiac transplantation. J Clin Endocrinol Metab 82(5): diarrhea in acutely ill patients. JPEN 15:277-280, 1991
1497-1506, 1997 25. Food and Drug Administration: Safety Alert: Hazards of precip-
5. Cutie AJ, Altman E, Lenkel L: Compatibility of enteral products itation associated with parenteral nutrition. Am J Hosp Pharm
with commonly employed drug additives. JPEN 7:186-191, 1983 51:1427-1428, 1994
6. Niemiec PW, Vanderveen TW: Compatibility considerations in 26. Allwood MC, Kearney MC: Compatibility and stability of addi-
parenteral nutrient solutions. Am J Hosp Pharm 41:893-911, tives in parenteral nutrition admixtures. Nutrition 14:697-706,
1984 1998
7. Bullock C, Clark JH, Fitzgerald JF, et al: The stability of ami- 27. Robinson LA, Wright BT: Central venous catheter occlusion
kacin, gentamicin, and tobramycin in total nutrient admixtures. caused by body-heat-mediated calcium phosphate precipitation.
JPEN 13:505-509, 1989 Am J Hosp Pharm 39:120-121, 1982
8. Mitchell JF: Oral dosage forms that should not be crushed, 1998 28. Total parenteral nutrition/total nutrient admixture. USP DI
update. Hosp Pharm 33:399-415, 1998 Update, Vol I and II. United States Pharmacopeial Convention
9. National Advisory Group on Standards and Practice Guidelines Inc, Rockville, MD, 1996, pp 66-71
for Parenteral Nutrition: Safe practices for parenteral nutrition 29. Chan, L: Redefining drug-nutrient interactions. NCP 15(5):245-
formulations. JPEN 22:49-66, 1998 252, 2000
 SECTIONX: Life Cycle and Metabolic Conditions

PREGNANCY Research Council has established recommended daily

allowances (RDAs) for oral intake. Pregnant women
Background should receive approximately 300 additional calories
The correlation between maternal nutrition and per day during the second and third trimester to meet
healthy babies has been well established. Adequate the increased demands of pregnancy.~ An additional 10
nutrition before and during pregnancy is necessary to to 14 g of protein per is needed to support fetal
achieve optimal health of the pregnant mother and her day
growth and development. Conditions such as physio-
baby. Maternal malnutrition can have a profound logic stress, trauma, and sepsis may require increased
effect on the growth and development of the unborn intake of calories and protein to achieve the desired
child and lead to poor pregnancy outcomes, including weight gain.
low-birth-weight infants, intrauterine growth retarda- Women with symptoms affecting nutrient intake,
tion, and increased prenatal morbidity and mortal- evidence of fluid and/or electrolyte imbalance or who
ity.2,3 Women with a low prepregnancy weight-for- are unable to achieve adequate weight gain during
height are at greatest risk for giving birth to a low- pregnancy are at nutrition risk and should undergo
birth-weight1 infants when maternal weight gain is formal nutrition assessment with development of a
inadequate nutritioncare plan.4 In addition to the nutrition
During normal pregnancy, nutrient absorption is not assessment data obtained for nonpregnant patients,
adversely affected. Conditions that may impair absorp- prepregnancy weight, weight history during preg-
tion, have an impact on gastrointestinal function, or nancy, measurement of fundal height, fetal ultra-
increase the demand for nutrients during pregnancy sound, and urine ketones are useful in evaluation of
include hyperemesis gravidarum, pancreatitis, chole- nutrition status and fetal growth. The interpretation
cystitis, motility disorders, small bowel obstruction, of biochemical indices for assessment of nutrition sta-
inflammatory bowel disease, short bowel syndrome, tus must allow for changes in values associated with
and trauma. the normal physiologic changes of pregnancy.4
Indications for SNS in pregnancy are the same as for
Evidence nonpregnant patients. If the gastrointestinal tract is
Maternal weight gain is indicator of the ade-
functional, EN should be considered before initiating
a key PN. Russo-Stieglitz et al6 evaluated the perinatal out-
quacy of maternal and fetal nutrition status.4 Current comes and complications of PN in pregnancy. Sixteen
recommendations for optimum weight gain during of 26 patients required PN for hyperemesis gravida-
pregnancy are based on body mass index (BMI = rum. They reported favorable fetal outcomes. Maternal
weight (kg)/height2 (m2)).. Normal BMI values range complications included hyperglycemia and central
from 20 to 26; a value greater than 26 or less than 20
venous catheter complications. Large controlled stud-
is designated as overweight or underweight, respec- ies are lacking; however, numerous case reports sup-
tively.~ The Committee on Nutritional Status and port the safety and effectiveness of PN during
Weight Gain During Pregnancy recommends a total pregnancy.
weight gain of 28 to 40 pounds for underweight women
compared with a gain of 15 to 25 pounds for overweight Special Considerations
women. Normal weight women are encouraged to gain
25 to 35 pounds. The rate of weight gain should be 2 to When conventional approaches using diet mod-
5 pounds (total) in the first trimester, increasing to 0.5 ifications and supplementations to attain adequate
to 1 pound each week in the second and third tri- weight gain are unsuccessful, SNS may become
mesters. Teenagers who are within 2 years postmen- necessary.
arche and black women should gain in the upper range Maternal hyperglycemia is associated with
to reduce the prevalence of low-birth-weight infants in increased fetal morbidity. 17-20 Maternal blood glucose
these groups. The recommendation for women bearing levels should be maintained within the range of
twins is 35 to 45 pounds. approximately 90 to 120 mg/dL. 17 Blood glucose mon-
Additional calories and protein are required during itoring should be performed during and after SNS
pregnancy to meet the demands of both mother and infusions.
fetus and achieve optimum weight gain. The National Maternal folic acid deficiency contributes to the

45SA
46SA

development of neural tube defects. The United States 10. Charlin V,

Borghesi L, Hasbun, et al: Parenteral nutrition in
Public Health Service recommends that all women who hyperemesis gravidarum. Nutrition 9(1): 29-32, 1993
11. Caruso A, De Carolis S, Ferrazzani S, et al: Pregnancy outcome
are capable of becoming pregnant should consume 0.4
and total parenteral nutrition in malnourished pregnant women.
mg/d of folic acid for the purpose of reducing their risk Fetal Diagn Ther 13:136-140, 1998
of having a pregnancy affected with neural tube 12. Hatjis CG, Meis PJ: Total parenteral nutrition in pregnancy.
defects. Specific folate supplementation is recom- Obstet Gynecol 66(4):585-588, 1985
13. Greenspoon JS, Rosen DJD, Ault M: Use of the peripherally
mended for women who previously have had an infant inserted central catheter for parenteral nutrition during preg-
or fetus with a neural tube defect. These women should
nancy. Obstet Gynecol 81(5):831-834, 1993
be advised to take supplemental folic acid, 0.4 mg/d, at 14. Mamel JJ, Kuznicki M, Carter M, et al: Total parenteral nutri-
the time they decide to become pregnant. 21 Pregnant tion during pregnancy in a patient requiring long-term nutrition
women should consume 0.6 mg/d of folate.22 support. Nutr Clin Pract 13:123-128, 1998
15. Wolk RA, Rayburn WF: Parenteral nutrition in obstetric
There is no apparent correlation between premature patients. Nutr Clin Pract 5:139-152, 1990
labor or increased uterine irritability and lipid infu- 16. Watson LA, Bommarito AA, Marshall JF: Total peripheral par-
sion using currently available soybean and soybean/ enteral nutrition in pregnancy. JPEN 14(5):485-489, 1990
safflower lipid emulsions. 6,9,23,24 17. Moore TR: Diabetes in pregnancy. In Maternal-Fetal Medicine,
4th ed., Creasy RK, Resnik R (eds). WB Saunders, Philadelphia,
1999, p 964
Practice Guidelines
.

18. Philipps AF: Carbohydrate metabolism in the fetus. IN Fetal

Pregnancy and Neonatal Physiology, Polin RA, Fox WW (eds). WB Saun-
ders, Philadelphia, 1998, pp 560-573
19. Skyler JS, OSullivan MJ, Holsinger KK: The relationship
1. Pregnant women are at nutrition risk and should between maternal glycemia and macosomia. Diabetes Care 3:3,
undergo nutrition screening to identify those who 1980
formal nutrition with devel- 20. Sosenko IR, Kitzmiller JL, Loo SW, et al: The infant of the
require assessment
diabetic mother. N Engl J Med 301:16, 1979
opment of a nutrition care plan. (B) 21. Centers for Disease Control: Recommendations for the use of
2. In pregnant women who require SNS, baseline folic acid to reduce the number of cases of spina bifida and other
needs should be supplemented with an additional neural tube defects. MMWR 41(no. RR-14):1-7, 1992
300 kcal/d and 10 to 14 g/d of protein during the 22. Subcommittee on Interpretation and Uses of Dietary Reference
second and third trimester. (B) Intakes and the Standing Committee on the Scientific Evalua-
tion of Dietary Reference Intakes, Food and Nutrition Board,
3. PN is indicated for pregnant patients at risk for Institute of Medicine. Dietary reference intakes: Applications in
malnutrition because of a nonfunctioning gastro- dietary assessment. National Academy Press, Washington, DC,
intestinal tract or inability to tolerate EN. (C) 2001
4. Maternal blood glucose should be maintained 23. Amato P, Quercia RA: A historical perspective and review of the
within the range of 90 to 120 mg/dL. (C) safety of lipid emulsion in pregnancy. Nutr Clin Pract 6:189-
192, 1991
5. Intravenous lipid emulsions may be used safely in 24. Greenspoon JS, Safarik RH, Hayashi JT, et al: Parenteral nutri-
pregnant women to provide a source of isotonic tion during pregnancy: lack of association with idiopathic pre-
term labor or preeclampsia. J Reprod Med 39(2): 89-91, 1994
nonprotein calories and avoid essential fatty acid
deficiency. (C)
6. All women of child-bearing age who are capable of
NEONATOLOGY: PREMATURE INFANT
becoming pregnant should consume at least 0.4
mg/d of folic acid, using specific supplementation Background
if necessary. (A)
Premature neonates are categorized by birth weight
and gestational age. Table I summarizes the terminol-
REFERENCES
ogy used to classify premature infantsB
1. Institute of Medicine (IOM) Subcommittee on Nutritional Status Numerous physiologic factors differentiate preterm
and Weight Gain During Pregnancy. Nutrition During Preg- and term infants. Preterm infants have: low carbohy-
nancy. National Academy Press, Washington, DC, 1990
2. Smith CA: Effects of maternal under nutrition upon newborn
infants in Holland: 1944-1945. J Pediatr 30:229-243, 1947
3. Naeve RL: Weight gain and the outcome of pregnancy. Am J TABLE I
Obstet Gynecol 135:3-9, 1979
Terminology used to classify premature infants
4. Wagner BA, Worthington PA, Russo-Stieglitz, et al: Nutritional
management of hyperemesis gravidarum. Nutr Clin Pract 15(2):
153-155, 65-76, 2000
5. National Research Council (NRC). Recommended Dietary Allow-
ances, 10th ed. National Academy Press, Washington, DC, 1989
6. Russo-Stieglitz KE, Levine AB, Wagner BA, et al: Pregnancy
outcome in patients requiring parenteral nutrition. J Maternal
Fetal Med 8:164-167, 1999
7. Chevreau N, Anthony PS, Kessinger K: Managing hyperemesis
gravidarum with home parenteral nutrition: treatment param-
eters and clinical outcomes. Infusion 5(8):22-28, 1999
8. Wiedner LC, Fish J, Talabiska DG, et al: Total parenteral nutri-
tion in pregnant patient with hyperemesis gravidarum. Nutri-
tion 9(5): 446-449, 1993
9. Levine MG, Esser D: Total parenteral nutrition for the treat-
ment of severe hyperemesis gravidarum: maternal nutritional
effects and fetal outcome. Obstet Gynecol 72(1):102-107, 1988
 47SA

drate and fat stores; elevated metabolic rates due to a 1hospital stay, and feeding morbidity. Growth in early
higher percentage of metabolically active tissue; high 1life and at discharge were significantly improved in the
evaporative losses; and immature gastrointestinal sys- aggressively
a fed group.
tems. Because of these differences, the nutrition needs The benefits of EN as little as 0.5 to 1 mL/h via a tube
of this population differ from term infants. PN, incor- Ifeeding, to ELBW and VLBW infants are well docu-
porating protein, carbohydrate and fat infusion, should imented. EN promotes normal gut motility, improved

be started as soon as clinically possible, preferrably on feeding

I tolerance, lactase activity and reduces the risk
the first day of life, to prevent a starvation state, nor- iof sepsis.11 The risk of necrotizing enterocolitis in this

malize serum glucose levels, and improve protein bal- population can be minimized by avoiding rapid
ance.2 Nutrient delivery is provided in quantities to advancement of the feeding regimen.
promote growth matching in utero accretion rates. Perinatal SNS may have long-term consequences in
preterm infants. Reports from a randomized feeding
trial of standard term formula versus preterm formula
Evidence
indicate that infants fed standard term formula have
Early parenteral nutrition (PN) support in the lower verbal IQ scores and overall IQ scores. 12 This
extremely low birth weight (ELBW) and very low birth cohort of preterm infants has been compared with age
weight (VLBW) infants, beginning on day 1 of life, is appropriate term infants at 8 to 12 years of age. 13
advocated for numerous reasons. Infusing parenteral Former preterm infants were shorter and weighed less
amino acids and glucose decreases protein catabolism than their full-term peers. There was no difference in
when compared with glucose infusion alone.33 A bone mineralization found between the groups once
decrease in the incidence of hyperglycemia and hyper- bone mineral content was adjusted for body weight.
kalemia has been documented when amino acid infu- Maximizing linear growth potential in the preterm
sions are begun on day 1 of life.4 Experimental evi- population may be essential in improving bone miner-
dence indicates that amino acid infusion may enhance alization.14,15
glucose-stimulated insulin secretion, aiding the pre-
vention and treatment of hyperglycemia.l1 Practice Guidelines .

Protein requirements in ELBW and VLBW infants Neonatology: Premature Infant ,

are dependent on the clinical situation and nutrition

goals at any given time. In the first weeks of life, 1 to 1. Preterm infants are at nutrition risk and should
1.5 g/kg per day of protein intake should prevent pro-
undergo nutrition screening to identify those who
tein catabolism. To promote in utero growth rates, 3.5
require formal nutrition assessment with devel-
to 3.85 g/kg per day protein is required.5 Term infants . f&dquo;t .. , . , /&dquo;T&dquo;&dquo;IIo
B

opment ot a nutrition care plan. iv>

can achieve positive nitrogen balance at a protein level 2. When indicated, PN should be started in preterm
of 2.5 g/kg per day. infants on day 1 of life, if clinically possible. (B)
Energy intake also ettects mtrogen balance. Glucose 3. Concurrent EN in infants receiving PN should be
and fat calories must be administered concurrently to started as soon as clinically possible. (C)
promote anabolism. Fifty to 60 kcal/kg per day meets 4. Protein should be given to stable ELBW and
minimal energy requirements in ELBW infants, but VLBW infants at a rate of 3.5 to 3.85 g/kg per
the maximal protein accretion rate is achieved at 100
2 day. (B)
to 120 kcal/kg per day intake in most preterm infants.2 5. Energy should be administered at a rate of 100 to
Glucose administration in ELBW and VLBW infants to 120 kcal/kg per day to stable preterm infants
meet basal requirements can be predicted from endoge- anabolism. (A)
nous glucose production, which approximates 6 mg/kg
6. Intravenous glucose administration should be
per minute. The upper limit of intake is dependent on the advanced as tolerated to 10 to 13 mg/kg per
infants maximal glucose oxidative capacity. This rate is minute to meet caloric goals. (A)
estimated to be 12 to 13 mg/kg per minute.6 Along with 7. Intravenous fat emulsion should be administered
intravenous lipid emulsion, this amount of glucose is over 24 hours up to a maximum rate of 3 g/kg per
sufficient to achieve caloric goals for weight gain.
Intravenous fat administration should be initiated
day. (B)
within the first 3 days of life to prevent fatty acid
deficiency. A deficiency state can be avoided with as REFERENCES
little as 0.5 to 1 g/kg per day of fat emulsion.7 Maxi- 1. Hay WW Jr: Assessing the effect of disease on nutrition of the
mally tolerated fat delivery in the preterm population preterm infant. Clin Biochem 29:399-417, 1996
is 3 g/kg per day. There is little clinical evidence to 2. Thureen PJ, Hay WW Jr: Intravenous nutrition and postnatal
of the micropremie. Clin Perinatol 27:197-234, 2000
support the practice of gradually increasing daily fat 3. growth
Battaglia FC, Thureen PJ: Nutrition of the fetus and premature
intake to promote lipid clearance.8 Lipid emulsion infant. Nutrition 13:903-907, 1997
delivered over 24 hours by constant infusion maxi- 4. Micheli J-L, Schutz Y, Junod S, et al: Early postnatal intrave-
mizes lipid clearance.9 nous amino acid administration to extremely low-birth-weight
infants. IN Hay WW Jr (ed). Seminars in Neonatal Nutrition and
Aggressive SNS, using both parenteral and enteral Metabolism, vol. 2, Ross Products Division, Abbott Laboratories,
support, in VLBW infants has recently been
Columbus, OH, 1994, pp 1-3
explored.l It was hypothesized that improved energy 5. Ziegler EE: Protein in premature feeding. Nutrition 10:69-72,
intake has an impact on growth, pulmonary morbidity, 1994
48SA

6. Jones MO, Pierro A, Hammond P, et al: Glucose utilization in the for-height are converted to a standard deviation score
surgical newborn infant receiving total parenteral nutrition. (Z-score) 16,17 using software available from the Centers
J Pediatr Surg 28:1121-1124, 1993
7. Foote KD, MacKinnon MJ, Innis S: Effect of early introduction of
for Disease Control and Prevention 18; undernutrition
formula versus fat free parenteral nutrition on essential fatty is classified as a Z score less than -2.0, a cutoff equiv-
acid status of preterm infants. Am J Clin Nutr 54:93, 1992 alent to the 2.3 percentile.l9 The recently released,
8. Brans YW, Andrew DS, Carrillo DW, et al: Tolerance of fat 2000 NCHS growth curves reflect the racial/ethnic
emulsions in very-low-birth-weight neonates. Am J Dis Child
142:145, 1988 composition of the US population,2 and the third
9. Spear ML, Stahl GE, Paul ME, et al: Effect of heparin dose and rather than fifth percentile can be used to classify
infusion rate on lipid clearance and bilirubin binding in prema- undernutrition, because it more closely approximates a
ture infants receiving intravenous fat emulsions. J Pediatr 112: Z score of less than -2.0. The updated charts also
94, 1988 include body mass index (BMI) curves, to aid early
10. Wilson DC, Cairns P, Halliday HL, et al: Randomised controlled
trial of an aggressive nutritional regimen in sick very low birth identification of obeSity.20 FTT also has been defined as
a fall of two or more major centile lines on reference
weight infants Arch Dis Child Fetal Neonatal Ed 77:F4-F11,
1997 curves once a stable weight pattern has been
11. Newell SJ: Enteral feeding of the micropremie. Clin Perinatol
27:221-234, 2000
reached, 12 failure to gain weight on two successive
12. Lucas A, Morley R, Cole TJ: Randomised trial of early diet in measurements,l9 or as a decrease in Z score.21,22 A
consensus definition specifying the magnitude or time
preterm babies and later intelligence quotient. Br Med J 317:
1481-1487, 1998 interval of growth delay is lacking.22
13. Fewtrell MS, Prentice A, Jones SC, et al: Bone mineralization Type and severity of undernutrition previously have
and turnover in preterm infants at 8-12 years of age: The effect been differentiated as mild, moderate, and severe, and
of early diet. J Bone Miner Res 14:810-820, 1999
as wasting (acute) malnutrition and stunting (chronic)
14. Lucas A, Fewtrell MS, Prentice A, et al: Effects of growth during
infancy and childhood on bone mineralization and turnover in malnutrition, using the Waterlow criteria.23 Short
preterm children aged 8-12 years Acta Paediatr 89:148-153, stature may indicate past nutritional deficits or long-
2000
15. MS, Cole TJ: Fetal origins of adult disease-the hypothesis revis-
term, continuing processes; because this distinction
ited. Br Med J 319:245-249, 1999
has different implications for intervention, the term
&dquo;chronic&dquo; malnutrition is now discouraged.l9 Further-
more, the Waterlow criteria and other criteria based on
NEONATOLOGY: PEDIATRIC
UNDERNUTRITION (FAILURE TO THRIVE) percent of median23 are age biased,21,24 and Z score
decrements are recommended to classify severity of
Background underweight, wasting, and stunting.9
Risk factors for developing undernutrition in the
Despite increases in the prevalence of childhood obe- United States include low birth weight25 and chronic
sity in the United States,1 pediatric undernutrition diseases of infancy as well as complex social factors
remains an important clinical and public health prob-
(including poverty, parental stress, parental health
lem. The prevalence of undernutrition can range from beliefs,2 excess fruit juice consumption,26 and parent-
1% to 10% in different clinical settings. Among low- child interaction difficulties .27 Oral-motor dysfunction
income children, recent national data document linear and poor feeding skills may also play a role in the
growth retardation in 8%;3 12% of children live in development of undernutrition. 28,29
households classified as food insecure with moderate or
severe hunger.4 Undernutrition may be associated
Evidence
with decreases in immune function and physical activ-
ity, motor and cognitive delay, and poor school perfor- Assessment of undernutrition is initiated by history
mance.2 Effects of undernutrition on behavior and cog- and physical exam.12,30 Nutrition history, including
nitive processes rarely can be isolated from social and feeding behavior and environment, should be included
environmental variables5,6 ; however, these &dquo;effects&dquo; in the formal nutrition evaluation. Family history
may also relate to emotional responses to stress should include biological parent heights and weights
rather than irreversible effects on brain function. 1,8 and sibling growth patterns. Social history should
Infant undernutrition has been identified as an cover parental age, life stresses, economic supports (eg,

independent risk factor for neglect in preschool years,9 means-tested benefit programs) and domestic violence.
and, in combination with neglect, associated with When one risk factor is identified, others need to be
lower levels of cognitive function than either condition thoroughly evaluated because multiple risk factors
alone. 10 may have a cumulative detrimental effect on cognitive
The term &dquo;failure to thrive&dquo; (FTT), lacks consistent function. 10 A review of systems should be performed to
definition 11 limiting scientific study across popula- rule out underlying medical conditions.
tions.l2 FTT is considered a clinical indicator of nutri- Anthropometric measurements should be carefully
tion status, i3 reflecting organic, nonorganic, or mixed obtained and plotted on growth charts. Maximum
etiology. 14 The term &dquo;pediatric undernutrition&dquo; cur- weight attained between 4 and 8 weeks of age is a
rently is preferred, emphasizing growth2 delay and de- better predictor of weight at 1 year of age than birth
emphasizing broad etiologic categories.2 weight and should be used in place of birth weight as
Undernutrition has been defined in clinical practice the reference percentile. 31 Corrected age should be
as weight-for-age or weight-for-height less than the used with premature infants until 24 months for
fifth percentile on the NCHS/WHO growth charts.15 weight, 40 months for height, and 18 months for head
For surveillance purposes, weight-for-age or weight- circumference.32
 49SA

A comprehensive physical examination including thrive specialty clinics is less clear, with one study
inspection and palpation of hair, skin, oral mucosa, showing no additional benefit of home intervention on
muscle, and subcutaneous fat stores is a fundamental growth or development.4o
part of the assessment. Attention to eye contact, vocal- In preterm low-birth-weight infants, regular home
ization, response to cuddling, and interest in the envi- health visits do not decrease the incidence of undernu-
ronment can give insight into the presence or absence trition .41 When undernutrition does develop in this
of psychosocial or environmental deprivation .30 Obser- population, home health visits are associated with
vation of a feeding allows for assessment of both the higher IQ scores at 36 months of age.41 In stunted
parent-child dynamic and oral-motor or swallowing dif- children, psychosocial intervention has been shown to
ficulties .30 Ideally, a formal psychosocial evaluation of confer additional benefits on cognitive development
the childs behavior and relationship with caregivers when compared with nutrition supplementation
and environment, as well as cultural variables, is per- alone.42 Among preterm infants with low birth
formed by a trained professional on the multidisci- weights, home environments have been found to be less
plinary team.33 stimulating in those who develop undernutrition.43
Management of undernutrition ideally takes place in Approximately 1.7 million children in the United
the outpatient setting. The goal of treatment is weight States have elevated lead levels.44,45 Blood lead levels
are negatively associated with linear growth, and prev-
gain. This is generally achieved by increased caloric alence of high blood lead levels is greater among chil-
intake.34 Catch up weight gain (rate of weight gain
that exceeds average weight gain for a given age group) dren with growth delay.46,47 Iron deficiency affects 3%
of young children.48 Although not linked directly to
may require 50% greater calories and protein than is
required for normal growth.34 Catch up growth calorie growth deficiency, iron deficiency can lead to increased
needs can be calculated as follows: kcal/kg needed =
absorption of lead (and other toxins) from the gastro-
intestinal tract46 and may be accompanied by zinc defi-
RDA kcal/kg (age appropriate) X ideal weight/actual
weight, using fiftieth percentile as ideal weight. Catch
ciency.46 Although there is limited evidence that zinc
supplementation enhances growth in US children with
up growth protein requirements can be calculated sim- undernutrition, supplementation has been associated
ilarly using the age appropriate RDA for protein. The with improved linear growth in developing countries.49
best way to increase caloric intake is by increasing
caloric density of formula for infants and with high Practice Guidelines
.

calorie additives (peanut butter, whole milk, etc) for

children. Intake of low caloric density foods such as soft
I I W Pediatric Undernutrition
I ,
I
drinks and juices should be decreased. Attention must
of course be paid to medical conditions, nutrition 1. Clinicians should define pediatric undernutrition
requirements, gastrointestinal tolerance, and renal as either: weight for age or weight for height less
solute load when developing a feeding plan.34,35 than the third percentile (less than -2.0 weight
Close monitoring should be performed regularly for age or weight for height Z-score) on the 2000
(weekly to monthly) with anthropometry and plotting NCHS growth charts or a fall across two or more
on growth curves. Triceps skinfold is a useful measure- centile lines on the NCHS growth charts once a
ment to monitor because changes in weight and skin- stable growth pattern has been reached. (B)
fold occur most rapidly in the course of nutrition reha- 2. Severity of wasting and stunting should be
bilitation.34 Most children treated for undernutrition assessed (Z score less than -2.0 [moderate], less
gain weight and grow well. Nonetheless, one fourth to than -3.0 [severe]) and past or continuing causes
one half of infants diagnosed with failure to thrive will of growth delay documented. (B)
remain small. 30 3. A careful history and physical exam should be
A multidisciplinary approach to evaluation and performed to assess risk factors for undernutri-
treatment of children with undernutrition has been tion and to evaluate resources available to treat
associated with faster weight than treatment in undernutrition. (C)
gain
the primary care setting alone. 6 Extensive laboratory 4. A multidisciplinary team approach, including a
,

is of limited value in most cases of undernutri- dietitian, social worker, nurse, behavior special-
testing
tion,3 and testing is clearly not indicated for all ist, and physician, should be convened to diag-
patients. Physical examination and history should nose, treat, and monitor undernourished pa-
guide the selection of tests. Appropriate screening lab- tients. (B)
oratory tests may include hematocrit, urinary analysis 5. Periodic re-evaluation of nutrition status should
and culture, BUN, calcium, electrolytes, HIV antibody, be performed using anthropometric and clinical
and Mantoux tubercillin skin test. 31 examination assessment tools. (B)
The role of home visits has been evaluated in several
recent studies with varying results. In the primary
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care setting, the use of home health visitors has been
associated with faster growth, 29,38 improved home 1. Troiano RP, Flegal KM: Overweight children and adolescents;
environments and mothers perceived stress,~8 and bet- description, epidemiology and demographics. Pediatrics 27:225-
234, 1998
ter language skills development.39 The utility of a : Kessler D: Failure to thrive and pediatric undernutrition: His-
2.

home health visitor for children attending failure to torical and theoretical context. IN Kessler D, Dawson P (eds).
50SA

Failure to Thrive and Pediatric Undernutrition. Paul H. Brookes 26. Smith MM, Lifshitz F: Excess fruit juice consumption as a con-
Publishing Co, Baltimore, MD, 1999 tributing factor in nonorganic failure to thrive. Pediatrics 93(3):
3. Healthy People 2010 Conference Edition. US Department of 438-443, 1994
Health and Human Services, 2000 27. Rathbun JM, Peterson KE: Nutrition in failure to thrive. IN
4. Federal Interagency Forum on Child and Family Statistics (Fed- Grand RJ, Sutphen JL, Dietz WH (eds). Pediatric Nutrition:
eral Interagency Forum on Child and Family Statistics): Theory and Practice. Butterworths, Boston, 1987
Nations Children Gain in Many Areas, July 13, 2000 28. Reilly SM, Skuse DH, Wolke D, et al: Oral-motor dysfunction in
5.. Metallinos-Katsaras E, Gorman KS: Effects of undernutrition children who fail to thrive: Organic or non-organic? Dev Med
on growth and development. IN Kessler D, Dawson P (eds). Child Neurol 41(2):115-122, 1999
Failure to Thrive and Pediatric Undernutrition. Paul H. Brookes 29. Wright C, Birks E: Risk factors for failure to thrive: A pop-
Publishing Co, Baltimore, MD, 1999 ulation-based survey. Child Care Health Dev 26(1):5-16,
6. Gorman KS: Malnutrition and cognitive development: Evidence 2000
from experimental/quasi-experimental studies among the mild- 30. Kirkland RT. Failure to Thrive. IN McMillan JA, DeAngelis
to-moderately malnourished [Review]. J Nutr 125(8 Suppl): CD, Feigin RD, et al (eds). Oskis Principals and Practices of
2239S-2244S, 1995 Pediatrics. Lippincott Williams and Wilkins, Baltimore,
7. Levitsky DA, Strupp BJ: Malnutrition and the brain: Changing 1999
concepts, changing concerns. J Nutr 124:2212S-2220S, 1995 31. Edwards AG, Halse PC, Parkin JM, et al: Recognizing failure to
8. Strupp BJ, Levitsky DA: Enduring cognitive effects of early thrive in early childhood. Arch Dis Child 65(11):1263-1265, 1990
malnutrition: a theoretical appraisal. J. Nutr 125:2221S-2232S, 32. Bithoney WG, Dubowitz H, Egan H: Failure to thrive/growth
1995 deficiency. Pediatr Rev 13(12):453-460, 1992
9. Skuse DH, Gill D, Reilly S, et al: Failure to thrive and the risk of 33. Black M, Cureton P, et al: Behavior Problems in Feeding: Indi-
child abuse: a prospective population survey. J Med Screening vidual, Family and Cultural Influences. IN Kessler D, Dawson P
2(3):145-149, 1995 (eds). Failure to Thrive and Pediatric Undernutrition. Paul H.
10. Mackner LM, Starr RH Jr, Black MM: The cumulative effect of Brookes Publishing Co., Baltimore, MD, 1999
neglect and failure to thrive on cognitive functioning. Child 34. Peterson KE, Washington J, Rathbun JM: Team management of
Abuse Negl 21(7):691-700, 1997 failure to thrive. J Am Diet Assoc 84(7):810-815, 1984
11. Wilcox WD, Nieburg P, Milller DS: Failure to thrive: A continu- 35. Cunningham KF, McLaughlin M. Nutrition. IN Kessler D, Daw-
ing problem of definition. Clin Pediatr 28:391-394, 1989 son P (eds). Failure to Thrive and Pediatric Undernutrition. Paul
12. Duggan C: Failure to thrive: Malnutrition in the outpatient H. Brookes Publishing Co, Baltimore, MD, 1999
setting. IN Walker WA, Watkins JB (eds). Nutrition in Pediat- 36. Bithoney WG, McJunkin J, Michalek J, et al: The effect of a
rics: Basic Science and Clinical Applications. BC Decker, Inc, multidisciplinary team approach on weight gain in nonorganic
Hamilton, Ontario, 1996 failure-to-thrive children. J Dev Behav Pediatr 12(4):254-258,
13. Peterson KE, Chen LC: Defining undernutrition for public 1991
health purposes in the United States. J Nutr 120(8):933-942, 37. Sills RH: Failure to thrive. The role of clinical and laboratory
1990 evaluation. Am J Dis Child 132(10):967-969, 1978
14. Homer C, Ludwig S: Categorization of etiology of failure to 38. Reifsnider E: Reversing growth deficiency in children: The effect
thrive. Am J Dis Child 135:848-851, 1981 of a community-based intervention. J Pediatr Health Care 12(6
15. Hamill PVV, Drizd T, Johnson CL, et al: Physical growth: Pt 1):305-312, 1998
National Center for Health Statistics percentiles. Am J Clin 39. Black MM, Dubowitz H, Hutcheson J, et al: A randomized clin-
Nutr 32:607-629, 1979 ical trial of home intervention for children with failure to thrive.
16. Dibley MJ, Goldsby JB, Staehling NW, et al: Development of Pediatrics 95(6):807-814, 1995
normalized curves for the international growth reference: His- 40.
torical and technical considerations. Am J Clin Nutr 46:736-
Raynor P, Rudolf MC, Cooper K, et al: A randomised controlled
trial of specialist health visitor intervention for failure to thrive.
748, 1987 Arch Dis Child 80(6):500-506, 1999
17. Dibley MJ, Staehling NW, Neiberg P, et al: Interpretation of 41. Casey PH, Kelleher KJ, Bradley RH, Kellogg KW, Kirby RS,
Z-score anthropometric indicators derived from the international
Whiteside L: A multifaceted intervention for infants with failure
growth reference. Am J Clin Nutr 46:749-762, 1987 to thrive. A prospective study. Arch Pediatr Adolesc Med
18. Dean AG, Dean JA, Coulombier D, et al: Epi Info, Version 6: A
Word-Processing, Database, and Statistics Program for Public 148(10):1071-1077, 1994
Health on IBM-compatible Microcomputers. Centers for Disease 42. Grantham-McGregor SM, Walker SP, Chang SM, et al: Effects of
Control and Prevention, Atlanta, GA, 1995 early childhood supplementation with and without stimulation
19. World Health Organization: Physical Status: The Use and Inter- on later development in stunted Jamaican children. Am J Clin

pretation of Anthropometry, WHO Technical Report Series No. Nutr 66(2):247-253, 1997
854, Geneva: WHO, 1995, pp 198-224, Chapter 5: Infants and 43. Kelleher KJ, Casey PH, Bradley RH, et al: Risk factors and
children; section 5.3 and 5.4 outcomes for failure to thrive in low birth weight preterm infants
20. NCHS: New pediatric growth charts provide tool to ward off [published erratum appears in Pediatrics 92(1):190, 1993]. Pedi-
future weight problems. National Center for Health Statistics, atrics 91(5):941-948, 1993
Division of Data Services, Hyattsville, MD, 2000 44. Satcher D: Screening young children for lead poisoning: Guid-
21. Peterson KE, Rathbun JM, Herrera MG: Growth data analysis ance for state and local public health officials. Atlanta, Centers
in failure to thrive treatment and research. IN Drotar D (ed). for Disease Control and Prevention
New Directions in Failure to Thrive: Implications for Research 45. Pirkle JL, Brody DJ, Gunter EW, et al: The decline in blood lead
and Practice. Plenum Press, New York, 1985 levels in the United States. JAMA 272:284-291, 1994
22. Sherry B: Epidemiology of inadequate growth. IN Kessler D, 46. Cutts D, Geppert J: Anemia, lead exposure, renal disease and
Dawson P (eds). Failure to Thrive and Pediatric Undernutrition. dental caries. IN Kessler D, Dawson P (eds). Failure to Thrive
Paul H. Brookes Publishing Co., Baltimore, MD, 1999 and Pediatric Undernutrition. Paul H. Brookes Publishing Co,
23. Waterlow JC, Buzina R, Keller W, et al: The presentation and Baltimore, MD, 1999
use of height and weight data for comparing the nutritional 47. Ballew C, Khan LK, Kaufmann R, et al: Blood lead concentration
status of groups of children under the age of 10 years. Bull WHO and childrens anthropometric dimensions in the Third National
55(4):489-498, 1977 Health and Nutrition Examination Survey (NHANES III), 1988
24. Gorstein J: Assessment of nutritional status: Effects of different to 1994. J Pediatr 134(5):623-630, 1999
methods to determine age on the classification of undernutrition. 48. Looker AC, Dallman PR, et al: Prevalence of iron deficiency in
Bull WHO 67:143-150, 1989 the United States. JAMA 277:973-976, 1997
25. Pugliese MT, Weyman-Daum M, Moses N, et al: Parental health 49. Brown KH, Peterson JM, Allen LH: Effect of zinc supplementa-
beliefs as a cause of nonorganic failure to thrive. Pediatrics tion on childrens growth: A meta-analysis of intervention trials.
80(2):175-182, 1987 Bibliotheca Nutritio et Dieta 54:76-83, 1998
 51SA

GERIATRICS Limited exposure to sunlight, the use of sunscreens,

and intake of dairy products contribute to low vitamin
Background D levels in the elderly. These low levels are associated
The physiologic changes that occur with advancing with poor bone density and reduced muscle strength as
age affect nutritional requirements, independent of well as function. 5 Along with vitamin D, calcium
1
disease or rehabilitation demands. requirements have attracted much attention in recent
The major physiologic changes that occur are as fol- years. Recommended dietary intake has increased
lows : a reduction in lean body mass, a decline in bone from 800 to 1200 or 1500 mg/d to reduce the risk of
density, an increase in total body fat with a redistribu- osteoporosis.
tion of fat stores, and a decrease in total body water.
These physiologic alterations occur in all people as Dehydration can be very debilitating in elderly per-
they age. They occur at different rates among individ-
sons. Adaptation to inadequate fluid intake and
increased requirements due to fever and excessive heat
uals dependent upon nutritional intake throughout
earlier life stages, the presence and progression of is impaired. Symptoms of dehydration, hypotension,
chronic disease, and episodes of acute illness. elevated body temperature, constipation, nausea, vom-
Distinguishing between physiologic age-induced iting, mucosal dryness, decreased urine output, and
changes and nutritional deficiencies may be difficult. mental confusion are rarely attributed to fluid imbal-
These abnormalities alter physical strength and the ances and are, therefore, often overlooked. A reason-
functional and cognitive capacity of the elderly. The able estimate of fluid needs for elderly persons is
basal requirements to maintain homeostasis, the approximately 30 mL/kg actual body weight with a
demands of chronic disease, and the extraordinary minimum intake for all healthy older adults being 1500
needs of acute illness make the provision of nutrition mL/d.8 Inadequate fluid intake in the institutionalized
care to elderly patients challenging.
elderly results from impaired access to dietary fluid,
voluntary restriction of fluid to avoid incontinence, and
Evidence
inadequate fluid in SNS.9
Lower calorie intake and immobility contribute to Malnutrition is a problem that often goes unrecog-
reduced retention of dietary nitrogen, therefore nized in elderly patients.1-0 Because of the physiologic
requiring more dietary protein to achieve nitrogen changes that occur with advancing age, standard
balance in older subjects. Surgery, sepsis, long nutrition assessment parameters may not be appropri-
bone fractures, and unusual losses such as those ate for older adults.11-14 Few of the standard measures
that occur with burns or gastrointestinal disease of nutrition status have reference values for adults
increase the need for dietary protein beyond the over 60 years of age. For older adults, nutrition assess-
augmented needs induced by age and immobility. ment should include evaluation of physical status,
Often, clinicians have been wary of providing ade- including a review of anthropometric measures, bio-
quately high levels of protein for fear of precipitat- chemical assessment, oral health status, and medica-
ing renal disease. There is no evidence that dietary tion review; functional status including activities of
protein impairs renal function in individuals who
daily living and instrumental activities of daily living;
do not have preexisting renal disease.33
cognitive and psychologic function; and socioeconomic
The ability to metabolize carbohydrates declines factors. 11-14 It is
with age.4 Fasting blood glucose levels tend to increase
important to recognize that indicators
for older adults are often reflective of something differ-
slowly over time to a mean of 140 mg/dL for individuals ent than they are for younger patients. Low serum
over age 65. As such, carbohydrate intake should be
for example, may indicate a serious medi-
approximately 55% to 60% of total calories with an cholesterol,
cal problem independent of heart disease. 15 The elderly
emphasis on complex carbohydrates to enhance colon
may be subclinically undernourished and may require
motility.
Subclinical deficiencies of water-soluble vitamins, more time to respond appropriately
to a physiologic
stress (trauma, surgery, sepsis), thereby influencing
particularly vitamin B-12, vitamin B-6, folate and their nutrition status. 10,16
ascorbic acid are likely in elderly persons.5 Epidemio-
logic studies show that low vitamin levels in elderly
subjects are associated with declining cognitive func- Special Considerations
tion .5 Vitamin B-12 and folate stores may be low due to
decreased absorption induced by gastric mucosal atro- The use of specialized nutrition support (SNS) in
phy6 or diets low in fat that reduce vitamin B-12 elderly patientsthat requires consideration of the physio-
intake. Ribaya-Mercado found that normal vitamin logic changes occur with age, cognitive status,

B-6 doses were insufficient to replete stores in depleted polypharmacy and potential drug interactions, hydra-
elderly subjects, suggesting higher doses are required tion status, and prognosis. Many older individuals
to replete vitamin deficient states in this age group. have living wills, durable medical power of attorney
There is an age-related decrease in whole blood, serum, assignments, and multiple comorbidities. Careful con-
and plasma leukocyte ascorbic acid levels although sideration of the long-term prognosis is necessary for
absorption appears normal in elderly subjects. For older patients; if there is a reasonable expectation of
vitamin C, repletion of stores occurs rapidly with usual recovery, aggressive nutrition intervention is a legiti-
replacement doses. mate option. Nutrition support used to extend life
52SA

is generally undesirable inter- 15. Rudman D, Mattson DE, Nagraj HS, et al: Prognostic signifi-
or prolong dying an
cance of serum cholesterol in nursing home men. JPEN 12:155-
vention and often eliminated as an option in living 158, 1988
wills. 16. Sullivan DH, Walls RC, Lipschitz DA: Protein-energy undernu-
trition and the risk of mortality within 1 yr of hospital discharge
in a select population of geriatric rehabilitation patients. Am J
..
Clin Nutr 53:599-605, 1991
,

1.Elderly patients (age greater than 65 years) are at OBESITY

nutrition risk and should undergo nutrition
Background
screening to identify those who require formal
nutrition assessment with development of a Obesity is the most common chronic disease in the
nutrition care plan. (B) United States, and its incidence is increasing at an
2. Age and life style parameters should be used to alarming rate. Recent data document that over 50% of
assess the nutrition status of elderly persons. (C)
adults are overweight [with a BMI 25 to 29 (kg/m2)], 15%
are obese (BMI 30-34, WHO Class I), 5% are seriously
3. Potential drug-nutrient interactions should be
obese (BMI 35-40, WHO Class II), and 3% have clinically
assessed in all elderly patients receiving medica-
severe obesity (BMI > 40, WHO Class III).
tions. (B)
The physical, psychological, and economic burden
4. Diet and SNS prescriptions for elderly persons that severe
should take into consideration altered nutrient
obesity places on those afflicted and on
society is enormous. Obesity is an independent risk
requirements observed in this age group. (B) factor for death from all causes and is associated with
numerous potentially life-threatening comorbid condi-
tions, including type 2 diabetes mellitus, hypertension,
REFERENCES
hyperlipidemia, coronary artery disease, obstructive
1. Chernoff R: Demographics of aging. IN Chernoff R (ed). Geriatric sleep apnea, and several forms of Mortal-
mali~nancy.2
Nutrition: The Health Professionals Handbook, 2nd ed. Aspen ity from obesity increases with BMI. It is estimated
Publishers, Inc, Gaithersburg MD, 1999, pp 1-12 that obesity causes in excess of 300,000 premature
2. Campbell WW, Crim MC, Dallal GE, et al: Increased protein deaths each year in the United States, second only to
requirements in elderly people: New data and retrospective reas- tobacco usage. In addition, obesity is associated with
sessments. Am J Clin Nutr 60:501-509, 1994
numerous life style-limiting complications, such as
3. Carter WJ: Macronutrient requirements for elderly persons. IN
Chernoff R (ed): Geriatric Nutrition: The Health Professionals arthritis, gastroesophageal reflux, gallstones, urinary
Handbook, 2nd edition, Gaithersburg MD, Aspen Publishers, stress incontinence, venous stasis disease, abdominal
Inc, 1999, pp 13-26 wall hernias, infertility, and depression.2
4. American Diabetes Association: Nutrition recommendations and
principles for people with diabetes mellitus. Diabetes Care Obesity may also affect the outcome of hospitalized
21(suppl 1):S32-S36, 1998 patients. Obese patients have a higher incidence of
5. Rosenberg IH, Miller JW: Nutritional factors in physical and wound infections and hernias than lean counterparts
cognitive functions of elderly people. Am J Clin Nutr 55 :1237S- and may have a higher incidence of respiratory, car-
12435, 1992 diac, and thromboembolic complications, although5
6. Suter PM: Vitamin status and requirements of the elderly. IN
Chernoff R (ed). Geriatric Nutrition: The Health Professionals these latter associations are much less clearly defined.5
Handbook, 2nd ed. Aspen Publishers, Inc, Gaithersburg MD, Because of the prevalence of obesity, obese individ-
1999, pp 27-62 uals are frequently encountered in the hospital setting.
7. Ribaya-Mercado JD, Russell RM, Morrow FD, et al: Vitamin B-6 A retrospective review of general, thoracic, urologic,
deficiency elevates serum insulin in elderly subjects. Ann NY and gynecologic surgical patients noted that 37% of the
Acad Sci 531-533, 1990
8. Holben DH, Hassell JT, Williams JL, et al: Fluid intake com- elective adult surgical population were overweight
pared with established standards and symptoms of dehydration [BMI > 27 (kg/m2)] and 17% were severely overweight
among elderly residents of a long-term care facility. J Am Diet (BMI > 3 1).6 Thus, an estimate for the incidence of
Assoc 99(11):1447-1450, 1999
9. Chernoff R: Nutritional requirements and physiological changes
obesity of 35% to 40% for the hospitalized population in
in aging: Thirst and fluid requirements. Nutr Rev 52(8)II:S3-S5, general is probably reasonable, if not low. Neverthe-
1994 less, considerable confusion exists regarding whether,
10. Sullivan DH, Sun S, Walls RC: Protein-energy undernutrition when, how, and what to feed, hospitalized obese
among elderly hospitalized patients: A prospective study. J Am
Diet Assoc 281(21):2013-2019, 1999
patients.77
11. Mitchell CO, Chernoff R: Nutritional assessment of the elderly.
IN Chernoff R (ed). Geriatric Nutrition: The Health Profession- Evidence
als Handbook, 2nd ed. Aspen Publishers, Inc, Gaithersburg MD,
1999, pp 382-415
12. Guigoz Y, Vellas B, Garry PJ: Assessing the nutritional status of Obesity and malnutrition are not mutually exclu-
the elderly: The Mini Nutritional Assessment as part of the sive. In fact, obesity can be considered a form of mal-
geriatric evaluation. Nutr Rev 54(1Pt 2):S59-S65, 1996 nutrition (overnutrition). Obese individuals should be
13. Morrow FD: Assessment of nutritional status in the elderly: assessed using the same approach as nonobese
Application and interpretation of nutritional biochemistries. patients, based on history, physical exam, and labora-
Clin Nutr 5:112-120, 1986
14. Finucane P, Rudra T, Hsu R, et al: Markers of the nutritional tory studies. Catabolic illness (trauma, burns, sepsis),
status in acutely ill elderly patients. Gerontology 34:304-309, prolonged ventilator dependence, cancer (especially if
1988 receiving chemotherapy or radiation therapy), and
 53SA

involuntary recent weight loss increase the risk for positive nitrogen balance, and enhanced protein anab-
malnutrition and significant loss of lean body mass. On olism, wound healing, and immune function.
the other hand, significant voluntary weight loss in a Data concerning the safety and efficacy of hypocaloric
monitored, balanced-deficit program does not appear to nutritional regimens in acutely ill obese patients is accu-
increase risk for nutrition-related adverse outcome.8 mulating. Four prospective studies have been performed
Nutrition support should be initiated expeditiously to date demonstrating that obese patients given hypoca-
in obese patients with illnesses that produce signifi- loric nutrition support can achieve positive nitrogen bal-
ance comparable to controls.2~25 In addition, others have
cant catabolism. For patients who were relatively
advocated the use of various hypocaloric regimens in
healthy before the onset of their current illness or
those undergoing elective surgery support should be hospitalized obese patients with varying degrees of met-
abolic stress.26-29 Although not specifically studied, such
considered after a period of 5 to 7 days without oral
a high-protein regimen should probably not be adminis-
intake, especially if it does not appear likely that the tered to patients with significant renal or hepatic dys-
individual will be consuming greater than 50% of esti-
mated needs within the next 3 to 4 days. Starvation or function, which generally mandates some restriction of
protein intake, to avoid severe azotemia (BUN > 100
&dquo;letting them live off their fat&dquo; is not an appropriate mg/dL) and hepatic encephalopathy.
strategy. It places these patients at risk for loss of lean Determination of the route of administration of SNS
body mass because metabolic stress and results in is also similar to that in nonobese patients. If no con-
&dquo;mixed fuel&dquo; (carbohydrate, protein, and fat) utiliza- traindication to EN exists, this should be attempted
tion, as opposed to the response seen with simple star- first. Parenteral access and long-term enteral access
vation.9 can be difficult in obese patients. Central venous can-
The most accurate method for determining nutri- nulation tends to be increasingly difficult because, as
tional requirements in obese individuals is indirect
body fat increases, the normal anatomic landmarks are
calorimetry.lO,l1 However, because indirect calorime- obscured.5 When placing enteral access devices such
try is expensive to perform and not universally avail- as gastrostomy or jejunostomy tubes, careful consider-
able, the development of prediction equations that ation must be given to placement of the tube exit site in
would be more widely applicable has been advocated. relation to skin creases.
Predictive equations based on normal populations,
such as the Harris-Benedict equations, have been Practl*[Ce Guidelines
shown to underestimate the resting energy expendi-
ture of obese individuals when IBW is used and over- Obesity
estimate energy expenditure when actual body weight
is used in the equations. 12,13 This has resulted in con- 1. Obese patients are at nutrition risk, and should
troversy regarding the most appropriate weight to be undergo nutrition screening to identify those who
used when calculating energy needs-IBW or actual require formal nutrition assessment with devel-
body weight. 14 Some clinicians use an &dquo;adjusted&dquo; body opment of a nutrition care plan. (B)
2. When possible, energy requirements of obese
weight [(actual BW X 0.25) + IBW], which represents
an attempt to account for the increase in lean body patients should be assessed using indirect calo-
mass seen in the obese patient. 15 rimetry because predictive equations have consid-
In addition to the Harris-Benedict equations, which erable limitations in estimating energy require-
can be used in acutely-ill patients in conjunction with ments in obese patients. (B)
&dquo;stress factors,&dquo; several other equations have been 3. Hypocaloric nutrition regimens with supplemen-
devised for estimating energy needs which may be tal protein are recommended in the treatment of
applicable in obese patients.13-17 However, studies mild to moderately stressed obese patients. (A)
comparing the accuracy of predictive formulas with REFERENCES
indirect calorimetry have found their utility to be
limited. 18,19 1. Flegal KM, Carroll MD, Kuczmarski RJ, et al: Overweight and
obesity in the United States: Prevalence and trends 1960-1994.
Int J Obes 22:39-46, 1998
Special Considerations 2. Pi-Sunyer FX: Medical hazards of obesity. Ann Intern Med 119:
655-660, 1993
Starvation or semi-starvation has been successfully 3. Hubert H, Feinleib M, McNamara PM, et al: Obesity as an
independent risk factor for cardiovascular disease: A 26-year
used as a treatment for obesity in otherwise healthy
follow-up of participants in the Framingham heart study. Circu-
obese individuals for some time.2 Adaptive changes lation 67:968-977, 1983
during starvation reduce energy requirements and 4. Kushner RF: Body weight and mortality. Nutrition Rev 51:127-
allow fat depots to be utilized for energy, while sparing 136, 1993
5. Flancbaum L, Choban PC: Surgical implications of obesity. Ann
muscle protein from excessive catabolism. In this set- Rev Med 49:215-234, 1998
ting, the administration of adequate amounts of exog- 6. Choban PS, Heckler R, Burge J, et al: Nosocomial infections in
enous protein (approximately 1 g/kg IBW) results in obese surgical patients. Am Surg 61:1001-1005, 1995
nitrogen equilibrium or positive nitrogen balance.21,22 7. Ireton-Jones CS, Francis C: Obesity: nutrition support practice
and application to critical care. Nutr Clin Pract 10:144-149,
Hypocaloric feeding of obese hospitalized patients 1995
has several theoretical advantages, including: avoid- 8. Martin LF, Tjiauw-Ling T, Holmes DA, et al: Can morbidly obese
ance of complications related to impaired glucose/
patients safely lose weight preoperatively? Am J Surg 169:245-
insulin metabolism, improved ventilatory dynamics, 253, 1995
54SA

9. Cerra FB: Hypermetabolism, organ failure, and metabolic sup- mones. The stress response leads to peripheral insulin
port. Surgery 10:1-14, 1987 resistance along with increased proteolysis and glu-
10. Flancbaum L, Choban PS, Sambucco S, et al: Comparison of
indirect calorimetry, the Fick method, and prediction equations coneogenesis and resulting hyperglycemia. Near nor-
in estimating energy requirements in critically ill patients. Am J mal glucose control is the goal in ambulatory, healthy
Clin Nut 69:461-466, 1999 subjects with type 1 and type 2 diabetes in order to
11. Brandi LS, Bertolini R, Calafa M: Indirect calorimetry in criti-
prevent or delay the development of microvascular
cally ill patients: Clinical applications and practical advice.
Nutrition 13:349-35, 1997 complications (in the retina, kidney, and peripheral
12. Pavlou KN, Hoefer MA, Blackburn GL: Resting energy expendi- nerves). There is increasing evidence that glucose con-
ture in moderate obesity. Ann Surg. 203:136-141, 1986 trol is important in hospitalized patients because
13. Daly JM, Heymsfield SB, Head CA, et al: Human energy require-
ments: Overestimation by widely used prediction equation. Am J
hyperglycemia can adversely affect immune function
and fluid balance.
Clin Nutr 42:1170-1174, 1985
14. Ireton-Jones CS, Turner WW Jr: Actual or ideal body weight: Appropriate nutrition therapy is a vital component
which should be used to predict energy expenditure? J Am Diet in the treatment of DM. Timely nutrition assessment
Assoc 91:193-195, 1991 and initiation of medical nutrition therapy may help to
15. Wilken K: Adjustment for obesity. ADA Renal Practice Group
prevent the development of complications over the long
Newsletter, Winter 1984, run. In the past, individuals with DM were instructed
16. Ireton-Jones CS: Evaluation of energy expenditure in obese
to follow strict diets containing specific amounts of
patients. Nutr Clin Pract 4:127-129, 1989
17. Ireton-Jones, Turner WW Jr, Liepa GU, et al: Equations for the foods with careful monitoring of carbohydrate intake
estimation of energy expenditure in patients with burns with and complete avoidance of simple carbohydrates,
special reference to ventilatory status. J Burn Care Rehabil including sucrose. Recommendations for carbohydrate
33-333, 1992 have been liberalized with emphasis placed on intake
18. Amato P, Keating KP, Quericia RA, et al: Formulaic methods of
estimating caloric requirements in mechanically ventilated of complex carbohydrates and fiber. The American Dia-
obese patients: A reappraisal. Nutr Clin Pract 10:229-230, 1995 betes Association recommends that for otherwise
19. Glynn CC, Greene GW, Winkler MF, et al: Predictive versus
measured energy expenditure using limits-of-agreement analy-
healthy patients, protein comprise 10% to 20% of total
sis in hospitalized obese patients. JPEN 23:147-154, 1999 calories, with no specific guidelines for carbohydrate
20. Bray GA: The obese patient. WB Saunders Company, Philadel- and fat other than to individualize intake based on
phia, PA, 1976 eating habits and goals of therapy.2,3 Recommenda-
21. Strang JM, McClugage HB, Evans FA: Further studies in the tions for macronutrient formulation of EN or PN do not
dietary correction of obesity. Am J Med Sci 179:687-694, 1930 differ from standard dietary recommendations for dia-
22. Strang, JM, McClugage HB, Evans FA: The nitrogen balance
during dietary correction of obesity. Am J Med Sci 181:336-349,
betic patients.4 It is probably more important to avoid
1931 overfeeding total calories.5,6
23. Dickerson RN, Rosato EF, Mullen JL: Net protein anabolism The major goal in patients with diabetes receiving
with hypocaloric parenteral nutrition in obese stressed patients. SNS is optimal blood glucose control and the avoidance
Am J Clin Nutr 44:747-755, 1986
24. Burge JC, Goon A, Choban PS, et al: Efficacy of hypocaloric total
of hyper- and hypoglycemia and the sequelae of meta-
parenteral nutrition in hospitalized obese patients: A prospec- bolic alterations such as fluid imbalance and dehydra-
tive, double-blind randomized trial. JPEN 18:203-207, 1994 tion, ketoacidosis, and hyperosmolar hyperglycemic
25. Choban PS, Burge JC, Scales D, et al: Use of hypocaloric paren- state (hyperosmolar nonketotic coma), infection, and
teral nutrition in obese hospitalized patients: A double-blind,
randomized, prospective trial. Am J Clin Nutr 66:546-550 ,1997
neurological injury.4 Indications for SNS in diabetic
26. Boschert K, Dickerson RA, Kudsk KA, et al: Clinical outcome of patients are not different from nondiabetic patients in
hypocaloric enteral tube feeding in obese trauma ICU patients need of such therapy. Patients with permanent injury
[Abstract]. Nutr Clin Pract 15:S12, 2000 or stroke or those recovering from surgery, acute ill-
27. Pasulka PS, Kohl D: Nutrition support of the stressed obese
ness, or trauma may require short-term EN until safe
patient. Nutr Clin Pract 4:130-132, 1989 transition to oral diet can be made. In patients in
28. Baxter JK, Bistrian BR: Moderate hypocaloric parenteral nutri-
tion in the critically ill, obese patient. Nutr Clin Pract 4:133-135, whom tube feeding is contraindicated or in situations
1989 of tube feeding intolerance, PN may be used.
29. Shikora SA, Muskat PC: Protein-sparing, modified-fast total
parenteral nutrition formulation for a critically-ill, morbidly
obese patient. Nutrition 10:155-158, 1994 Evidence
30. Shikora SA: Nutrition support of the obese patient. Nutr Clin
Care 2:231-238, 1999 Multicenter trials have shown that intensive insulin
therapy using multiple injections per day can lead to
decreased risk for long-term complications in ambula-
DIABETES MELLITUS
tory, healthy individuals with type 1 diabetes and for
Background people with type 2 diabetes.10,11 During short-term
hospitalization, hyperglycemia can adversely affect
Diabetes Mellitus (DM) is a serious metabolic disor- fluid balance and immune function. Studies document
der caused by an absolute (type 1) or a relative (type 2) that hyperglycemia is associated with abnormalities in
lack of insulin that may lead to alterations in metabo- white cell and complement function. Increasing clinical
lism of carbohydrate, protein, and fat. In addition, seri- evidence links hyperglycemia with increased risk for
ous illness may cause hyperglycemia in patients with- infection. A retrospective review of patients undergo-
out a prior diagnosis of diabetes or may worsen blood ing cardiac operation found a significant relationship
glucose control in critically ill patients who have pre- between elevated blood glucose levels 48 hours after
existing DM. This is thought to be due to release of surgery and increased risk for deep wound infection in
various inflammatory mediators, cytokines, and hor- patients with DM. Implementation of a strict protocol
 55SA

for blood glucose management in the postoperative paresis requires special consideration im designing and
period led to a significant decrease in deep wound :implementing SNS. Alterations in gastric emptying
infections.7 Several prospective studies found that may lead to difficulty achieving adequate blood glucose
postoperative hyperglycemia in patients with DM was control due to mismatching of insulin action and nutri-
related to a significant increase in the incidence of ,ent absorption. Pharmacologic treatment of gastropa-
infections.&dquo;,9 It appears reasonable to aim for a blood resis is possible. Gastroparesis in and of itself is not an
glucose range of 100 to 200 mg/dL while minimizing indication for PN. Enteral feedings can be successfully
the incidence of hypoglycemia.~2-14 Because intensive administered using
postpyloric feeding access along
insulin therapy may increase the risk for hypoglyce- with or a venting gastrostomy if
promotility agents
mia, it is important to closely monitor blood glucose needed. If EN is used, the initial formula should con-
levels when providing SNS to individuals with DM. tain only moderate amounts of fat (30% of total calo-
The use of EN and PN poses special challenges in
ries) and should be fiber free, because both fat and fiber
managing blood glucose levels. A retrospective analysis may slow gastric emptying.
of 65 patients with DM who required SNS over a
10-year period found that one third of patients with
type 2 diabetes required insulin during PN; patients Special Considerations
with type 1 diabetes required an increase from their
,preadmission insulin dose during PN.15 The likelihood forSpecialinformulas have been developed and marketed
of a patient requiring a major change from preadmis- use patients with DM. Several studies have
sion diabetes therapy depended on severity of the examined glycemic response while feeding enteral for-
underlying illness, the amount of calories provided, mulations that are lower in carbohydrate and higher in
and the type of feeding (PN). Insulin therapy may also fat content compared with standard products.19
need to be adjusted or initiated in patients not previ- Although one study reported an improved glycemic
ously requiring insulin. Initial insulin requirements response to the lower carbohydrate formula, another
for EN can be estimated based on the percentage of demonstrated that glycemic response was variable in
usual intake being provided by the feeding solution. As each patient.2o,21 The results of these studies are dif-
with PN, basal insulin requirements should be pro- ficult to apply to most clinical settings, because sub-
vided along with sliding scale coverage while feedings jects consumed small amounts of formula over time or
are being advanced. If the feeding is providing 25% of were given one meal but were not enterally fed. A
usual intake, then 15% to 25% of usual insulin can be study comparing enteral feedings of standard and dia-
given, with increases in daily insulin dose based on betic formulas in nursing home residents with DM
feeding rate and blood glucose levels. Regular insulin failed to show a significant difference in plasma glucose
should be used until tolerance of EN is demonstrated. or
The dose and frequency of administration of interme- in blood
Hgb Alc. 22 Dietary fiber intake may also play a role
glucose management, although further
diate-acting varies with the route of SNS administra- research is needed to determine the most appropri-
tion. Glucose levels should be monitored until they
stabilize.l6 Insulin infusion should be initiated if glu- ate form (soluble or insoluble) and amount of fiber
cose goals cannot be achieved with subcutaneous
needed.23 Based on available research, there is not
administration. Oral diabetic agents are appropriate sufficient evidence at this time to recommend routine
for use in stable patients with type 2 diabetes who have use of specialized enteral formulas for patients with
normal hepatic and renal function and are receiving DM or abnormal glucose control. More research is
EN. needed on the effect of different types of fat on long-
When initiating PN, insulin
therapy should be con- term outcomes in enterally fed patients with DM.19
tinued in patients with type 1 diabetes and in patients
with type 2 diabetes who previously required insulin. Practice Guidelines
.

Insulin therapy should be initiated in patients with Diabetes mellitus

blood glucose levels consistently greater than 200
mg/dL. It is recommended that initially 0.1 unit of 1. Patients with diabetes mellitus are at nutrition
regular insulin be added for each gram of dextrose in risk and should undergo nutrition screening to
PN solutions in order to meet basal insulin require- identify those who require formal nutrition
ments. 17 Parenteral dextrose should be kept constant assessment with development of a nutrition care
until blood glucose levels are controlled. Depending on plan. (A)
the level of glucose control, patients may require 2. In ambulatory, otherwise healthy people with dia-
increased insulin in the PN, additional subcutaneous betes mellitus, strict glucose control is recom-
insulin, or an insulin infusion. Because there is a vari- mended to decrease the incidence of diabetes-re-
able amount of insulin binding to PN bags and tubing, lated complications. (A)
depending on materials used, it is important to be 3. Blood glucose levels should be maintained in the
aware of this and adjust insulin dosage accordingly. 100 to 200 mg/dL range in hospitalized patients
Gastroparesis, abnormal gastric emptying, and with diabetes mellitus. (A)
impaired small bowel motility occur in a significant 4. The macronutrient composition of EN and PN
number of persons with DM and may be exacerbated provided to patients with DM should be individ-
by poor blood glucose control. Gastroparesis may make ualized and avoid administration of excess calo-
glucose control more difficult. 18 The presence of gastro- ries. (B)
56SA

REFERENCES ETHICAL AND LEGAL ISSUES

1. Rayfield EJ, Ault MJ, Keusch GT, et al: Infection and diabetes:
the case for glucose control. Am J Med 72:439-450, 1982
Introduction
2. American Diabetes Association: Nutrition recommendations and
Specializednutrition support is provided when
principles for people with diabetes mellitus. Diabetes Care
22(Suppl 1):S42-S45, 1999 patients unable to take adequate hydration or
are
3. Garg A, Bantle J, Henry R, et al: Effects of varying carbohydrate nutrients independently by mouth. SNS is considered a
content of diet in patients with NIDDM. JAMA 271:1421-1428, medical therapy. Withholding or withdrawing SNS
1994 often involves different considerations than other life-
4. Wright J: Total parenteral nutrition and enteral nutrition in sustaining therapies, in part because of emotional, reli-
diabetes. Curr Opin Clin Nutr Met Care 3:5-10, 2000
5. American Diabetes Association: Maximizing the role of nutrition gious, and symbolic meanings. Since this organization
in diabetes management. American Diabetes Association, Alex- last published ethical and legal guidelines about SNS,L
andria, VA, 1994 little has changed in the legal or ethical approaches to
6. Parillo M, Rivellese AA, Ciardullo AV, et al: A high monounsat- withholding or withdrawing specialized nutrition sup-
urated fat/low carbohydrate diet improves peripheral insulin port. However, additional evidence has accumulated
sensitivity in non-insulin dependent diabetic patients. Metabo- about the natural course of certain subsets of patients
lism 41:1371-1378, 1992
who may require this support. This information has
7. Zerr KJ, Furnary AP, Grunkemeier GL, et al: Glucose control
lowers the risk of wound infection in diabetics after open heart significant implications for caregivers.
operations. Ann Thorac Surg 63:356-361, 1997 The use of SNS involves understanding the medical
8. Pomposelli JJ, Baxter JK, Babineau TJ, et al: Early postopera- indications, including benefits and burdens. Next, it
tive glucose control predicts nosocomial infection rate in diabetic involves applying these interventions in a moral, eth-
patients. JPEN 22:77-81, 1998 ical, and legal construct that is satisfactory to patients,
9. Golden SH, Peart-Vigilance C, Kao WH, et al: Perioperative
families, and caregivers.
glycemic control and the risk of infectious complications in a
cohort of adults with diabetes. Diabetes Care 22:1408-1414,
1999
10. DCCT Research Group: The effect of intensive treatment of Evidence
diabetes on the development and progression of long-term com-
plications of insulin-dependent diabetes mellitus. N Engl J Med Consideration of the ethical and legal aspects of
329:977-986, 1993 delivering SNS first requires choosing therapy that
11. UK Prospective Diabetes Study (UKPDS) Group: Intensive blood is medically appropriate. There are a wide variety
control with sulfonylureas or insulin compared with conven- of patients who may require SNS. Some authors make
tional treatment and risk of complications in patients with type a distinction between those who cannot physically
2 diabetes (UKPDS 33). Lancet 352:837-853, 1998
or metabolically take adequate hydration and nutri-
12. Baxter JK, Babineau TJ, Apovian CM, et al: Perioperative glu-
cose control predicts increased nosocomial infection in diabetics
ents from those who choose not to eat or drink. In
Crit Care Med 18:S207, 1990 general, it is medically indicated and ethically re-
13. DCCT Research Group: Hypoglycemia in the diabetes control quired to administer specialized nutrition to patients
and complications trial. Diabetes 46:271-286, 1997 with anatomic or metabolic diseases. The ethical, legal,
14. Hirsch IB, Paauw DS, Brunzell J: Inpatient management of and moral debates surround patients with fatal dis-
adults with diabetes. Diabetes Care 18:870-878, 1995
eases, progressive dementia, and persistent vegetative
15. Park RH, Hansell DT, Davidson LE, et al: Management of dia-
betic patients requiring nutritional support. Nutrition 8:316-
state.
320, 1992 When deciding to administer SNS, caregivers need
16. McMahon MM, Hurley DL: Enteral nutrition and diabetes mel- to know the risk of intervention as well as the evidence
litus. IN Rombeau JL, Rolandelli RH (eds). Clinical Nutrition: regarding use in selected populations. For example,
Enteral and Tube Feeding, 3rd ed. WB Saunders, Philadelphia, recent evidence has shown that gastrostomy tubes
1997 are of doubtful effectiveness in the late stages of
17. McMahon MM: Management of hyperglycemia in hospitalized
cancer or AIDS.2 In addition, studies have shown
patients receiving parenteral nutrition. Nutr Clin Pract 12:35- that hospitalized patients who require gastrostomy
38, 1997
18. Horowitz M, Wishart JM, Jones KL, et al: Gastric emptying in tube placement have a high complication rate, and
diabetes: An overview. Diabetes Med 13(Suppl):S16-S22, 1996 patients with dementia who require gastrostomy tubes
19. Coulston AM: Enteral nutrition in the patient with diabetes due to anorexia have a high 30-day and 1-year
mellitus. Curr Opin Nutr Met Care 3:11-15, 2000
20. Peters AL, Davidson MB, Isaac RM: Lack of glucose elevation
mortality.3-5 This information enables members of the
after simulated tube feeding with low carbohydrate, high fat
health care team to advise patients and their families
enteral formula in patients with type I diabetes. Am J Med about the medical appropriateness of these therapies.
87:178-182, 1989 Health care professionals have come to propose a more
21. Peters AL, Davidson MB: Effects of various enteral feeding prod- .

prudent use of SNS in these populations. 6,7 There

ucts on post-prandial blood glucose response in patients withL remains a need for additional studies of costly and
type I diabetes. JPEN 16:69-74, 1992
22. Craig LD, Nicholson S, Silverstone FA, et al: Use of a reduced- _
potentially hazardous nutrition support interven-
carbohydrate, modified-fat enteral formula for improving meta- _ tions.88
bolic control and clinical outcomes in long-term care residents; In an otherwise psychologically competent and
with Type 2 diabetes: Results of a pilot study. Nutrition 14:529- -

informed adult, choosing not to eat or drink (eg, polit-

534, 1998 ical protest) is an autonomous decision that should be
23. Thomas BL, Laine DC, Goetz FC: Glucose and insulin response
in diabetic subjects: Acute effects of carbohydrate level and the~ respected by physicians and caregivers, even if it
addition of soy polysaccharide in defined formula diets. Am J r results in the persons death. This is supported legally
Clin Nutr 48:1048-1052, 1988 and ethically in the United States9-11 but not every-
 57SA

where (eg, in Israel, societal respect for individual life tional protection for infants, for whom adequate nour-
is considered more important than individual auton- ishment and hydration is mandated even in irrevers-
omy, and patients may be fed against their will).12 ible coma, presumably because of the completely
Patients with anorexia nervosa or dementia have psy- dependent nature of all newborns. Withdrawal of this
chological disorders that result in malnutrition. It is support, once started, may be discussed by caregivers
considered legal and ethical to administer specialized and requested by parents. If there is a disagreement,
nutrition to patients with these disorders, although it ethics consultation and mediation should occur before
may not always be effective medically. Patients who seeking legal involvement and review.-15
forcibly remove enteral or intravenous feeding tubes Although withdrawing and withholding treatment
may be considered to have refused this method of feed- are equally justifiable from an ethical and legal per-
ing, but if their psychological competence is in doubt, spective, it is often harder for caregivers to withdraw
they may be restrained for ongoing feeding. Patients support already initiated than to withhold it.11 This is
who are deemed psychologically competent and remove due to concern that
their feeding tubes or intentionally tamper or contam- with
withdrawing therapy in patients
end-stage disease may hasten their death. How-
inate them should be allowed to refuse this therapy.
ever, it is important to understand that withdrawal of
Much of the debate about administration of SNS
or SNS often allows death from the natural
would be avoided if every patient had an unambiguous hydration
course of the disease itself. Although physicians gen-
living will outlining advance directives and if this doc- erally believe it is ethical to withdraw nutrition and
ument were used appropriately. This document would
in certain patients,16 significant debate con-
indicate whether (and for how long) patients would hydration
tinues whether dying patients suffer from thirst or
desire certain treatments and services. The Patient
at the end of life.17-19
Self-Determination Act of 1990 mandated that all hunger
Fears about withdrawing treatment that has already
health care institutions receiving Medicare and Med-
icaid funding must provide patients with written infor- started may prevent initiation of therapies in patients
with poor or uncertain prognoses and therefore deprive
mation regarding their states law about advance direc-
tives as well as their individual rights to refuse a patient of potential benefit. An approach to this con-
treatment. 13 Unfortunately, despite this legislation, cern may be to start such therapy with defined goals
most patients do not have a living will, and many and end points, thereby limiting the therapy prospec-
patients with living wills do not specify nutritional tively.In cases in which there is disagreement or uncer-
needs in their directives. Even when a well-executed
advance directive is available, family dynamics, cul- tainty about the course of action for a patient who
tural differences between caregivers and patients, and requires artificial hydration or feeding, an ethics con-
sultation should be obtained. Many hospitals now sup-
many other factors may have the practical effect of
negating the directives. When an advance directive is port a diverse group of professionals and lay people
not available, an identified durable power of attorney who constitute an ethics consultation service. Individ-
for health care is legally authorized to make decisions uals with specific expertise in nutrition support should
about withholding or withdrawing therapies. 14 In the be members of this group.o This group may provide an
absence of an unambiguous living will or durable analysis of the special circumstances of individual
power, the courts have identified surrogates to act as cases, offer opinions, mediation skills, And if necessary,
decision-makers. This occurs in a defined order, usu- recommend legal involvement.21 Recent work has dem-
ally consisting of the patients spouse, followed by any onstrated that effective use of ethics consultation may
adult children, followed by parents. be cost saving as we11.22
Many times, surrogate decision makers do not know
the wishes of the patient and must rely on the guidance Practice Guidelines
.

of experienced clinicians and caregivers. It is impor- Ethical ., Legal Issues

tant that caregivers consider the social and cultural
implications of feeding and understand the medical, 1. Legally and ethically, SNS should be considered a
ethical, and legal ramifications in order to help medical therapy. (A)
patients and families make the best decisions about 2. Care providers should be familiar with current
their care. When it remains unclear what the patient
evidence of the benefits and burdens of SNS. (C)
would have desired, guidelines from the Hastings Cen-
ter provide assistance in surrogate decision-making.
3. Patients should be encouraged to have living wills
These guidelines require evaluating the burdens and and/or advance directives and to discuss with
benefits of an intervention from the patients perspec- their loved ones their wishes in the event of a
tive and choosing therapies with a higher benefit-to- serious or terminal accident or disease. (C)
burden ratio. When it is uncertain what this ratio is, 4. Adult patients or their legally authorized surro-
the guidelines recommend administering the inter- gates have the right to accept or to refuse SNS. (A)
vention. 5. The benefits and burdens of SNS, and the inter-
In the case of young children, parents have a moral ventions required to deliver it, should be consid-
and legal obligation to provide the necessary care for ered before offering this therapy. (B)
them. This care includes nutrition support in the form 6. Institutions should develop clear policies regard-
of hydration or feeding. Federal law provides addi- ing the withdrawal or withholding of SNS and
58SA

communicate these policies to patients in ac- health care professionals are paying increased atten-
cordance with the Patient Self-Determination tion to the quality of life of their patients. Health-
Act. (A) related quality of life (HRQOL) has become an increas-
ingly important consideration in the treatment of
REFERENCES patients. However, this field of research is relatively
new, and there is insufficient evidence to support the
1. A.S.P.E.N Board of Directors: Ethical and legal issues in special-
ized nutrition support. JPEN 17(Suppl):50SA-52SA, 1993
issuance of practice guidelines for use of HRQOL tools
2. Powell-Tuck J: Nutrition support in advanced cancer. J Roy Soc in routine practice. There is also insufficient evidence
Med 90(11):591-592, 1997 to differentiate between various nutrition support
3. Abuksis G, Mor M, Segal N, et al: Percutaneous endoscopic interventions in specific therapeutic areas based solely
gastrostomy: High mortality rates in hospitalized patients. Am J on HRQOL information. This discussion will highlight
Gastroenterol 95(1):128-132, 2000
4. Sanders DS, Carter MJ, DSilva J, et al: Survival analysis in the importance of HRQOL methodologies in refining
percutaneous endoscopic gastrostomy feeding: A worse outcome and improving nutrition support therapies in the
in patients with dementia. Am J Gastroenterol 95(6):1472-1475, future.
2000
5. Nair S, Hertan H, Pitchumoni CS: Hypoalbuminemia is a poor
HRQOL has been defined as &dquo;patients appraisals of
their current level of functioning and satisfaction with
predictor of survival after percutaneous endoscopic gastrostomy
in elderly patients with dementia. Am J Gastroenterol 95(1): it compared with what they perceive to be ideal.&dquo; This
133-136, 2000 definition incorporates &dquo;the impairments, functional
6. Finucane TE, Christmas C, Travis K: Tube feeding in patients states, perceptions, and social opportunities that are
with advanced dementia: A review of the evidence. JAMA
282(14):1365-1370, 1999
influenced by disease, injury, treatment, or policy.&dquo;
7. Gillick MR: Rethinking the role of tube feeding in patients with The purpose of HRQOL measurement is not to eval-
advanced dementia. N Engl J Med 342(3):206-210, 2000 uate symptoms; rather it is used to describe the
8. August DA: Creation of a specialized nutrition support outcomes
research consortium: If not now, when? JPEN 20(6):394-400,
patients subjective experience. As such it is critical to
1996
keep in mind that HRQOL should incorporate those
9. Quill TE, Byock IR: Responding to intractable terminal suffer- aspects (often called domains) of their life that are
ing: the role of terminal sedation and voluntary refusal of food affected by their health. In general, these domains
and fluids. ACP-ASIM End-of-Life Care Consensus Panel. Amer- include physical, psychological, social and spiritual
ican College of Physicians-American Society of Internal Medicine
components. A narrower subset of domains is typically
[erratum in Ann Intern Med 20;132( 12):1011, 2000]. Ann Intern assessed to focus on those domains
Med 132(5):408-414, 2000 likely to be influ-
10. Snyder L: Life, death, and the American College of Physicians: enced by the intervention of interest.
The Cruzan case. Ann Intern Med 112(11):802-804, 1990 Nutrition intervention can affect a variety of
11. American College of Physicians: Ethics Manual, 4th ed. Ann domains, either by improving health status or through
Intern Med 128(7):576-594, 1998 factors associated with treatment.3-9 Physically,
12. Glick SM: Unlimited human autonomy-a cultural bias? N Engl
J Med 336(13):954-956, 1997 important domains may include physical functioning,
13. Areen J: Advance directives under state law and judicial deci- activities of daily living, recreation, and fatigue. In the
sions. Law Med Health Care 1-2:91-100, 1991 psychological/emotional area important domains
14. Annas GJ: The health proxy and the living will. N Engl
care include depression, anxiety/fear, body image, and inde-
J Med 324(17):1210-1213, 1991
15. Mayo TW: Forgoing artificial nutrition and hydration: Legal and pendence. The social area may incorporate family and
ethical considerations. Nutr Clin Pract 11(6):254-264, 1996 marital relationships, sexual life, and social interac-
16. Payne K, Taylor RM, Stocking C, et al: Physicians attitudes tions. Additional domains may well include financial
about the care of patients in the persistent vegetative state: A status, appetite/eating/hunger, symptoms, and overall
national survey. Ann Intern Med 125(2):104-110, 1996 or general health.
17. McCann RM, Hall WJ, Groth-Juncker A: Comfort care for ter-
A number of tools have been used to assess HRQOL.
minally ill patients. The appropriate use of nutrition and hydra-
tion. JAMA 272(16):1263-1266, 1994 These can be divided into two groups: generic HRQOL
18. Vullo-Navich K, Smith S, Andrews M, et al: Comfort and inci- measures, which are designed to be used across a wide
dence of abnormal serum sodium, BUN, creatinine and osmo-
range of diseases, and disease-targeted measures,
lality in dehydration of terminal illness. Am J Hosp Palliat Care which are developed to focus on a specific disease.
15(2):77-84, 1998
19. Printz LA: Terminal dehydration, a compassionate treatment. Generic measures are often less sensitive than disease-
Arch Intern Med 152(4):697-700, 1992 targeted measures, but have the advantage that they
20. Dorner B, Gallagher-Allred C, Deering CP, et al: The "to feed or can be used to make comparisons across a number of
not to feed" dilemma. J Am Diet Assoc 97(10 Suppl 2):S172- diseases. Examples of generic measures that have been
S176, 1997 used for patients receiving nutrition therapy include:
21. La Puma J, Schiedermayer D, Siegler M: How ethics consulta-
tion can help resolve dilemmas about dying patients. West J Med the Short Form-36 (SF-36), the EuroQol EQ-5D, the
163(3):263-267, 1995 Profile of Mood States, the Nottingham Health Profile,
22. Heilicser BJ, Meltzer D, Siegler M: The effect of clinical medical the Quality of Well-Being scale, the Sickness Impact
ethics consultation on healthcare costs. J Clin Ethics 11(1):31-
38 2000
Profile (SIP), Rosenbergs Self Esteem scale, the Nor-
--, ----
ton scale, and the Barthel Activities of Daily Living
Index. Disease-targeted measures have included: the
QUALITY OF LIFE QOL for liver transplants, the Inflammatory Bowel
Disorder QOL form (IBDQOL), and the European
Background Organization for Research and Treatment of Cancer
As attention has shifted from purely life-saving tech- (EORTC) core questionnaire, along with the head and
nologies to those that improve patients experiences, , neck and the esophageal modules of the EORTC.
 59SA

Evidence may include a disease-targeted measure. Such tools

focus on the specific disease (ie, cancer, inflammatory
HRQOL research in nutrition support is still in its bowel disease, AIDs, etc). Examples of disease-targeted
infancy. Currently HRQOL investigations do not lead measures include the EORTC (with appropriate mod-
to any solid conclusions. There are, however, two areas
of research where HRQOL methods have shed some ules), the FACT, and the IBDQOL.
light. First, using cross-sectional HRQOL data (obser- Practice ~. .

vations for multiple patients at a single point in time),

researchers have shown that patients requiring nutri- Quality , ,
tion support have worse HRQOL compared with those
not requiring support. Second, longitudinal HRQOL 1. The subjective patient experience receiving SNS
data (observations for each patient at multiple points should be measured with an HRQOL tool. (B)
in time) show that SNS generally leads to improved 2. A nutrition support HRQOL tool should include
HRQOL. generic and disease targeted measures for either
More specifically, cross-sectional data analysis cross-section and/or longitudinal observations. (C)
shows that (1) patients receiving HPN are worse off
than the normal population and have a HRQOL com-
parable or worse than those with chronic renal failure REFERENCES
treated by dialysis 10-15; (2) patients receiving HPN
1. Cella DF, Tulsky DS: Measuring quality of life today: Method-
may be worse off than patients with anatomical or
functional short bowel disease not receiving HPN 16,17; ological aspects. Oncology 5:29-38, 1990
2. Patrick DL, Erickson P: Health Status and Health policy: Qual-
(3) opiate-dependent patients are worse off than non- ity of life in Health Care Evaluation and Resource Allocation.
opiate-dependent patients receiving HPN18; and (4) Oxford University Press, New York, 1993
caregivers of patients on long-term HPN have lower 3. Detsky AS, McLaughlin JR, Abrams HB, et al: Quality of life of
HRQOL. patients on long term total parenteral nutrition at home. J Gen
Intern Med 1:26-33, 1986
HRQOL improvements related to nutrition support 4. Herfindal ET, Bernstein LR, Kudzia K, et al: Survey of home
show by longitudinal evaluations that (1) nutrition nutritional support patients. JPEN 13:255-261, 1989
support may provide HRQOL improvement, although 5. Malone M: Quality of life of patients receiving home parenteral
the burden of invasive support may be associated with orenteral nutrition support. PharmacoEconomics 5(2):101-108,
some decline in psychosocial domains 19 -24; (2) patients 1994
6. Maunder RG, Cohen Z, McLeod RS, et al: Effect of interven-
with weight in the less-than-desirable range experi- tion in inflammatory bowel disease on health-related quality of
ence HRQOL improvements with HPN, whereas life: A critical review. Qual Life IBD Treat 38(11):1147-1161,
patients with weight in the desirable range do not25; (3) 1995
7. Grindel CG, Whitmer K, Barsevick A: Quality of life and nutri-
patients who receive an intestinal transplant experi- tional support in patients with cancer. Cancer Pract 4(2): 81-87,
ence better HRQOL than those receiving HPN16,17; and
1996
(4) an oral, semi-elemental diet provides better 8. Kotler DP: Management of nutritional alterations and issues
HRQOL outcomes than TPN in AIDs patients.26 concerning quality of life. J Acquir Immune Defic Synd Human
Retrovirol 16(Suppl 11):S30-S35, 1997
9. Richards DM, Irving MH: Cost-utility analysis of home paren-
Special Considerations teral nutrition. Br J Surg 83:1226-1229, 1996
10. Smith CE: Quality of life in long-term total parenteral nutrition
In an ideal academic environment, one would patients and their family caregivers. JPEN 17(6): 501-506, 1993
disease- or nutrition-specific HRQOL tool 11. Carlson GL, Maguire G, Williams N, et al: Quality of life on home
develop a
parenteral nutrition: A single centre study of 37 patients. Clin
and then validate it in the appropriate patient popula- Nutr 14:219-228, 1995
tion. The time and resources necessary for this 12. Richards DM, Irving MH: Assessing the quality of life on
approach in each and every disease state is generally patients with intestinal failure on home parenteral nutrition.
not available. In our resource-constrained environ- Gut 40:218-222, 1997
13. Reddy P, Malone M. Cost and outcome analysis of home paren-
ment, researchers may be best served by using a mod- teral and enteral nutrition. JPEN 22(5):302-310, 1998
ular approach in which the core HRQOL measure 14. Jeppesen PB, Langholz E, Mortensen PB: Quality of life in
remains the same and only disease-specific compo- patients receiving home parenteral nutrition. Gut 44:844-852,
nents change for the specific disease of interest. The 1999
core may consist of a generic measure and a nutrition- 15. Schneider SM, Pouget I, Staccini P, et al: Quality of life in
long-term home enteral nutrition patients. Clin Nutr 19(1):23-
targeted component. The generic measure is useful for 28, 2000
making comparisons across populations and to evalu- 16. Rovera GM, DiMartini A, Schoen RE, et al: Quality of life of
ate unpredicted HRQOL effects. The nutrition-tar- patients after intestinal transplantation. Transplantation 66(9):
geted component includes those domains not assessed 1141-1145, 1998
17. DiMartini A, Rovera GM, Graham TO, et al: Quality of life after
by the generic measure and would focus on nutrition- small intestinal transplantation and among home parenteral
specific effects such as fatigue, body image, and symp- nutrition patients. JPEN 22(6):357-362, 1998
toms. The nutrition-targeted component can consist of 18. Richards DM, Scott NA, Shaffer JL, et al: Opiate and Sedative
scales from existing measures (for example, the fatigue Dependence Predicts a Poor Outcome for patients Receiving
scale from the Functional Assessment of Cancer Ther- Home Parenteral Nutrition: JPEN 21(6): 336-338, 1997
19. King LA, Carson LF, Konstantinides RN, et al: Outcome assess-
apy (FACT) and the sexual function scale from the ment of home parenteral nutrition in patients with gynecologic
Medical Outcomes Study). malignancies: What have we learned in a decade of experience?
In addition to the core HRQOL measure, researchers Gynecol Oncol 53:377-382, 1993
60SA

20. Siskind MS, Lien Y-HH: Effect of intradialytic parenteral nutri- 24. Roberge C, Tran M, Massoud C, et al: Quality of life and home
tion onquality of life in hemodialysis patients. Int J Artifical enteral tube feeding: A French prospective study in patients
Organs 16(8):599-603, 1993 with head and neck or oesophageal cancer. Br J Cancer 82(2):
21. Edwards MW, Drexler AM, Aboulafia DM, et al: Efficacy of total 263-269, 2000
parenteral nutrition in a series of end-stage AIDS patients: A 25. Jamieson CP, Norton B, Lakeman M, et al: The quantitative
case-control study. AIDS Patient Care STDs 11(5):323-329, 1997 effect of nutrition support on quality of life in outpatients. Clin
22. Torelli GF, Campos AC, Meguid MM: Use of TPN in terminally Nutr 16:25-28, 1997
ill cancer patients. Nutrition 15(9):665-667, 1999 26. Kotler DP, Fogleman L, Tierney AR: Comparison of total paren-
23. Beattie AH, Prach AT, Baxter JP, et al: A randomised controlled teral nutrition and an oral, semielemental diet on body compo-
trial evaluating the use of enteral nutritional supplements post- sition, physical function, and nutrition-related costs in patients
operatively in malnourished surgical patients. Gut 46:813-818, with malabsorption due to acquired immunodeficiency syn-
2000 drome. JPEN 22(3):120-126, 1998
 SECTION XI: Specific Guidelines for Disease-Adults

CARDIAC DISEASE mias, and renal failure) and mortality has been shown
in some although not all studies in cardiac surgery
Background .

patients. Abel et a1,6 in 100 consecutive adults under-

Cardiac cachexia is a syndrome of severe malnutri- going cardiac surgery, found no strong correlations
tion that occurs in a minority of patients with New between anthropometric or biochemical measurements
York Heart Association class III or IV congestive heart of malnutrition or decreased cell-mediated immunity
failure (CHF). It involves depletion of lean body mass and postoperative morbidity and mortality. They did
(including vital organs such as the heart) leading to point out, however, that most of their patients had
declines in performance status and immune function. arteriosclerotic disease and were not at high risk for
Presence of cachexia is associated with decreased sur- cachexia. They concluded that routine nutrition assess-
vival in patients with congestive heart failure. A classic ment is of little value in management of these patients.
description of cardiac cachexia was published by Pitt- In a more recent study, Ulicny et al prospectively
man and Cohen in 1964.1 examined 221 adult cardiac surgery patients.7 They
The cause of cardiac cachexia is multifactorial.2 The found no significant correlations between visceral pro-
fatigue seen in CHF patients leads to decreased phys- tein status, acute phase protein response, or delayed
ical activity that in turn leads to decreased lean body hypersensitivity reaction and development of sternal
mass. Anorexia is a common finding and may be wound infection. Again, however, most of their patients
related to drug therapy, bowel edema leading to gas- had normal preoperative nutrition status.
trointestinal hypomotility and nausea, and restriction Several recent studies have identified a correlation
to a bland, low-sodium diet. The bowel edema may also between blood glucose control and incidence of postop-
result in nutrient malabsorption in the intestine. Dys- erative infectious complications, especially sternal
pnea may lead to increases in resting energy expendi- wound infections. In addition, Babineau et al5 dem-
ture in this population. Increase in energy expenditure
onstrated a higher prevalence of diabetes and
may also be related to the compensatory activation of
the sympathetic nervous system. hyperglycemia in patients requiring PN after CPB
Recent research has focused on the role of cytokines compared with CPB patients not requiring PN.
in the pathogenesis of cardiac cachexia.3 In particular, Other authors have suggested that a prolonged time
elevated circulating levels of tumor necrosis factor- to enteral alimentation after coronary bypass graft-
alpha (TNF) have been demonstrated in patients with ing is a risk factor for the development-of postoper-
severe CHF, especially in those with cachexia. ative infections.8
Although elevation of TNF might initially have a ben- The objectives for nutrition management of patients
eficial effect by accelerating catabolism of muscle tis- with chronic congestive heart failure include reduction

sue to provide substrates for a hepatic acute-phase in the workload of the heart, maintenance of dry
response, continued elevation leading to continued loss weight, and maintenance of optimal nutrition status.9
of lean body mass is deleterious. General nutrition intervention includes sodium and
Postoperative open heart surgery patients with com- fluid management. Although sodium and fluid restric-
plications are another population with potential need tion are often necessary, each situation must be
for nutritional support.4 In one study, 5% of patients assessed individually. For example, a sodium depletion
undergoing cardiopulmonary bypass (CPB) developed syndrome may sometimes occur, especially in elderly
postoperative complications necessitating PN.~ Only a patients put on strict sodium restriction. In addition,
minority of open heart surgery patients will demon- supplementation of magnesium and potassium may be
strate the frank cardiac cachexia of congestive heart necessary in patients receiving diuretics.
failure described above. Although theoretically SNS might be useful in
achieving and maintaining better nutrition status in
Evidence patients with cardiac cachexia, clinical trial data sup-
porting this hypothesis are scarce. Heymsfield and
A correlation between preoperative malnutrition and Casper studied continuous nasogastric feeding to pro-
increased postoperative morbidity (such as infectious mote accrual of lean body mass in undernourished
complications, respiratory failure, pneumonia, arrhyth- patients with moderate to severe CHF.1 Over a
61SA
62SA

2-week period, patients had a net loss of extracellular In the post-CPB patient requiring SNS, pancreatitis
fluid with a gain in lean body mass; cardiac function may develop. Babineau and colleagues reported a mild
was unchanged. form of pancreatitis characterized by hyperlipasemia
Paccagnella et al studied the effects of nutrition sup- and early intolerance to EN into the stomach or duo-
port pre- and postoperatively in six patients with mal- denum in post-CPB patients.14 The incidence of symp-
nutrition secondary to severe mitral valve disease and tomatic hyperlipasemia was 1.3%. Although these
congestive heart failure. 11 Four of the patients received authors did not recommend avoidance of enteral feed-
oral food plus PN for 2 weeks preoperatively and for 3
weeks postoperatively, whereas two of the patients
ing in the critically ill patient post CPB, they did rec-
ommend caution with monitoring of the serum lipase
only received the PN postoperatively. Hemodynamic and consideration of feeding distal to the ligament of
function, oxygen consumption, and carbon dioxide pro- Treitz.
duction were not adversely affected by the PN. Visceral
Patients requiring PN after cardiac surgery have
protein levels were improved in these patients at week been shown to have a higher prevalence of volume
2 or 3 postoperatively compared with 2 weeks preoper-
atively. Other clinical findings included a decrease in overload, hyponatremia, metabolic alkalosis, and ure-
anorexia and proteinuria over the study period. The mia compared with similar patients not requiring PN.
authors concluded that nutrition support could be These factors should be taken into account when for-
safely given to such patients and that such support mulating SNS for this population. For example, use of
improves clinical status. concentrated stock solutions to decrease fluid load and
In an early study of the effect of nutrition support in decrease the acetate to chloride ratio in the solution
malnourished patients on outcome after cardiac sur- should be considered.
gery, Abel et al gave PN containing approximately A serious but potentially fatal rare complication of
1000 kcal and 5 g nitrogen per day to 20 patients for 5 early jejunal feeding after surgery in trauma patients
days immediately postoperatively. 12 There was no is bowel necrosis. Some research indicates that
effect on morbidity and mortality in comparison to decreased mesenteric blood flow is a risk factor for
malnourished and nonmalnourished controls not development of this complication,15 although another
receiving PN. The malnourished patients in this study series of case reports does not corroborate these find-
were truly depleted, having a weight loss of at least 4.5
ings. i6 Because of the potential for this serious compli-
kg over 12 months, a body weight less than 85% of cation, many clinicians are hesitant to initiate jejunal
ideal, or giving a clinical impression of malnutrition on feedings in a patient who is hemodynamically unstable
the basis of physical examination. and thus may not have good blood flow to the gastro-
In a more recent study, Otaki studied 25 patients intestinal tract. Although this issue has not been stud-
with New York Heart Association Class IV heart fail- ied specifically in the cardiac surgery population, a
ure with body weights less than 80% of ideal. 13 Eigh-
prudent approach would be to delay jejunal feedings
teen of the patients were given 5 to 8 weeks of preop- until the patient is hemodynamically stable and to
erative PN containing 1000 kcal and 6 g nitrogen daily. monitor closely for abdominal distention after initia-
The other 7 patients were not given preoperative PN. tion of tube feedings.
Patients receiving PN had a mortality rate of 17%
compared with 57% for those without PN. Patients Practice ,. .
.

with preoperative nutrition support also had signifi- Cardiac Disease ,

cant decreases in the incidence of postoperative respi-

ratory failure. 1. Patients with cardiac cachexia or who develop
complications after CPB are at nutrition risk, and
Special Considerations should undergo nutrition screening to identify
Nutrition assessment of the patient with cardiac those who require formal nutrition assessment
with development of a nutrition care plan. (B)
cachexia may be challenging. Excess extracellular fluid
2. The use of PN should be reserved for those cardiac
as well as malnutrition may contribute to decreases in
visceral protein markers such as albumin and trans- patients having postoperative complications that
ferrin. Although total body weight may be decreased preclude use of the gastrointestinal tract. (C)
3. In the cardiac surgery patient, EN should be
when compared with premorbid body weight, the
excessive extracellular fluid may mask weight loss. An deferred until the patient is hemodynamically
entire spectrum of malnutrition occurs in patients with stable. (C)
chronic congestive heart failure; on one end of the
spectrum are the classic cases of cardiac cachexia with REFERENCES
severe loss of lean body mass, whereas other cases are
1. Pittman JG, Cohen P: The pathogenesis of cardiac cachexia.
less pronounced. A loss of greater than 10% of lean N Engl J Med 271:403-409, 1964
body mass has been used to define cardiac cachexia; 2. Freeman LM, Roubenoff R: The nutrition implications of cardiac
unfortunately, in the clinical setting a good estimation cachexia. Nutr Rev 52:340-347, 1994
of loss of lean body mass may be very difficult to deter- 3. Anker SD, Coats AJS: Cardiac cachexia. A syndrome with
mine. This definition is felt to be helpful, however, impaired survival and immune and neuroendocrine activation.
Chest 115:836-847, 1999
because at this level reduced immune function can 4. Ulicny KS, Hiratzka LF: Nutrition and the cardiac surgical
2
generally be documented.2 patient. Chest 101:836-842, 1992
 63SA

5. Babineau TJ, Bollinger WS, Forse RA, et al: Nutrition support malnourished COPD patients. 4 Both ventilatory drive
for patients after cardiopulmonary bypass: required modifica- and the response to hypoxia are decreased in malnour-
tions of the TPN solution. Ann Surg 228:701-706, 1998
6. Abel RM, Fisch D, Horowitz J, et al: Should nutritional status be ished COPD patients.5 Alteration in immune function
assessed routinely prior to cardiac operation? J Thorac Cardio- occurs in malnourished COPD patients and may influ-
vasc Surg 85:752-757, 1983 ence the frequency and severity of pulmonary infec-
7. Ulicny KS: Sternotomy infection: poor prediction by acute phase tions. 3,5
response and delayed hypersensitivity. Ann Thor Surg 50:949- Nutrition assessment in patents with COPD is nec-
958, 1990
8. Ford EG, Baisden CE, Matteson ML, et al: Sepsis after coronary essary to identify those with a higher risk of an adverse
bypass grafting: Evidence for loss of the gut mucosal barrier. outcome. A thorough nutrition history, including eval-
Ann Thor Surg 52:514-517, 1991 uation of weight history, nutrient intake, and medica-
9. Hughes C, Kostka P: Chronic congestive heart failure. IN Mod- tion usage will help to develop nutrition goals.3 Nutri-
ern Nutrition in Health and Disease, 9th ed. Shils ME, Olson JA,
Shike M, et al (eds). Williams and Wilkins, Philadelphia, 1999, tion assessment via a multiparameter approach has
pp 1229-1234 been shown to be useful in identifying malnutrition in
10. Heymsfield SB, Casper K: Congestive heart failure: Clinical the COPD patient with acute respiratory failure.
management by use of continuous nasoenteric feeding. Am J ARDS is characterized by severe hypoxemia, diffuse
Clin Nutr 50:539-544, 1989
11. Paccagnella A, Calo MA, Caenaro G, et al: Cardiac cachexia: pulmonary infiltrates, and reduced pulmonary compli-
ance. The degree of hypoxemia is defined by the ratio of
Preoperative and postoperative nutrition management. JPEN
18:409-416, 1994 arterial oxygen concentration to fractional inspired
12. Abel RM, Fischer JE, Buckley MJ, et al: Malnutrition in cardiac oxygen (PaO2/FiO2) with a ratio equal to or less than
surgical patients: Results of a prospective, randomized evalua- 200 diagnostic for ARDS. The etiology of ARDS is mul-
tion of early postoperative parenteral nutrition. Arch Surg 111:
45-50, 1976
tifactorial with sepsis
being the predominant underly-
13. Otaki M: Surgical treatment of patients with cardiac ca- ing cause.6 Inflammatory mediators, including prosta-
chexia&mdash;An analysis of factors affecting operative mortality. glandins and leukotrienes derived from arachidonic7
Chest 105:1347-1351, 1994 acid metabolism, are implicated in acute lung injury.7
14. Babineau TJ, Hernandez E, Forse RA, et al: Symptomatic hyper-
Critical illness can result in altered nutrition status
lipasemia after cardiopulmonary bypass: implications for enteral to the inflammatory response. Marked pro-
nutritional support. Nutrition 9:237-239, 1993 secondary
15. Smith-Choban P, Max MH: Feeding jejunostomy: a small bowel tein catabolism in the absence of exogenous intake can
stress test? Am J Surg 155:112-117, 1988 result in respiratory muscle impairment and decreased
16. Schunn DCG, Daly JM: Small bowel necrosis associated with visceral proteins, factors that may be obstacles to
postoperative jejunal tube feeding. J Am Coll Surg 180:410-416, 8
1995 weaning ventilatory support.8
Evidence
PULMONARY DISEASE
The strong association between nutrition and lung
Background function has been appreciated for many years. In fact,
Nutrition and pulmonary disease are closely related. it is often stated that, &dquo;death from starvation is death
Alterations in nutrition status will have an impact on from pneumonia.&dquo; It is clear that patients with protein-
pulmonary function and conversely, pulmonary func- calorie malnutrition have an increased incidence of
tion can alter nutrition status. Pulmonary disease as pneumonia, respiratory failure, and ARDS.8 At the
presented here will address chronic obstructive pulmo- same time, many patients with COPD have uninten-

nary disease (COPD) and acute respiratory distress tional weight loss.
syndrome (ARDS) SNS is used frequently in patients with COPD, acute
COPD is an obstructive airway disease limiting air- respiratory failure, and ARDS. Unless other clinical
flow which occurs either by destruction of alveoli conditions or complications are present, patients with
(emphysema), by a narrowing of small airways (chronic COPD can improve their nutritional status with oral
bronchitis), or from a combination of both processes. supplements or enteral tube feeding. Patients with
Patients with COPD frequently demonstrate clinical acute respiratory failure or ARDS rarely meet their
sequalae of both emphysema and chronic bronchitis.
nutritional needs orally so they often receive EN or, in
Malnutrition in COPD is common. The incidence of cases where the gastrointestinal tract is not functional
altered nutrition status ranges from 19% to 74%, with or accessible, PN.
a greater incidence in hospitalized patients with acute Nutrition assessment in pulmonary disease is chal-
respiratory failure. 1,2 Decreases in albumin, trans- lenging.9 In COPD, overfeeding with resultant produc-
ferrin, and prealbumin concentrations occur in COPD tion of excess carbon dioxide is the primary concern. A
patients with acute respiratory failure.2 Weight loss number of disease specific predictive formulas have
occurs frequently in COPD. Weight loss is caused by been developed to estimate energy requirements in
.

increased resting energy expenditure, reduced nutri- these patients, but none has been clinically validated.99
ent intake, and inefficient fuel metabolism. Weight, Indirect calorimetry has also been advocated, but is not
loss is known to occur in up to 50% of COPD patients , of proven benefit.10 The situation is similar in patients
who require hospitalization and is an independent pre- .
with ARDS; predictive equations exist and indirect
dictor of mortality. Loss of both fat mass and fat-free~ calorimetry is advocated, but there is no proven opti-
mass occur, with the depletion of fat-free mass carrying; mal approach to nutrition assessment or estimation of
functional implications. 1,3 caloric requirements.9lo
Malnutrition in COPD adversely affects pulmonary T Each of the macronutrients used in SNS has an
function. Respiratory muscle strength is impaired iri individual respiratory quotient (RQ) when metabolized
64SA

for energy. RQ is determined by dividing the C02 pro- Moderate doses of each of the macronutrients appear
duced by the O2 consumed metabolizing the substrate. to be optimal when providing SNS to patients with
The individual RQs for glucose, protein, and fat oxida- pulmonary disorders.11 Both glucose and protein
tion are approximately 1.0, 0.8, and 0.7, respectively. administration have been shown to stimulate ven-
The lower RQ for fat oxidation has created interest in tilatory drive independently after a period of semi-
using it as a major energy component in patients where starvation. However, excessive glucose administration
excessive C02 production is undesirable. Decreased (>5mg/kg per minute) clearly increases C02 produc-
C02 production and a lower RQ have been demon- tion to levels making it difficult to wean patients from
strated when patients have 50% of nonprotein calories mechanical ventilation. Excessive protein administra-
provided as lipid compared with 100% glucose in an tion theoretically could stimulate ventilatory drive to
overfed state. However, when total calories are pro-
the point of patient fatigue. Rapid administration of
vided in moderate amounts (eg, 30% above basal
intravenous lipid (3 mg/kg per minute) may cause sig-
energy expenditure), manipulation of the macronutri- nificant increases in vascular resistance in
ents has little effect on CO2 production, minute venti-
patients with ARDS. 9
pulmomary
lation, and presumably Rt~,11-14 The production of Fluid accumulation and pulmonary edema in pa-
excessive CO2 secondary to nutrition support occurs
tients with ARDS are associated with a poor clinical
when patients are overfed (eg, two times basal energy
oUtCoMe.20 Therefore, it is prudent to use a fluid-re-
expenditure in patients with uncomplicated respira- stricted nutrient formulation in patients whose hemo-
tory failure).11
Most patients with acute respiratory failure and dynamic status necessitates fluid restriction.
many with ARDS can receive EN because their gastro-
Phosphate is essential for the synthesis of ATP and
intestinal tract is accessible and functional. Several 2,3 DPG, both of which are critical for optimal pulmo-
nary function. Normal diaphragmatic contractility is
EN products were developed with a high-fat, low-car- dependent on adequate provision of phosphate. There-
bohydrate composition because of the theoretical fore, particular attention to phosphate balance is nec-
advantage of the lower CO2 production from fat oxida- essary in the patient with underlying pulmonary dis-
tion. Controlled trials in stable outpatients with COPD
ease or acute respiratory failure. Length of hospital
have demonstrated decreased CO2 production, O2 con-
stay and time receiving mechanical ventilation is
sumption, and RQ in patients receiving a high-fat increased in critically ill patients who become
enteral formula compared with a high-carbohydrate
enteral formula; however, the data do not demonstrate hypophosphatemic when compared with those patients
who do not develop this metabolic complication.21
improved clinical outcomes. 15,11 Patients with acute Phosphate replacement in patients with hypophos-
respiratory failure who received high-fat EN also have phatemia receiving SNS is crucia1.22
demonstrated decreased CO2 production and RQ when
compared with those receiving a high-carbohydrate Practice ,..
.

enteral formulation. One study of high fat EN did show

significant reductions in both PaCo2 before extubation Pulmonary Disease ,

and time receiving mechanical ventilation, although

the sample size was quite small.&dquo; 1. Patients with COPD or ARDS are at nutrition

Because ARDS is associated with elaboration of risk and should undergo nutrition screening to
inflammatory cytokines such as interleukin-1, inter- identify those who require formal nutrition
leukin-6, and interleukin-8, nutrition formulations assessment with development of a nutrition care
have been developed containing fatty acids that can plan. (B)
potentially downregulate the inflammatory response. 2. Energy intake should be kept at or below esti-
One study compared the use of a high-fat enteral for- mated needs in patients with pulmonary disease
mulation supplemented with n-3 fatty acids (fish oil and demonstrated carbon dioxide retention. (B)
and borage oil) and antioxidants with a standard high- 3. Routine use of modified carbohydrate and fat
fat enteral formulation. The patients receiving this nutrition formulations in patients with pulmo-
immune-modulating enteral formula spent less time nary disease is not warranted. (B)
receiving mechanical ventilation, less time in the 4. Provision of a modified enteral formulation con-
intensive care unit, and a decreased incidence of organ taining n-3 fatty acids may be beneficial in the
failure.77 patient with early ARDS. (B)
5. A fluid-restricted nutrient formulation should be
used in patients with ARDS whose hemodynamic
Special Considerations status necessitates fluid restriction. (B)
Patients with COPD often have accompanying 6. Serum phosphate levels should be monitored
weight loss. Although decreased nutrient intake sec- closely in patients with pulmonary disease. (B)
ondary to the work of breathing had long been sus-
pected as the primary cause of this weight loss, it is REFERENCES
now clear that weight-losing COPD patients are hyper-
metabolic.l8 This demonstrates a poor adaptive 1. J: The pulmonary cachexia syndrome: aspects of
Congleton
energy balance. Proc Nutr Soc 58:321-328, 1999
response to weight loss. Most patients with other dis- 2. Laaban JP, Kouchakji B, Dore MF, et al: Nutritional status of
ease states will demonstrate a decrease in resting patients with chronic obstructive pulmonary disease and acute
energy expenditure after weight loss. respiratory failure. Chest 103:1362-1368, 1993
 65SA

3. Donahoe M: Nutritional aspects of lung disease. Resp Care Clin when severe hepatocellular dysfunction occurs, be-
NA 4(1):85-111, 1998 -ause the liver role in the metabolism,
4. Gosker HR, Wouters E, van der Vusse G, et al: Skeletal muscle
plays pivotal
a

dysfunction in chronic obstructive pulmonary disease and storage, and distribution of nutrients. Liver disease
chronic heart failure: Underlying mechanisms and therapy per- ~an be divided into several categories that include
spectives. Am J Clin Nutr 71:1033-1047, 2000 iuration (acute vs chronic), pathophysiology (hepato-
5. Pingleton SK: Enteral nutrition in patients with respiratory cellular vs and
disease. Eur Respir J 9:364-370, 1996
cholestasic), etiology (viral, alcohol,
toxin,
autoimmune). Cirrhosis occurs when chronic
6. Bernard GR, Artigan A, Brigham KL, et al: The American-
European Consensus Conference on ARDS: Definitions, mecha- leads
iniury to irreversible scarringof the liver. Mal-
nisms, relevant outcomes and clinical trial coordination. Am J nutrition has been most studied in
extensively patients
Resp Crit Care Med 149:818-824, 1994 with end stage a modest amount of informa-
cirrhosis;
7. Gadek J, DeMichele S, Karlstad M, et al: Specialized enteral tion nutrient status is available
nutrition improves clinical outcomes in patients with or at risk or
regarding concerning
acute respiratory distress syndrome: a prospective, blinded, ran-
with acute alcoholic
patients hepatitis,cholestatic liver
domized, controlled multicenter trial. Crit Care Med 27:1409- and fulminant
disease, hepaticfailure.
1420, 1999 Mortality is increased when malnutrition occurs in
8. Radrizzani D, Iapichino G: Nutrition and lung function in the
critically ill patient. Clin Nutr 17:7-10, 1998
patients with either acute or chronic liver diseases.l>2
9. Hogg J, Lapholz A, Reid-Hector J: Pulmonary disease. IN
Assessment of PCM in the setting of liver disease is
The Science and Practice of Nutrition Support. A Core Cur- particularly difficult because many of the common
riculum. Gottschlich MM (ed). Kendall/Hunt, Dubuque, IA, nutrition assessment parameters (eg, serum albumin)
2001, pp 491-516 are directly affected by hepatic dysfunction even in the
10. Sherman MS: Parenteral nutrition and cardiopulmonary dis- absence of undernutrition. The assessed presence of
ease. IN Clinical Nutrition: Parenteral Nutrition. Rombeau JL,
Rolandelli RH (eds). WB Saunders, Philadelphia, 2000, pp 335- PCM in liver disease patients reflects true malnutri-
352 tion, severity of liver disease, or a combination of both.
11. Talpers SS, Romberger DJ, Bunce SB, et al: Nutritionally asso- The presence of factors associated with PCM has
ciated increased carbon dioxide production: excess total calories been associated with a poor prognosis in patients
vs. high proportion of carbohydrate calories. Chest 102:551-555,
1992 awaiting liver transplantation, in cirrhosis with decom-
12. Sullivan DJ, Marty TL, Barton RG: A case of overfeeding com- pensation, and in cirrhotics undergoing abdominal
plicating the management of adult respiratory distress syn- surgery.3-5 Preoperative malnutrition has also been
drome. Nutrition 11:375-378, 1995 associated with increased operative blood loss, longer
13. Kiiski R, Takala J: Hypermetabolism and efficiency of CO 2 intensive care unit length of stay, increased mortality,
removal in acute respiratory failure. Chest 105; 1198-1203,
1994 and higher total hospital charges after liver transplan-
14. Van den Berg B, Stam H: Metabolic and respiratory effects of tation. Whether PCM is an independent predictor of
enteral nutrition in patients during mechanical ventilation. survival or just a reflection of the severity of liver
Intensive Care Med 14:206-211, 1988 disease remains controversial.77
15. Kuo CD, Shiao GM, Lee JD: The effects of high fat and high
The prevalence of PCM in patients with liver disease
carbohydrate diet loads on gas exchange and ventilation in
COPD patients and normal subjects. Chest 104:189-196, has been reported to range from 10% to 100%. This
1993 broad range reflects a variety of factors that include
16. Akrabawi SS, Mobarhan S, Stoltz RR, et al: Gastric emptying, etiology, severity and type of liver disease, the methods
pulmonary function, gas exchange, and respiratory quotient used to perform the nutrition assessment, and the set-
after feeding a moderate versus high fat enteral formula meal in
chronic obstructive pulmonary disease patients. Nutrition ting where these surveys were performed. PCM has
12:260-265, 1996 been noted to be as low as 20% for patients with com-
17. Al-Saady NM, Blackmore CM, Bennet ED: High fat, low carbo- pensated alcoholic liver disease in the community and
2 and reduces the period of
hydrate enteral feeding lowers PaCO as high as 100% in hospitalized patients with acute
ventilation in artificially ventilated patients. Intensive Care
Med 15:290-295, 1989
alcoholic hepatitis.8 More recent surveys report the
18. Schols AM, Soeters PB, Mostert R, et al: Energy balance in prevalence of PCM to range from 27% to 87% in
chronic obstructive pulmonary disease. Am Rev Respir Dis 143: patients with cirrhosis.9
1248-1252, 1991 The pathophysiology of malnutrition in liver disease
19. Venus B, Smith RA, Patel C, et al: Hemodynamic and gas is complex and often includes multiple processes. Gas-
exchange alterations during Intralipid infusion in patients with trointestinal symptoms which limit food intake are
adult respiratory distress syndrome. Chest 95:1278-1281, 1989
20. Simmons RS, Berdine GG, Seidenfeld JJ, et al: Fluid balance common and include anorexia, early satiety secondary
and the adult respiratory distress syndrome. Am Rev Respir Dis to ascites, altered taste due to zinc and magnesium
135:924-929, 1987 10
21. Marik PE, Bedigian MK: Refeeding hypophosphatemia in criti-
deficiency, nausea, and vomiting. Dietary intake may
also be limited through the prescription of protein and
cally ill patients in an intensive care unit. Arch Surg 131:1043-
1047, 1996 salt restricted diets. Fat malabsorption secondary to
22. Clark CL, Sacks GS, Dickerson RN, et al: Treatment of the diminished production of bile acids can occur in
hypophosphatemia in patients receiving specialized nutrition cholestatic liver disease or when pancreatic exocrine
support using a graduated dosing scheme: Results from a pro- insufficiency accompanies alcoholic liver disease. Mal-
spective clinical trial. Crit Care Med 23:1504-1511, 1995
absorption can occur with drugs such as lactulose and
neomycin or when severe portal hypertension leads to
LIVER DISEASE protein losing enteropathy.
Altered amino acid metabolism is a hallmark of liver
Background disease, characterized by low levels of circulating
Protein calorie malnutrition (PCM) and nutritional branched-chain amino acid (BCAA; leucine, isoleucine
deficiencies are common in liver diseases, especially and valine) and elevated levels of circulating aromatic
66SA

amino acids (AAA; phenylalanine, tyrosine, and tryp- with malnutrition, the impact of nutrition therapy on
tophan) and methionine. Endogenous leucine flux, an outcomes in patients with liver disease varies with the
indicator of protein breakdown, and leucine oxidation indication.ls-23
are increased in the postabsorptive state, and whole The multifactorial wasting condition that is so fre-
body protein synthesis in response to a meal is atten- quently encountered in patients with Child-Pugh-Tur-
uated. &dquo; cotte class B and C cirrhosis may predispose to enceph-
The metabolism of carbohydrate and fat is also alopathy (skeletal muscle is the second largest site of
altered in cirrhosis and can be characterized as a more ammonia metabolism) and other complications of liver
rapid transition from the fed to the starved pattern of disease. Fortunately, muscle wasting/negative nitro-
substrate use. After an overnight fast, patients with gen balance has been shown to be ameliorated by the
stable cirrhosis derive approximately 75% of their cal- administration of 1.0 g/kg per day of standard pro-
ories from fat, as opposed to only 35% for healthy tein .2 The preferential early utilization of fat and pro-
controls.12 One of the mechanisms responsible for this tein that occurs in patients with cirrhosis can be ame-
metabolic pattern is the presence of marked insulin liorated by frequent feeding. A late evening meal has
resistance which occurs with cirrhosis.13 been shown to have a positive effect on nitrogen bal-
Increased nutritional requirements may occur ance in patients with cirrhosis when compared with an

acutely in cirrhosis (eg, due to ascites generation, equicaloric diet without a late evening meal.25
spontaneous bacterial peritonitis, or variceal hemor- The particularly high prevalence of malnutrition
rhage).14 Muller et al, in a study of 123 stable patients among patients with alcoholic liver disease and the
with various stages and etiologies of liver disease, association of negative nitrogen balance with subse-
found that resting energy expenditure, when expressed quent mortality has led to a relatively large number of
per unit of lean body mass, was increased, normal or clinical trials of nutrition therapies in this group.
decreased in 18%, 51%, and 31% of the patients, Despite initial promise, the aggregated evidence sug-
respectively, when compared with noncirrhotic con- gests that parenterally and/or enterally administered
trols. 12 The degree of increased energy requirement SNS (with or without branched-chain amino acid-
correlated with diminished body cell mass but not with enriched preparations) does not confer a medium or
the etiology or duration of liver disease in this study. long-term survival benefit to patients with acute alco-
Biochemical parameters, such as bilirubin or albumin, holic hepatitis.26 It is important to note, however, that
were predictive of hypercatabolism. Estimates of
not patients with alcoholic hepatitis who do not achieve a
the caloric needs of patients with cirrhosis, when based positive nitrogen balance have very poor survival
on the Harris-Benedict equation, are frequently inac- rates, although cause and effect have not been demon-
curate, tending to underestimate the caloric needs of strated. Administration of a nitrogen balance main-
patients with cirrhosis by 15% to 18% when compared taining diet, using standard amino acid mixtures/food
with measurement using indirect calorimetry. 15 preparations, with concomitant replacement of potas-
Nutrition assessment of patients with liver disease is sium, phosphate, magnesium, and thiamine should be
difficult because many of the traditional indices of considered in patients hospitalized with alcoholic liver
nutrition status are altered in liver disease indepen- disease.
dent of nutrition status (eg, serum albumin, prothrom- Even subclinical hepatic encephalopathy, present in
bin time, and ideal body weight). Although adverse approximately 75% of patients with cirrhosis, can
outcomes are associated with the presence of one or attenuate quality of life and should be treated. Lactu-
more indices of malnutrition, no single nutrition lose administration and replacement of zinc, when
parameter is able to consistently identify patients with deficient, are almost always sufficient therapy. Protein
cirrhosis who are likely to experience poor outcomes. A restriction is rarely necessary in the short-term and
multivariate approach to nutrition assessment is rec- never in the medium or long term. Branched-chain
ommended. The subjective global assessment (SGA) of amino acid-enriched, aromatic amino acid-deficient
nutrition status, modified for patients with cirrhosis, is nutrition supplements are the most extensively
a simple, reproducible and validated method that studied and utilized nutrition therapy in patients
includes nutrition history, physical examination and with liver disease.27-29 This is based on the theory that
simple anthropometrics.16 In addition, because of the higher levels of aromatic amino acids generate false
frequency of micronutrient deficiencies in this popula- neurotransmitters, promoting encephalopathy. Of the
tion, serum levels of zinc, vitamins A, D, E, and pro- nine published randomized, controlled trials of the use
thrombin time should also be periodically measured. of branched-chain amino acid-enriched formulas to
treat hepatic encephalopathy, six demonstrated no
Evidence
benefit, two found improved morbidity but unaltered
Nutritional deficiencies are common among patients mortality, and the ninth found significant improve-
with compensated cirrhosis and ubiquitous in patients ments in both mortality and response of encephalopa-
with decompensated liver disease. Although protein thy. Thus there is no consensus concerning the use of
calorie malnutrition is often the most clinically appar- branched-chain amino acid-enriched supplements in
ent manifestation of malnutrition in this population, the treatment of acute hepatic encephalopathy. Con-
deficiencies of micronutrients, particularly of vitamins versely, these supplements appear to be of clear benefit
A, D, E, and K17 and zinc,18 are also prevalent. to patients with cirrhosis who exhibit evidence of
Although there is overwhelming evidence that the chronic hepatic encephalopathy and who are intolerant
incidence of complications of liver disease increases of standard protein sources.
 67SA

For acute, overt hepatic encephalopathy, acute with- idiuretic agents to control ascites, less weight loss after
drawal of protein from the diet while precipitating Ihepatectomy, and less deterioration of liver function
causes of encephalopathy are sought, has been shown among patients receiving perioperative nutrition sup-
to be a cornerstone of therapy. The administration of a port. These benefits were seen predominantly in the
disaccharide, such as lactulose or lactitol, has been patients with underlying cirrhosis who underwent
repeatedly demonstrated to be effective and safe ther- major hepatectomy. Based on these results, periopera-
apy. 30 Zinc, deficiency of which is a near constant find- tive nutrition support should be considered in patients
ing in patients with advanced stages of liver disease, undergoing liver resection for hepatocellular carci-
may be supplemented empirically, as there is reason- noma associated with cirrhosis.
able evidence that supplementation is associated with

improvement in amino acid metabolism and clinical PracticeGuidelines.

grade of encephalopathy.3i Liver Disease ,

After successful reversal of hepatic encephalopathy,

nitrogen balance-maintaining quantities of standard 1. Patients with liver disease are at nutrition risk and
proteins should be reintroduced into the diet. In the should undergo nutrition screening to identify those
unusual patient who is not able to tolerate at least 1.0 who require formal nutrition assessment with
g/kg/per day of standard protein without becoming of a nutrition care
development (B)plan.
encephalopathic, despite optimal pharmacological 2. Nutrition assessment in patients with liver dis-
therapy, nutritional supplementation with vegetable ease should include screening for micronutrient
proteins and, if necessary, branched-chain amino acid- deficiencies, including vitamins A, D, E, and K,
enriched formulas should be considered. Both of these and zinc. (B)
agents have been shown to produce clinical improve- 3. Patients with cirrhosis should divide their caloric
ment in chronic hepatic encephalopathy while allowing intake into 4 to 6 meals per day, including a late
adequate amounts of protein to be consumed. Medium- evening snack. (B)
and long-term protein restriction are contraindicated 4. Protein restriction should be implemented for the
in patients with cirrhosis. acute management of overt hepatic encephalopa-
thy. (A)
Special Considerations 5. Protein restriction should not be implemented
Fulminant hepatic failure is associated with a 1- to
chronically in patients with liver disease. (B)
6. Use of branched-chain amino acid-enriched diets
4-fold increase in the rate of protein catabolism, with a and SNS formulas is only indicated in chronic
concomitant loss of capacity for ammonia remova1.32 In
encephalopathy unresponsive to pharmacother-
addition, glucose metabolism is greatly altered, a con- apy. (B)
dition characterized by diminished insulin sensitivity, 7. Perioperative nutrition support should be used in
high levels of insulin and glucagon, and a tendency to patients undergoing liver resection for hepatocel-
develop hypoglycemia.33 Unfortunately, the ideal lular carcinoma associated with cirrhosis. (A)
method of preventing hypoglycemia and glucopenic
brain injury has not been established. Certainly, blood REFERENCES
glucose levels require frequent monitoring; continuous 1. Abad-Lacruz A, Cabre E, Gonzalez-Huix F, et al: Routine tests of
infusions of 10% to 20% dextrose should be initiated renal function, alcoholism, and nutrition improve the prognostic
after the onset of hypoglycemia. Almost every other accuracy of Child-Pugh score in nonbleeding advanced cirrhotics.
facet of nutrition therapy in the setting of fulminant Am J Gastroenterol 88:382-387, 1993
2. Chedid A, Mendenhall CL, Gartside P, et al: Prognostic factors in
hepatic failure is controversial. Although branched- alcoholic liver disease. VA Cooperative Study Group. Am J Gas-
chain amino acid-enriched and medium chain troenterol 86:210-216, 1991
triglyceride-supplemented preparations offer theoret- 3. Madden AM, Bradbury W, Morgan MY: Taste perception in
ical advantages over standard amino acid and lipid cirrhosis. Its relationship to circulating micronutrients and food
preparations, the relative benefits of these nutrients in preferences. Hepatology 26:40-48, 1997
4. Kalman DR, Saltzman JR: Nutrition status predicts survival in
the support of patients with fulminant hepatic failure cirrhosis. Nutr Rev 54:217-219, 1996
have not been formally studied in a randomized, con- 5. Selberg O, Bottcher J, Tusch G, et al: Identification of high- and
trolled fashion. Intuitively, patients with fulminant low-risk patients before liver transplantation. A perspective
cohort study of nutritional and metabolic parameters in 150
hepatic failure who require pxolonged hospitalization patients. Hepatology 25:652-657, 1997
seem to merit nutrition support and are usually given
6. Ricci P, Therneau TM, Malinchoc M, et al: A prognostic model for
it. Such support is, however, empiric in terms of com- the outcome of liver transplantation in patients with cholestatic
position and route. liver disease. Hepatology 25:672-677, 1997
Fan et al, in a large randomized, controlled study, 7. Merli M, Riggio O, Dally L: Does malnutrition affect survival in
cirrhosis? PINC Hepatol 23:1041-1046, 1996
demonstrated that patients undergoing resection of
8. Morgan MY: Alcohol and nutrition. Br Med Bull 38:21-29, 1982
hepatocellular carcinoma who received 14 days of peri- 9. McCullough AJ, Bugianesi E: Protein calorie malnutrition and
operative intravenous nutrition support in addition to the etiology of cirrhosis. Am J Gastroenterol 92:734-738, 1997
their oral diet, experienced lower overall postoperative 10. Gloria L, Cravo M, Camilo ME, et al: Nutritional deficiencies in
chronic alcoholics. Relation to dietary intake and alcohol con-
morbidity when compared with a control group not sumption. Am J Gastroenterol 92:485-489, 1997
receiving SNS (34% versus 55%; relative risk, 0.66), 11. McCullough AJ, Mullen KD, Tavill AS, et al: In vivo differences
predominantly because of fewer septic complications.34 between the turnover rates of leucine and leucines ketoacid in
There was also a reduction in the requirement for stable cirrhosis. Gastroenterology 103:571-578, 1992
68SA

12. Muller MJ, Lautz HU, Plogmann B, et al: Energy expenditure another 35%. The remaining 20% is divided between
j
and substrate oxidation in patients with cirrhosis. The impact of
cause, clinical staging and nutritional state. Hepatology 15:782-
idiopathic and miscellaneous causes. The inflamma-
794, 1992 tory response associated with acute pancreatitis can
13. Petrides AS, Groop LC, Riely CA, et al: Effect of physiologic lead to a spectrum of pancreatic injury that ranges
hyperinsulinemia on glucose and lipid metabolism in cirrhosis. from mild edema to necrosis. Significant ischemia
J Clin Invest 88:561-570, 1991 of the gland predisposes to severe hemorrhage and
14. Charlton MR. Energy and protein metabolism in alcoholic liver
disease. Clin Liver Dis 2:781-798, 1998 necrosis, which in turn, predisposes to secondary
15. Shanbhogue RL, Bistrian BR, Jenkins RL, et al: Resting energy infection.2-4 The severity of the injury determines the
5
expenditure in patients with end-stage liver disease and in nor- prognosis and dictates the therapy.5
mal population [see comments]. JPEN 11:305-308, 1987 Chronic pancreatitis (CP) results in fibrosis and per-
16. Hasse J, Strong S, Gorman MA, et al: Subjective global assess- manent glandular insufficiency while in AP pancreatic
ment. Alternative nutrition-assessment technique for liver-
function nearly always returns to normal.6 Prolonged
transplant candidates. Nutrition 9:339-343, 1993
17. DiCecco SR, Wieners EJ, Wiesner RH, et al: Assessment of heavy alcohol consumption is the most common cause
nutritional status of patients with end-stage liver disease under- of CP, whereas many of the other cases are due to
going liver transplantation. Mayo Clin Proc 64:95-102, 1989 cystic fibrosis or nutritional and inherited forms of the
18. Bode JC, Hanisch P, Henning H, et al: Hepatic zinc content in
disease. Patients can present with abdominal pain,
patients with various stages of alcoholic liver disease and in
patients with chronic active and chronic persistent hepatitis. maldigestion, and diabetes mellitus. The diagnosis of
Hepatology 8:1605-1609, 1988 CP is based on both radiographic and functional test-
19. Bienia R, Ratcliff S, Barbour GL, et al: Malnutrition and hospital ing. Pancreatic enzyme concentrations in the blood are
prognosis in the alcoholic patient. JPEN 6:301-303, 1982 often normal.
20. Garrison RN, Cryer HM, Howard DA, et al: Clarification of risk
factors for abdominal operations in patients with hepatic cirrho- Most patients with AP have a mild, self-limiting
sis. Ann Surg 199:648-655, 1984 illness that resolves with several days of supportive
21. Blendis LM, Harrison JE, Russell DM, et al: Effects of perito-
neovenous shunting on body composition. Gastroenterology
therapy. 78 Depending on the cause, these patients are
usually not malnourished and are able to eat within 5
90:127-134, 1986 to 7 days, so nutrition support is unnecessary.9 The
22. Shaw BW Jr, Wood RP, Gordon RD, et al: Influence of selected
patient variables and operative blood loss on six-month survival cumulative effects of repeated attacks of chronic
following liver transplantation. Semin Liver Dis 5:385-393, 1985 relapsing pancreatitis can lead to malnutrition.5 Pan-
23. Goldberg S, Mendenhall C, Anderson S, et al: VA Cooperative creatitis can lead to hypocalcemia and hypomag-
Study on Alcoholic Hepatitis. IV. The significance of clinically nesemia, liver function abnormalities, and abnormali-
mild alcoholic hepatitis&mdash;describing the population with mini-
mal hyperbilirubinemia. Am J Gastroenterol 81:1029-1034, ties of a number of other metabolic parameters.
1986 Approximately 5% to 15% of patients develop necrotiz-
24. Gabuzda GJ, Shear L: Metabolism of dietary protein in hepatic ing pancreatitis that predisposes them to complica-
cirrhosis. Nutritional and clinical considerations. Am J Clin tions and can have a mortality rate of 5% to 20%.8-12
Nutr 23:479-487, 1970
This severe form of the disease induces a catabolic
25. Swart GR, Zillikens MC, van Vuure JK, et al: Effect of a late
evening meal on nitrogen balance in patients with cirrhosis of state similar to that seen in trauma and sepsis, result-
the liver. Br Med J 299:1202-1203, 1989 ing in rapid weight loss and increased morbidity and
26. Fulton S, McCullough AJ: Treatment of alcoholic hepatitis. Clin
Liver Dis 2:799-820, 1998
mortality.13,14 Combinations of clinical and laboratory
27. Marchesini G, Bianchi G, Rossi B, et al: Nutritional treatment
parameters such as those described by Ranson 10 and
with branched-chain amino acids in advanced liver cirrhosis. J others&dquo; and by the APACHE II scoring system are
Gatroenterol 35:S1-S12, 2000 used to determine the severity of pancreatitis and to
28. Riordan SM, Williams R: Treatment of hepatic encephalopathy. assess prognosis.l6 Severe pancreatitis is character-
N Engl J Med 337:473-479, 1997 ized by the presence of three or more Ranson criteria or
29. Fabbri A, Magrini N, Bianchi G, et al: Overview of randomized
clinical trials of oral branched-chain amino acid treatment in eight or more APACHE II points. 17 Estimating the
chronic hepatic encephalopathy. JPEN 20:159-164, 1996 severity of the pancreatitis is important to the assess-
30. Butterworth RF: Complications of cirrhosis III. Hepatic enceph- ment of the need for SNS. In patients with severe
alopathy. J Hepatol 32:171-180, 2000 pancreatitis by Ranson criteria, measured energy
31. Marchesini G, Fabbri A, Bianchi G, et al: Zinc supplementation
and amino acid-nitrogen metabolism in patients with advanced expenditure has been shown to be as high as 50%
cirrhosis. Hepatology 23:1084-1092, 1996 greater than the resting energy expenditure as calcu-
32. OKeefe SJ, Abraham RR, Davis M, et al: Protein turnover in lated by the modified Harris-Benedict equation. 18 The
acute and chronic liver disease. Acta Chir Scand 507 (Suppl):91- most accurate measurement of caloric requirements is
101, 1981 with indirect calorimetry.
33. Vilstrup H, Iversen J, Tygstrup N: Glucoregulation in acute liver CP may result in malnutrition. Energy requirements
failure. Eur J Clin Invest 16(3):193-197, 1986
34. Fan ST, Lo CM, Lai EC, et al: Perioperative nutrition support in in underweight patients with CP may be 15% to 30%
patients undergoing hepatectomy for hepatocellular carcinoma. above the expected range compared with the Harris-
N Engl J Med 1994 Benedict equation. 19,20 The cause of this is unknown. It
has been suggested that moderate fat diets and pan-
PANCREATITIS creatic enzyme replacement be given when steatorrhea
is present .21 Low-fat diets, along with pancreatic
Background enzymes, are advised if steatorrhea does not improve.
Pancreatitis is a common disorder. The incidence of Patients should abstain from alcohol when AP or CP
pancreatitis appears to be increasing. Biliary obstruc- are present. Deficiencies in vitamin A and E have been
tion by gallstones accounts for about 45% of the cases of identified in CP.22 Deficiencies in vitamin C, riboflavin,
acute pancreatitis (AP) and alcohol is the cause in thiamin, and nicotinic acid have been shown in alcohol
 69SA

induced CP.23 Steatorrhea can lead to malabsorption of period, SNS is appropriate. Enteral feeding should be
calcium, magnesium and zinc. Vitamin B-12 malab- attempted first in the minority of patients with pan-
sorption is common, but deficiency is rare. Supplemen- creatitis who require SNS. If enteral feeding increases
tation for these micronutrients should be undertaken pain, ascites or fistulous output it should be discontin-
when deficiency is present. Diabetes should be man- ued. Patients with mild-to-moderate AP allowed an
aged to control blood sugars. Pain management can oral diet of clear liquids and nutritional supplements in
improve oral intake. addition to EN show improvement in markers of dis-
SNS does not consistently limit disease activity in ease activity. 35 Nutrition needs can safely be provided
patients with pancreatitis and therefore cannot be con- by EN in patients with acute pancreatitis. Recent data
sidered as primary therapy. Nutrition support for confirm earlier studies that suggested feeding jejunos-
patients with severe pancreatitis may prevent nutrient tomies are safe and effective and that formulas low in
deficiencies and preserve lean body mass and func-
fat are tolerated best. Patients given EN do better than
tional when nutrient intake falls below
capacity
needs.24,2 This distinction between nutrition support those given PN.36 PN should be reserved for those
as primary therapy for the disease versus its value as patients requiring SNS who are not able to tolerate
an adjunct to primary therapy is essential. The ratio-
EN.
nale and criteria for using nutrition support in the
setting of pancreatitis is similar to that for other dis- Special Considerations
eases. It is used to treat malnutrition when present
and to avoid the development of malnutrition resulting Pseudocysts, intestinal and pancreatic fistulae, pan-
from insufficient energy intake in the face of increased creatic abscesses, and pancreatic ascites are known
energy needs. complications of acute pancreatitis that occur in up to
25% of patients. Complications such as these can
make enteral feeding impossible. PN should be used
Evidence along with appropriate treatment for each or these
One of the major goals of the therapy of pancreatitis complications. Bowel rest with PN can lead to clinical
is to limit pancreatic secretion. This has led to the and radiographic improvement of pseudocysts, but PN-
belief that bowel rest might be useful as a primary related complications, mostly catheter-related infec-
treatment for pancreatitis. Although bowel rest cer- tions, makes the overall utility, as a primary treatment
for pseudocysts, questionable. 37
tainly decreases pain, there are no clinical trials that Case reports of lipid emulsions causing AP have
have shown that it decreases the morbidity or mortal-
raised some concern regarding lipid administration
ity of the disease. 26,27 The belief that pancreatic rest isin patients with pancreatitis.21 Fortunately, most pa-
beneficial probably explains why PN has been the
tients tolerate glucose- and lipid-based formulas quite
usual method of nutrition support in pancreatitis.
PN does not stimulate pancreatic secretion. 28-30 well .38 Because hypertriglyceridemia-induced pancre-
atitis is rare unless serum concentrations exceed 1000
Despite this potential benefit of PN, it is infrequently
needed as an adjunct to the supportive treatment of mg/dL, it is suggested that lipid emulsions be withheld
from patients with triglyceride concentrations exceed-
pancreatitis. In patients with mild disease who will 400 mg/dL.39 PN administration without lipid
probably be able to eat within 7 days, it is unnecessary. ing
In more severe pancreatitis when SNS is indicated, EN emulsions beyond 2 weeks is not advised because of the
is less expensive, reduces the incidence of infection, risk of development of essential fatty acid deficiency.
and may preserve gut integrity and gut barrier and
immune function.31 It facilitates transitional feeding. Practice Guidelines
.

If the GI tract is functioning normally, EN is well Pancreatitis

tolerated. The degree of pancreatic stimulation
depends on the location of the feeding tube in the 1. Patients with pancreatitis are at nutrition risk
gastrointestinal tract and the composition of the feed- and should undergo nutrition screening to iden-
ing. Less stimulation occurs the more distally the EN is tify those who require formal nutrition assess-
delivered.32 The advantages of EN observed in patients ment with development of a nutrition care plan. (B)
with trauma and sepsis have led to its use in patients 2. SNS should not be used routinely in patients with
with AP.33 Patients receiving EN have outcomes sim- mild to moderate acute pancreatitis. (B)
ilar to those seen in patients receiving PN. EN is safe, 3. SNS should be used in patients with acute or
effective, and less expensive than PN in patients with chronic pancreatitis to prevent or to treat malnu-
mild to moderate AP. 34,35 trition when oral energy intake is anticipated to
In severe pancreatitis, patients fed an elemental for- be inadequate for 5 to 7 days. (B)
mula via a nasojejunal feeding tube have significantly 4. EN is the preferred route of SNS in patients with
fewer septic events and fewer complications overall. pancreatitis and should be attempted before ini-
Enteral feeding of a semi-elemental low triglyceride tiating PN. (A)
diet is safe and cheaper than PN.34 5. PN should be used in patients with pancreatitis if
Patients with AP expected to resolve clinically over a SNS is indicated and EN is not tolerated. (B)
period of 5 to 7 days likely do not require SNS. In 6. Intravenous lipid emulsions are safe in acute pan-
patients who are unable to tolerate oral intake or who creatitis provided triglyceride levels are moni-
are anticipated to be undernourished for a prolonged tored and remain below 400 mg/dL. (B)
70SA

REFERENCES 28. Konturek SJ, Tasler J, Cieszkowski M, et al: Intravenous amino

acids and fat stimulate pancreatic secretion. Am J Physiol 236:
1. Steinberg W, Tenner S: Acute pancreatitis. N Engl J Med 330:
E676&mdash;E684, 1979
1198-1210, 1994 29. Kelly GA, Nahrwold DL: Pancreatic secretion in response to an
2. Klar E, Messmer K, Warshaw AL, et al: Pancreatic ischaemia in elemental diet and intravenous hyper-alimentation. Surg
experimental acute pancreatitis: Mechanisms, significance and Gynecol Obstet 143:87-91, 1976
therapy. Br J Surg 77:1205-1210, 1990 30. Edelman K, Valenzuela JE: Effect of intravenous lipid on human
3. Beger HG, Bittner R, Block S, et al: Bacterial contamination of pancreatic secretion. Gastroenterology 85:1063-1066, 1983
pancreatic necrosis: a prospective clinical study. Gastroenterol- 31. Cerra FB, Benitez MR, Blackburn GL, et al: Applied nutrition in
ogy 91:433-438, 1986 ICU patients: a consensus statement of the American College of
4. Gerzof SG, Banks PA, Robbins AH, et al: Early diagnosis of Chest Physicians. Chest 111:769-78, 1997
pancreatic infection by computed tomography-guided aspiration. 32. Ragins H, Levenson SM, Singer R, et al: Intrajejunal adminis-
Gastroenterology 93:1315-1320, 1987 tration of an elemental diet at neutral pH avoids pancreatic
5. Helton WS: Intravenous nutrition in patients with acute pancre- stimulation. Am J Surg 126:606&mdash;614, 1973
atitis. IN Clinical Nutrition: Parenteral Nutrition. Rombeau JL, 33. McClave SA, Greene LM, Snider HL, et al: Comparison of the
Caldwell MD (eds) WB Saunders, Philadelphia, 1993, pp 442- safety of early enteral vs. parenteral nutrition in mild acute
461 pancreatitis. JPEN 21:14-20, 1997
6. Banks PA: Acute and chronic pancreatitis. IN Gastrointestinal 34. Kalfarentzos F, Kehagias J, Mead N, et al: Enteral nutrition is
and Liver Disease. Feldman M, Scharschmidt BF, Sleisenger superior to parenteral nutrition in severe acute pancreatitis:
MH (eds). WB Saunders, Philadelphia, PA, 1998, pp 809&mdash;862 results of a randomized prospective trial. Br J Surg 84:1665&mdash;
7. Levelle-Jones M, Neoptolemos JP: Recent advances in the treat- 1669, 1997
ment of acute pancreatitis. Surg Ann 22:235-261, 1990 35. Windsor ACJ, Kanwar S, Li AGK, et al: Compared with paren-
8. Dammann HG, Dreyer M, Walter TA, et al: Prognostic indicators teral nutrition, enteral feeding attenuates the acute phase
in acute pancreatitis: Clinical experience and limitations. IN response and improves disease severity in acute pancreatitis.
Acute Pancreatitis. Beger HG, Buchler M (eds). Springer-Verlag, Gut 42:431-435, 1998
Berlin, Germany, 1987, pp 181-197 36. Pennington CR: Feeding the inflamed pancreas. Gut 42:315-
9. Sax HC, Warner BW, Talamini MA, et al: Early total parenteral 316, 1998
nutrition in acute pancreatitis: Lack of beneficial effects. Am J 37. Jackson MW, Schuman BM, Bowden TA, et al: The limited role
Surg 153:117-124, 1987 of total parenteral nutrition in the management of pancreatic
10. Ranson JHC, Rifkind KM, Roses DM, et al: Prognostic signs and pseudocyst. Am Surg 59:736-739, 1993
the role of operative management in acute pancreatitis. Surg 38. Silberman H, Dixon NP, Eisenberg D: The safety and efficacy of
Gynecol Obstet 139:69-81, 1974 a lipid-based system of parenteral nutrition in acute pancreati-
11. Beger HG: Surgical management of necrotizing pancreatitis. tis. Am J Gastroenterol 77:494&mdash;497, 1982
Surg Clin N Am 69:529-549, 1989 39. Adamkin DH, Gelke KN, Andrews BF: Fat emulsions and hyper-
12. Allardyce DB: Incidence of necrotizing pancreatitis and factors triglyceridemia. JPEN 8:563-567, 1984
related to mortality. Am J Surg 154:295-299, 1987
13. Feller JH, Brown RA, Toussant GPM, et al: Changing methods
in the treatment of severe pancreatitis. Am J Surg 127:196-201, SHORT-BOWEL SYNDROME
1974
14. Voitk A, Brown RA, Echave V, et al: Use of an elemental diet in Background
the treatment of complicated pancreatitis. Am J Surg 125:223&mdash;
Short-bowel syndrome (SBS) occurs when a combi-
227, 1973
15. Blaney SL, Imrie CW, ONeil J, et al: Prognostic factors in acute nation of loss of bowel due to resection and/or dys-
pancreatitis. Gut 25:1340-1346, 1984 function of the remaining bowel reduces intestinal
16. Knaus WA, Draper EA, Wagner DP, et al: APACHE II: a severity
of disease classification system. Crit Care Med 13:818&mdash;829, 1985
absorption such that fluid, electrolyte, macronutrient,
17. Summary of the international symposium on acute pancreatitis. mineral, and vitamin needs cannot be met through use
Atlanta, GA, September 11-13, 1992. Arch Surg 128:586-590, of standard oral or enteral feedings.- This syndrome
1993 occurs most commonly after surgery for Crohns dis-
18. Bouffard YH, Delafosse BX, Annant GJ, et al: Energy expendi- ease and mesenteric infarction in adults. Symptoms of
ture during severe acute pancreatitis. JPEN 13:26&mdash;29, 1989 SBS include large volume diarrhea, thirst, and weight
19. Dickerson RN, Vehe KL, Mullen JL, et al: Resting energy expen-
diture in patients with pancreatitis. Crit Care Med 19:484-490,
loss. Although malabsorption is primarily the result of
1991 a decrease in intestinal surface area, a decrease in
20. Hebuterne X, Hastier P, Peroux JL, et al: Resting energy expen- intestinal transit time contributes to the pathophysi-
diture in patients with alcoholic chronic pancreatitis. Dig Dis Sci
ology of this condition. Both nutrient and fluid absorp-
41:533&mdash;539, 1996 tion are compromised. The colon and ileocecal valve
21. Seidner DL, Fuhrman MT: Nutrition Support in Pancreatitis. IN
The Science and Practice of Nutrition Support: A Case-Based decrease intestinal transit time; however, in SBS both
Core Curriculum. Gottschlich MM (ed). American Society for the colon and ileocecal valve may have been resected.
Parenteral and Enteral Nutrition. Kendall-Hunt Publishing, The function of the residual proximal small bowel is
Dubuque, IA, 2001, pp 553&mdash;574 also important for absorption. Iron and most water-
22. Dutta SK, Bustin MP, Russell RM, et al: Deficiency of fat-soluble
vitamins in treated patients with pancreatic insufficiency. Ann
soluble vitamins are absorbed in the proximal jejunum.
Intern Med 1982, 97:549-552 Deficiencies are found in only the most severe cases of
23. Van Gossum A, Closset P, Noel E, et al: Deficiency in antioxidant short bowel. The terminal ileum is where vitamin B-12
factors in patients with alcohol-related chronic pancreatitis. Dig and bile salts are absorbed. When 100 cm or more of
Dis Sci 41:1225-1231, 1996
the terminal ileum has been resected, monthly B-12
24. Grant JP, James S, Grabowski V, et al: Total parenteral nutri-
tion in pancreatic disease. Ann Surg 200:627-631, 1984 injections are eventually required. Bile salts are
25. Kudsk KA, Campbell SM, OBrien T, et al: Postoperative jejunal required for micellar solubilization of dietary fat and
feedings following complicated pancreatitis. Nutr Clin Pract fat-soluble vitamins. After extensive ileal resections,
5:14-17, 1990 bile salts are malabsorbed, resulting in significant fat
26. Ranson JHC: Acute pancreatitis: pathogenesis, outcome, and
treatment. Clin Gastroenterol 13:843-863, 1984
and fat soluble vitamin malabsorption.
27. Kirby DF, Craig RM: The value of intensive nutritional support Complications of SBS include dehydration and
in pancreatitis. JPEN 9:353-357, 1985 weight loss from malabsorption of fluids and macronu-
 71SA

trients (carbohydrate, fat, and protein); electrolyte, day, if possible. Oral rehydration solutions, which con-
mineral, and trace element deficiencies; metabolic bone tain approximately 90 mEq/kg per liter of sodium, can
disease (osteoporosis and osteomalacia) from calcium also be used to help maintain fluid and electrolyte
and vitamin D malabsorption; cholelithiasis because of homeostasis postoperatively. 12 During the transitional
inadequate bile salt reserves; and nephrolithiasis. feeding period, the oral diet should be advanced slowly
Oxalate nephrolithiasis develops in the setting of ste- using small, frequent feedings of solid food. The PN is
atorrhea and the presence of an intact colon. Dietary reduced gradually as oral intake increases and the
oxalate usually binds to calcium and is excreted in the diarrhea decreases. From this point forward the
stool as an insoluble complex. In SBS, oxalate remains dietary management of the short bowel patient varies,
in a free unbound form that is easily absorbed in the depending on the presence or absence of a colon.
colon, because calcium has a greater affinity for unab- The colon is a very important digestive organ. It has
sorbed fatty acids.5 Patients with end-jejunostomies, the ability to absorb both fluid and electrolytes and has
on the other hand, are more prone to uric acid renal slower transit time in comparison with the small intes-
stones from recurrent episodes of dehydration. tine. The colon also has the capability to salvage
Two other entities that can occur in the pathophys- energy by converting complex carbohydrates to short-
iology of short bowel are gastric acid hypersecretion chain fatty acids through bacterial fermentation in the
and D-lactic acidosis. The acute acid hypersecretory colonic flora. 13 Noordgard et al 14 compared an isoca-
state after intestinal resection is usually transient (3 to loric diet of 60:20% or 20:60% carbohydrate to fat in
6 months) and unrelated to the length of intestinal eight short-bowel patients with colons and six patients
resection.6 The increased gastrointestinal acid load with end-jejunostomies. Patients with colons fed a
inactivates normal digestive enzymes such as pancre- high-carbohydrate, low-fat diet had reduced loss of
atic lipase and deconjugates intraluminal bile salts, total calories compared with the low-carbohydrate,
which further impairs fat and fat soluble vitamin high-fat diet. In contrast, patients with end-jejunosto-
absorption. D-lactic acid is produced by the fermenta- mies excreted equal amounts of calories on the high-
tion of malabsorbed carbohydrates in the colon. and low-carbohydrate diets. The study confirms the
Humans lack the enzyme necessary to metabolize findings of previous studies that patients with end-
D-lactic acid. D-lactic acidosis should be suspected when jejunostomies do not require a high-carbohydrate
there is unexplained metabolic acidosis in a patient diet.l5-16 With regard to the type of carbohydrate, com-
with short bowel and colonic continuity. Management plex carbohydrates are preferable to simple carbohy-
involves the use of carbohydrate-restricted diets. drates. Simple carbohydrates may result in significant
After intestinal resection, the remaining intestine osmotic diarrhea in patients with SBS and are not
undergoes both structural and functional changes that fermented to short-chain fatty acids. Marteau et al
increase nutrient and fluid absorption. These changes compared the tolerance of a diet providing 20 g/d of
are collectively termed intestinal adaptation.8 These lactose to a lactose-free diet in 14 patients with SBS. 17
changes begin to occur immediately after surgery and Eight patients had a colon and 6 patients had an end-
may continue for up to 2 years, or occasionally even jejunostomy. The presence of lactose did not cause
longer. The process of intestinal adaptation is pro- symptoms of intolerance, nor worsening of diarrhea in
moted by luminal nutrients. Besides having a direct either group. Patients with short bowel and colonic
trophic effect on the intestine, luminal nutrients stim- continuity should also be placed on a low-oxalate diet,
ulate both pancreatic and intestinal peptide secretion, especially if they are prone to oxalate nephrolithiasis
5
which promotes growth and function of the residual or have high 24-hour urinary oxalate levels.5
intestine.9 Fat-soluble vitamins (vitamins A, D, K, E) should be
monitored; these vitamins should be supplemented if
deficient. Water-soluble vitamins can usually be
Evidence
replaced with a daily oral multivitamin because they
The immediate postoperative period after intestinal are primarily absorbed in the proximal small intestine.
resection is characterized by significant fluid and elec- Monthly injections of vitamin B-12 should be given
trolytes losses. Most patients require PN for 1 or more when the terminal ileum has been resected. In
months after massive intestinal resection. Patients patients with continued weight, electrolyte, and fluid
with less than 100 cm of small bowel distal to the loss, PN is required even though some gut stimulation
ligament of Treitz and without a colon often require PN with oral or EN feedings is continued. The PN should
for an indefinite period. In contrast, 50 cm of small provide macronutrients, vitamins, minerals, and trace
bowel may suffice for adequate oral nutrition after a elements in amounts sufficient to maintain normal
period of adaptation if most of the colon is reserved.10 growth, development, and lean body mass. As the
During the initial adaptive phase, intravenous fluids intestine continues to adapt after resection, PN may be
and nutrients should be administered to match losses reduced or discontinued. Careful monitoring during
and maintain nitrogen balance. Hypersecretion of gas- this period of weight, fluid status, volume of diarrhea,
tric acid during this phase can result in significant and blood chemistries is essential.
fluid loss and should be treated with intravenous Ambulatory patients with SBS absorb less (one-third
H2-receptor antagonists, which can be placed in the PN to one-half less) calcium, magnesium, and zinc than
formulation.ll If stool volume increases with oral normal individuals.&dquo; Net negative calcium balance
intake, antidiarrheal agents should be used.2 The goal occurs before osteopenia is detected by bone mineral
is to keep stool losses less than approximately 2 L/d per density scans. Urinary magnesium falls before serum
72SA

Mg is low. 9 Patients with extensive small bowel resec- bowel transplantation would include those with PN
tion requiring PN have even lower absorption of these associated liver failure or recurrent catheter sepsis and
divalent ions and require intravenous replacement.2o lack of venous access.27
Treatment of ambulatory patients is usually success- Progressive, cholestatic liver failure may arise in
ful with oral therapy. The preparations with the high- patients with SBS who are PN dependent. The risk of
est content of calcium and magnesium (calcium carbon- this complication appears proportional to the length of
ate and magnesium oxide) are the least soluble and bowel resected. Weaning of PN if at all possible is the
have the lowest available content of the elemental ions. preferred method of treatment.
Thus, their use balances large delivery [400 mg of

calcium/g of calcium carbonate; 360 mg magnesium (15 Practice Guidelines

of
mEq)/600 mg magnesium oxide] against uncertain Short-Bowel Syndrome ,

solubility and absorption. Other preparations of cal-

cium include acetate, citrate, lactate, gluconate, glu- 1. Patients undergoing extensive bowel resection or
bionate, and phosphate salts. The carbonate salt is with short bowel syndrome are at nutrition risk
recommended for initial therapy. The diet should be and should undergo nutrition screening to iden-
supplemented with 800 mg of elemental calcium while tify those who require formal nutrition assess-
following the 24 urinary calcium excretion to ensure ment with development of a nutrition care plan. (B)
that it is brought into the normal range. If this fails, 2. Patients with SBS and an intact colon should
other more soluble salts, such as citrate or glubionate, receive diets rich in complex carbohydrates and
are used. Magnesium oxide can be used initially to add
low in fat. (A)
360 to 720 mg of elemental magnesium, remembering 3. A low oxalate diet should be given to patients with
that it can cause diarrhea. Other preparations include SBS and an intact colon. (A)
acetate, citrate, aspartate, hydroxide, lactate, and glu- 4. Monthly vitamin B-12 injections should be given
conate salts. The most soluble of these are the acetate, to patients with greater than 100 cm of the ter-
lactate, and gluconate forms; the latter is most readily minal ileum resected. (A)
available in the United States. The 500-mg tablet dose
5. PN should be administered to patients with SBS
of magnesium gluconate contains only 29 mg of ele-
if nutritional requirements cannot be met by oral
mental magnesium, so the liquid preparation (54 mg/5 or EN feeding. (A)
mL) is generally preferred.21
REFERENCES
Speciad Considerations
1. Scolapio JS, Fleming CR: Short bowel syndrome. Gastroenterol
PN in the setting of SBS is associated with compli- Clin N Am 27:467-479, 1998
cations, including catheter sepsis and liver disease.22 2. Scolapio JS, Camilleri MC: Motility considerations in short
To wean patients from the need for PN, methods of bowel syndrome. Dig Dis15:253-262, 1997
&dquo;intestinal rehabilitation&dquo; designed to increase the 3. Gerson CD, Coben N, Janowitz HD: Small intestinal absorptive
function in regional enteritis. Gastroenterology 64:907, 1973
absorptive capacity of the remaining intestine have 4. Manji N, Bistrian BR, Mascioli EA, et al: Gallstone disease
been studied. The combination of various trophic fac- in-patients with severe short bowel syndrome dependent on par-
tors including glutamine, human recombinant growth enteral nutrition. JPEN 13:461-464, 1989
hormone and a high-carbohydrate, low-fat diet was 5. Dobbins JW, Binder HJ: Importance of the colon in enteric
shown in an uncontrolled study of 8 patients with SBS hyperoxaluria. N Engl J Med 296:298-301, 1977
6. Windsor CW, Fejfar J, Woodward DA: Gastric secretion after
to significantly increase water, electrolyte, and carbo-
massive small bowel resection. Gut 10:779-786, 1969
hydrate absorption after 3 weeks of administration.23 7. Stolberg L, Rolfe R, Gitlin N, et al: D-lactic acidosis due to
The same authors expanded their study with an addi- abnormal gut flora. N Engl J Med 306:1344-1348, 1982
tional 31 patients using the same treatment regimen.24 8. Williamson RC: Intestinal adaptation: Structural, functional,
and cytokinetic changes. N Engl J Med 298:1393-1402, 1978
Forty percent of the treated patients were able to dis- 9. Dowling RH: Small bowel adaptation and its regulation. Scand J
continue parenteral nutrition. Because the study was Gastroenterology 74:53-74, 1982
uncontrolled, it is not clear whether the glutamine, 10. Lennard-Jones JE: Review article: Practical management of the
growth hormone, diet, or other factors contributed to short bowel. Aliment Pharmacol Ther 8:563&mdash;577, 1994
the favorable outcome. There have since been two con- 11. Cortot A, Fleming CR, Malagelada JR: Improved nutrient
trolled studies using this same treatment in patients absorption after cimetidine in short bowel syndrome with gastric
hypersecretion. N Engl J Med 300:79-80, 1979
with SBS, which did not find positive effects using this 12. Lennard-Jones: Oral rehydration solutions in short bowel syn-
specific treatment.25,26 drome. Clin Therap 12:129&mdash;137, 1990
Small bowel transplantation is also an option. Graft 13. Nordgaard I, Hansen BS, Mortensen PB: Colon as a digestive
survival has progressively increased. Rejection of the organ in patients with short bowel. Lancet 343:373-376, 1994
14. Nordgaard I, Hansen BS, Mortensen PB: Importance of colonic
graft and post transplant related lymphoma remaining support for energy absorption as small-bowel failure proceeds.
the biggest challenges after small bowel transplanta- Am J Clin Nutr 64:222&mdash;231, 1996
tion.27 Currently, the 5-year survival with PN is better 15. Woolf GM, Miller C, Kurian R, et al: Diet for patients with a
short bowel: High fat or high carbohydrate. Gastroenterology
than graft survival after small bowel transplanta-
84:823&mdash;828, 1983
tion . 22,27 Therefore, PN remains the treatment of 16. McIntyre PB, Fitchew M, Lennard-Jones JE: Patients with a
choice in patients with SBS who can not be maintained high jejunostomy do not need a special diet. Gastroenterology
orally or enterally. Potential candidates for small 91:25-33, 1986
 73SA

17. Marteau P, Messing B, Arrigoni E, et al: Do patients with short- restrictions, malabsorption of nutrients (primarily in
bowel syndrome need a lactose-free diet? Nutrition 13:13&mdash;16,
1997 CD), increased gastrointestinal losses associated with
18. Woolf GM, Miller C, Kurian R, et al: Nutritional absorption in denudation of mucosa and bleeding, increased nutrient
short bowel syndrome. Evaluation of fluid, calorie, and divalent requirements resulting from fever and inflammation,
cation requirements. Dig Dis Sci 32:8-15, 1987 and drug-nutrient interactions.
19. Fleming CR, George L, Stoner GL, et al: The importance of Proposed roles for SNS in CD have included correc-
urinary magnesium values in patients with gut failure. Mayo tion of malnutrition, use as primary therapy to induce
Clin Proc 71:21-24, 1996
20. Ladefoged K, Nicolaidou P, Jarnum S: Calcium, phosphorus, remission or to limit amount of surgical resection, peri-
magnesium, zinc, and nitrogen balance in patients with severe operatively as an adjunct to decrease postoperative
short bowel syndrome. Am J Clin Nutr 33:2137&mdash;2144, 1980 complications, to reverse growth retardation in chil-
21. Alpers DH, Stenson WF, Bier DM: Manual of Nutritional Ther- dren, to induce healing of enterocutaneous fistulae,
apeutics, 4th ed. Lippincott Williams & Wilkins, Baltimore, MD, and to provide long term nutrition in those with short
Chapter 7 (in press)
22. Scolapio JS, Fleming CR, Kelly D: Survival of home parenteral bowel syndrome. In UC, the use of nutrition support
nutrition patients: Twenty-years of experience at the Mayo has been directed toward achieving clinical remission
Clinic. Mayo Clinic Proc 74:217-222, 1999 to avoid surgery.
23. Byrne TA, Morrissey TB, Nattakom TV, et al: Growth hormone,
glutamine, and a modified diet enhance nutrient absorption in
patients with severe short bowel syndrome. JPEN 19:296&mdash;302, Evidence
1995
24. Byrne TA, Persinger RL, Young LS, et al: A new treatment for Prospective studies have evaluated the role of PN as
patients with short-bowel syndrome. Growth hormone, glu- primary therapy in CD. PN induces remission during
tamine, and a modified diet. Ann Surg 222:243&mdash;254; discussion acute attacks of CD, but upon resuming oral nutrition
254&mdash;255, 1995 recurrence rates are high and do not justify the cost or
25. Scolapio JS, Camilleri M, Fleming CR, et al: Effect of growth risk associated with PN.2-4
hormone, glutamine, and diet on adaptation in short-bowel syn-
drome: A randomized, controlled study. Gastroenterology 113: There is no therapeutic benefit of bowel rest in CD.
1074&mdash;1081, 1997 Prospective studies have compared the role of PN with
26. Szkudlarek J, Jeppesen PB, Mortensen PB: Effect of high dose bowel rest to EN.56 Clinical remission rates were sim-
growth hormone with glutamine and no change in diet on intes- ilar, with no evidence that bowel rest with PN had any
tinal absorption in short bowel patients: a randomised, double
blind, crossover, placebo controlled study. GUT 47:199-205, advantage in management of patients with active CD.
2000 Meta-analysis of 16 prospective randomized trials
27. Abu-Elmagd K, Reyes J, Todo S, et al: Clinical intestinal trans- showed that the frequency of clinical remission after
plantation: new perspectives and immunologic considerations. treatment with steroids was 80% compared with 60%
J Am Coll Surg 186:512-525, 1997 after treatment with an elemental or polymeric diet
alone. 7-9 Pooled data of studies comparing polymeric
INFLAMMATORY BOWEL DISEASE and elemental formulas showed no advantage for ele-
Background mental diets (65% versus 61% remission rates
Inflammatory bowel disease (IBD) includes both Although it had been proposed that IBD is associated
with markedly increased caloric requirements, it has
Crohns disease (CD) and ulcerative colitis (UC). CD
been demonstrated that in both inactive CD and in the
can involve any portion of the alimentary tract from
the mouth to the anus. Inflammation of the bowel is setting of active disease, total energy expenditure is
not significantly different than expected in nor-
patchy and involves the full thickness of the intestine. mals.1o,111 Although resting energy expenditure is
Fistulae to other segments of involved bowel, adjacent
increased in active CD, activity level in these patients
organs (bladder, uterus),and skin are common, occur- is decreased, making total energy expenditure identi-
ring in 20% to 40% of patients.
cal to normals.1
Ulcerative colitis (UC) is a mucosal disease
Published studies do not support the concept that
restricted to the colon. UC begins in the rectum and is
found in a continuous distribution without inter- improved nutrition status coupled with bowel rest
induce clinical remission and avoid colectomy in UC.23
spersed normal mucosa.
Malnutrition in CD, and to a somewhat lesser extent
in UC, is common. Depending on severity of disease, Special Considerations
weight loss has been reported in 65% to 78% of those High output CD fistulae may result in altered nutri-
with CD and in 18% to 62% of those with UC. Hypoalbu- tion status. Fluid, electrolyte, and zinc deficiencies
minemia is encountered in 25% to 80% of patients with may be particularly prominent. 12 Although approxi-
CD and in 26% to 50% of those with UC. Anemia occurs mately 38% of fistulae close spontaneously with bowel
in about half of patients with CD, primarily the result rest and PN, fistulae frequently recur when oral intake
of malabsorption, and in up to 80% of those with UC, is resumed. 13
largely caused by blood loss. Electrolytes are often In some patients with very extensive CD, prolonged
depleted as a result of diarrhea in both CD and UC. use of PN may be required when the oral or EN feeding
Vitamin and mineral deficiencies are usually more is not tolerated. PN is usually indicated for a limited
prominent in CD, but this is variable depending on the period of time until remission can be achieved with
location and degree of disease involvement. Mecha- steroids or surgical intervention is performed.
nisms contributing to malnutrition in IBD include Preoperative PN in CD has been investigated pri-
decreased food intake due to discomfort and diarrhea marily in retrospective studies. These have shown
being exacerbated by eating, as well as to dietary fewer postoperative complications, 14 an improved clin-
74SA

ical course,15 and a decreased length of bowel requiring active Crohns disease? A meta-analysis of the randomized con-
trolled trials. JPEN 19:356-362, 1995
resection, but at the expense of a longer hospitaliza- 9. Griffiths A, Ohlsson A, Sherman P, et al: Meta-analysis of
tion. 16 The latter study showed no significant differ- enteral nutrition as a primary treatment of active Crohns dis-
ence in postoperative complications. It appears that ease. Gastroenterology 108:1056-1067, 1995
the useof preoperative PN should be restricted to 10. Chan AT, Fleming CR, OFallon WM, et al: Estimated versus
malnourished patients with CD who cannot measured basal energy requirements in patients with Crohns
severely disease. Gastroenterology 91:75-78, 1986
tolerate EN and who are scheduled for elective or semi- 11. Stokes MA, Hill GL: Total energy expenditure in patients with
elective procedures. Crohns disease: Measurement by the combined body scan tech-
The only indication for dietary modification in nique. JPEN 17:3-7, 1993
patients with IBD is in CD when a nonobstructive 12. Yamazaki Y, Fukushima T, Sugita A, et al: The medical, nutri-
stricture precludes a normal, well-balanced diet. In tional and surgical treatment of fistulae in Crohns disease. Jpn
J Surg 20:376-383, 1990
this case, restriction of fiber is indicated. 13. Afonso JJ, Rombeau JL: Nutritional care for patients with
There may be a role for specific nutrients in UC. An Crohns disease. Hepato-gastroenterology 37:32-41, 1990
association has been observed between folic acid sup- 14. Rombeau JL, Barot LR, Williamson CE, et al: Preoperative total
plementation and a decreased relative risk of develop- parenteral nutrition and surgical outcome in patients with
ment of cancer or dysplasia in UC.18 Randomized con- inflammatory bowel disease. Am J Surg 143:139-143, 1982
15. Eisenberg HW, Turnbull JRB, Weakley FL: Hyperalimentation
trolled trials of omega-3 fatty acids as a nutritional as preparation for surgery in transmural colitis (Crohns dis-
supplement in UC provide evidence for a role in ease). Dis Colon Rectum 17:469-475, 1974
decreasing disease activity and in reducing steroid 16. Lashner BA, Evans AA, Hanauer SB: Preoperative total paren-
teral nutrition for bowel resection in Crohns disease. Dig Dis Sci
requirements.l9-21 34:741-774, 1989
17. Wilschanski M, Sherman P, Pencharz P: Supplementary enteral
nutrition maintains remission in paediatric Crohns disease. Gut
Practice ,.. .

38:543-548, 1996
Inflammatory Bowel Disease ,
18. Lashner B, Provencher K, Seidner D, et al: The effect of folic acid
supplementation on the risk for cancer or dysplasia in ulcerative
colitis. Gastroenterology 112:29-32, 1997
1. Patients with IBD are at nutrition risk and 19. Aslan A, Triadafilopoulos, G: Fish oil fatty acid supplementation
should undergo nutrition screening to identify in active ulcerative colitis: A double-blind, placebo-controlled,
those who require formal nutrition assessment crossover study. Am J Gastroenterol 87:432-437, 1992

with development of a nutrition care plan. (B) 20. Hawthorne AB, Daneshmend TK, Hawkey CJ, et al: Treat-
ment of ulcerative colitis with fish oil supplementation: a
2. EN should be used in CD patients requiring
prospective 12 month randomised controlled trial. Gut
SNS. (B) 33:922-928, 1992
3. PN should be reserved for those patients with IBD 21. Lorenz R, Weber PC, Szimnau P, et al: Supplementation with
in whom EN is not tolerated. (B) n-3 fatty acids from fish oil in chronic inflammatory bowel dis-
ease&mdash;a randomized, placebo-controlled, double-blind cross-over
4. In cases of fistulae associated with CD, a brief
trial. J Intern Med 225:225-232, 1989
course of bowel rest and PN should be
attempted. (B) SOLID ORGAN TRANSPLANTATION
5. Peri-operative SNS is indicated in patients with Background
IBD who are severely malnourished and in whom
surgery may be safely postponed. (B) The United Network of Organ Sharing (UNOS) esti-
6. SNS and bowel rest should not be used as primary mates that the number of solid organ transplants per-
therapies for UC or CD. (A) formed over the past decade has almost doubled to
nearly 22,000 annually. Unfortunately, because of a
limited number of donor organs, the number of recipi-
REFERENCES ents awaiting transplant is approximately 72,000, a
1. Kelly DG, Fleming CR: Nutritional considerations in inflamma- more than a three-fold increase over the same time.
tory bowel diseases. Gastroenterol Clin N Am 24:597-611, 1995 Malnutrition prior to transplantation has been
2. Dickinson RJ, Ashton MG, Axon ATR, et al: Controlled trial of
shown to increase morbidity and mortality after solid
intravenous hyperalimentation and total bowel rest as an
adjunct to the routine therapy of acute colitis. Gastroenterology organ transplant.2-5 Nutrition assessment iri these
79:1199-1204, 1980 patients is dependent on a carefully performed history
3. McIntyre PB, Powell-Tuck J, Wood SR, et al: Controlled trial of and physical examination. Objective measures such as
bowel rest in the treatment of severe acute colitis. Gut 27:481&mdash;
485, 1986
body weight, anthropometric measures, and visceral
4. Shiloni E, Coronado E, Freund HR: Role of total parenteral protein levels may be less sensitive in detecting the
nutrition in the treatment of Crohns disease. Am J Surg 157: degree of malnutrition as a result of fluid imbalance,
180&mdash;185, 1989 organ dysfunction, and surgical stress. 6-10
5. Lochs H, Meryn S, Marosi L, et al: Has total bowel rest a Nutrition care may need to be modified depending on
beneficial effect in treatment of Crohns disease? Clin Nutr 2:61-
the time in relation to transplantation. Patients can be
64, 1983
6. Greenberg GR, Fleming CR, Jeejeebhoy KN, et al: Controlled stratified into three stages: pretransplant, peri-opera-
trial of bowel rest and nutrition support in the management of tive, and posttransplant. Clinical guidelines for specific
Crohns disease. Gut 29:1309-1315, 1988 diseases should be followed for patients in the pre-
7. Trallori M, DAlbasio G, Milla M, et al: Defined-formula diets
versus steroids in the treatment of active Crohns disease. Scand
transplant stage. Immediately after transplantation,
J Gastroenterol 31:267-272, 1996
the goal of nutrition support is to promote wound heal-
8. Fernandez-Barares F, Cabre E, Esteve-Comas M, et al: How ing, support the bodys ability to fight infection, and to
effective is enteral nutrition in inducing clinical remission in allow for rehabilitation.&dquo; EN can be used in most
 75SA

patients requiring SNS after organ transplant. PN Hyperlipidemia, a potential long-term complication
may be necessary in malnourished patients with after transplantation, can be particularly problematic
severe cytomegalovirus esophagitis and gastroenteri- since it has been linked to transplant graft vasculopa-
tis, azathioprine induce pancreatitis, small bowel thy. This can result in coronary artery disease, chronic
obstruction, fistula formation, gastrointestinal bleed- rejection, and vanishing bile duct syndrome in heart,
ing, chylous ascites, and in the immediate postopera- kidney and liver transplant, respectively.l2 A variety of
tive stage of small bowel transplantation. Finally, the factors can contribute to this problem including under-
long-term care of patients during the posttransplant lying genetic abnormalities, dietary factors, obesity,
stage can be complicated by obesity, hypertension, dia- diabetes mellitus and corticosteroids. 21,29,30
betes mellitus, hyperlipidemia, and osteoporosis . 12-15
A comprehensive program to care for patients under-
Special Issues
going solid organ transplant should address all of these
issues. Experimental animal studies suggest that specific
nutrients may be used to modify outcomes after organ
Evidence transplant. Supplemental arginine and n-3 polyunsat-
urated fatty acids, alone and in combination, have been
Protein and energy requirements are affected by the shown to improve survival after transplantation in
stress of surgery, the use of immune modulating med- animal models.31-33 Growth hormone, insulin-like
ications, postoperative complications, and episodes of growth factor-1 (IGF-1) and homocysteine have been
acute rejection. Peri-operative energy requirements shown in similar models to improve graft and recipient
are similar to those necessary to support uncompli- surviva1.34-36 Nucleotide-free diets have been shown to
cated surgical procedures of a similar magnitude. enhance immunity and improve graft and host sur-
There requirements are generally 130 to 150% of basal vival.37 Although there is often little control over the
energy expenditure as determined by the Harris Bene- nutrition status of the donor, nutritional repletion of
dict equation or 35 kcal/kg of body weight. 2,6,16-20 donor swine has been shown to improve survival in the
Requirements may transiently increase as a result of recipient animals.38,39 The nutrient status of the donor
sepsis or acute rejection. Although energy require- may become a more important issue in the future with
ments are often estimated, they can be most reliably transplants from living-related donors.
determined using indirect calorimetry.
Balance studies suggest that protein requirements Practice ,.. .

after transplantation are modestly elevated, ranging Solid i

Organ Transplantation
from 1.5 to 2 gm/kg per day. This level of intake is in
part necessary because of the losses associated with 1. Patients in any stage of the transplant process are
surgical wounds, drains, and fistulae, and the increase at nutrition risk, and should undergo nutrition
in protein catabolism associated with corticosteroid screening to identify those who require formal
use.21-23 Protein requirements can decrease to 1 gm/kg nutrition assessment with development of a
as the dose of corticosteroids is reduced to maintenance nutrition care plan. (B)
levels.24 2. In the perioperative transplant period, patients
There are only a few prospective controlled trials should receive energy substrate similar to that
investigating the role of SNS in solid organ transplan- required in all postoperative patients. (B)
tation. Each involves the management of patients after 3. In the perioperative transplant period, patients
liver transplant. Reilly et a125 demonstrated a decrease should receive 1.5 to 2.0 g/kg per day protein. (B)
in intensive care unit length of stay in a group of 4. SNS should be provided to malnourished patients
patients receiving PN compared with patients who with complications or delayed oral intake after
received intravenous fluids. Wicks et a126 compared EN solid organ transplant. (B)
to PN and was unable to show a difference in time to an 5. Metabolic and nutrition complications of trans-
oral diet, intestinal or infectious compli-
cations. Hasse et al2 permeability
plantation, including obesity, hypertension, dia-
found that EN reduced the occur- betes mellitus, hyperlipidemia, and osteoporosis,
rence of viral infections after transplant compared should be treated with appropriate dietary and
with intravenous fluid. In all cases EN was delivered pharmacologic interventions. (C)
via nasojejunal feeding tube. These results suggest
that SNS provides a modest benefit for malnourished
REFERENCES
patients after liver transplantation and that EN is
medically equivalent to PN. 1. http: //www.unos.org
SNS should be administered cautiously to avoid 2. Frazier OH, Van Buren CT, Poindexter SM, et al: Nutritional
management of the heart transplant recipient. J Heart Trans-
postoperative hyperglycemia. Hyperglycemia has been plant 4:450-452, 1998
shown to impair wound healing and increase the risk of 3. Selberg O, Bottcher J, Tusch G, et al: Identification of high and
infection. Hyperglycemia after transplant is due to low risk patients before liver transplantation: A prospective
insulin resistance associated with surgical stress, cohort study of nutritional metabolic parameters in 150 patients.
infection, and corticosteroid administration .28 The 4. Hepatology 25:652-657, 1997
Harrison J, McKiernan J, Neuberger JM: A prospective study on
immune modulators tacrolimus and cyclosporine can the effect of recipient nutritional status on outcome in liver
contribute to hyperglycemia by inhibiting insulin transplantation. Transpl Int 10:369-374, 1997
secretion by the pancreas.l3 5. Pikul J, Sharpe MD, Lowndes R, et al: Degree of preoperative
76SA

malnutrition is predictive of postoperative morbidity and mor- 32. Elzinga L, Kelley VE, Houghton DC, et al: Model of experimental
tality in liver transplant recipients. Transplantation 57:469- nephrotoxicity with fish oil as the vehicle for cyclosporine. Trans-
472, 1994 plantation 43:271-274, 1987
6. Poindexter SM: Nutrition support in cardiac transplantation. 33. Otto DA, Kahn DR, Hamm HW, et al: Improved survival of
Top Clin Nutr 7:12-16, 1992 heterotopic cardiac allografts in rats with dietary omega-3 poly-
7. DeCecco SR,Wieners EJ, Wisner RH, et al: Assessment of nutri- unsaturated fatty acids. Transplantation 50:193-198, 1990
tional status of patients with end-stage liver disease undergoing 34. Ducloux D, Fournier V, Rebibou JM, et al: Hyperhomocysteine-
liver transplantation. Mayo Clin Proc 64:95-102, 1989 mia in renal transplant recipients with and without cyclospor-
8. Hasse J, Strong S, Gorman MA, et al: Subjective global assess- ine. Clin Nephrol 49:232-235, 1998
35. Cole DE, Ross HJ, Evovski J, et al: Correlation between total
ment: Alternative nutritional assessment technique for liver
transplant candidates. Nutrition 9:339-343, 1993 homocysteine and cyclosporine concentrations in cardiac trans-
9. Baron P, Waymack JP: A review of nutrition support for trans-
plant recipients. Clin Chem 44:2307-2312, 1998
36. Alexander JW, Valente JF, Greenberg NA, et al: Dietary amino
plant patients. Nutr Clin Pract 8:12-18, 1993 acids as new and novel agents to enhance allograft survival.
10. Lowell JA, Beindorff ME: Nutritional assessment and therapy in Nutrition 15:130-134, 1999
abdominal organ transplantation. IN Nutritional Support: The- 37. Van Buren CT, Kulkami AD, Schandle VB, et al: The influence of
ory and Therapeutics. Shikora S, Blackburn G (eds). Chapman & dietary nucleotides on cell-mediated immunity. Transplantation
Hall, Glasgow, Scotland, 1997, pp 422-488 36:350-352, 1983
11. Hasse JM: Recovery after organ transplantation in adults: The 38. Sadamori H, Tanaka N, Yagi T, et al: The effects of nutritional
role of postoperative nutrition therapy. Top Clin Nutr 13:15-26, repletion on donors for liver transplantation in pigs. Transplan-
1998 tation 60:317-321, 1995
12. Kobashigawa JA, Kasiske BL: Hyperlipidemia in solid organ 39. Ishikawa T, Yagi T, Ishine N, et al: Energy metabolism of the
transplantation. Transplantation 63:331-338, 1997 grafted liver and influence of preretrival feeding process on
13. Jindal RM: Post-transplant diabetes mellitus: A review. Trans- swine orthotopic liver transplantation. Transplantation 29:397-
plantation 58:1289-1298, 1994 399, 1997
14. Perez R: Managing nutrition problems in transplant patients.
Nutr Clin Pract 8:228-232, 1993
15. Meier-Kriesche H: Obesity and long-term allograft survival. GASTROINTESTINAL FISTULA
Transplantation 68:1294-1297, 1999 Background
16. Delafosse B, Faure JL, Biouffard Y, et al: Liver transplantation-
energy expenditure, nitrogen loss, and substrate oxidation rate Gastrointestinal fistulae result in diversion of intes-
in the first two postoperative days. Transplant Proc 21:2453- tinal contents to the skin or to another hollow viscous
2454, 1989 such as the urinary bladder, vagina, or another part of
17. Shanbhogue RLK, Bistrian BR, Jenkins RL, et al: Increased
protein catabolism without hypermetabolism after human ortho- the gastrointestinal tract. They occur as a result of
topic liver transplantation. Surgery 101:146-149, 1997 Crohns disease, abscess, surgery, trauma, ischemia,
18. Ragsdale D: Nutritional program for heart transplantation. irradiation, and/or tumor. The pathophysiologic conse-
J Heart Transplant 6:228-233, 1987
quences are determined by the site of the fistula in the
19. Zabielski P: What are the calorie and protein requirements dur-
ing the acute postrenal transplant period? Support Line 14:11- gastrointestinal tract, the site to which contents are
13, 1992 diverted, and the volume of fluid diverted. Even small
20. Kowalchuk D: Nutritional management of the pancreas trans- quantities of intestinal fluid may cause urinary or vag-
plant patient. Support Line 14:10-11, 1992 inal infection, skin irritation, or malabsorption. High-
21. Steiger U, Lippuner K, Jensen EX, et al: Body composition and
fuel metabolism after kidney grafting. Eur J Clin Invest 25:809- output fistulae, defined as loss of greater than 500 mL
816, 1995 of fluid daily, are usually the result of enterocutaneous
22. Seagraves A, Moore EE, Moore FA, et al: Net protein catabolic fistulae involving the proximal gastrointestinal tract.
rate after kidney transplantation: Impact of corticosteroid
They may cause substantial losses of fluid (500 to 4000
immunosuppression. JPEN 10:453-455, 1986 mL/d), electrolytes, protein, energy, vitamins, and
23. Hoy WE, Sargent JA, Freeman RB, et al: The influence of glu-
corticoid dose on protein catabolism after renal transplantation. trace minerals resulting in dehydration, acid-base
Am J Med Sci 291:241-247, 1986 imbalance, electrolyte imbalance, and malnutrition.
24. Hasse JM, Weseman RA: Solid organ transplantation. IN The These losses, together with food restriction to minimize
Science and Practice of Nutrition Support. A Core Curriculum.
Gottschlich MM (ed). Kendall/Hunt, Dubuque, IA, 2001, pp 107-
symptoms and hypercatabolism resulting from sepsis,
cause profound nutrient depletion and death if not
140
25. Reilly J, Mehta R, Teperman L, et al: Nutritional support after corrected. Mortality from gastrointestinal fistulae
liver transplantation: A randomized prospective study. JPEN results from sepsis, malnutritio i, and electrolyte
14:386-391, 1990 imbalance, often after several attempts to close the
26. Wicks C, Somasundaram S, Buarnason I, et al: Comparison of
fistula surgically. For external gastrointestinal tract
enteral feeding and total parenteral nutrition after liver trans-
plantation. Lancet 344:837-840, 1994 fistulae, mortality rates of 40% to 65% before 19701-5
27. Hasse JM, Blue LS, Liepa GU, et al: Early enteral nutrition have generally declined to 5% to 2 1%.1,6-9 Recent
support in patients undergoing liver transplantation. JPEN reports suggest no further decline in mortality rate but
19:437-443, 1995 possibly further improvement in the rate of nonsurgi-
28. Driscoll DF, Palombo JD, Bistrian BR: Nutritional and meta-
bolic considerations of the adult liver transplant candidate and
cal (spontaneous) closure Spontaneous closure rates
organ donor. Nutrition 11:255-263, 1995 from 15% to 80% are reported. 1,7,10,11 Malnutrition,
29. Moore R, Thomas D, Morgan E, et al: Abnormal lipid and other physiologic disturbances, and mortality are pro-
lipoprotein profiles following renal transplantation. Transplant portionately less in moderate-output fistulae (200 to
Proc 25:1060-1061, 1993
500 mL/d) and low-output fistulae (<200 mL/d).
30. Palmer M, Schaffner F, Thung SN: Excessive weight gain after
liver transplantation. Transplantation 51:797-800, 1991
31. Alexander JW, Levy A, Custer D, et al: Arginine fish oil, and Evidence
donor-specific transfusions independently improve cardiac allo-
graft survival in rats given subtherapeutic doses of cyclosporine. Most postoperative fistulae will heal without fur-
JPEN 22:152-155, 1998 ther surgery in the absence of distal obstruction,
 77SA

loss of bowel continuity, adjacent abscess, foreign vation of otherwise healthy individuals will lead to
body, cancer, or Crohns disease. There are no death in about 60 days, and infection and excessive
reported prospective, randomized, controlled clini- losses from high output fistulae can reasonably be
cal trials comparing the results of treatment which expected to reduce the time for death from starvation
includes SNS (EN or PN) with controls not receiving to 30 days. Therefore, even in the absence of random-
SNS for any type of gastrointestinal fistula. ized, controlled clinical data, nutrition support with
The improvement in mortality, especially for EN or PN should not be delayed beyond 7 to 14 days
patients with high output fistulae, over the past 40 in patients with gastrointestinal fistulae who are not
years, can be attributed to improvements in intensive eating.
care, antibiotic therapy, wound care, operative tech-
niques, and possibly SNS. Edmunds et a12 noted a 43% Special Considerations
mortality and significant malnutrition (47%, defined as Whether treatment with TPN and bowel rest
serum protein less than 5.6 g/100 mL and/or weight
loss of greater than 15 pounds) among 157 fistula increases the incidence of spontaneous fistula closure
or reduces the incidence of postoperative complications
patients seen at Massachusetts General Hospital
between 1946 and 1959. However, overall mortality among fistula patients is unclear. The primary role of
was not increased in the malnourished group with one
SNS in management of gastrointestinal fistulae is sup-
exception. Patients with lower bowel fistulae did have portive, that is, to prevent or treat malnutrition and
an increased mortality related to a high prevalence of
debilitation.8 Administration of octreotide plus PN did
cancer and malnutrition. Nonrandomized, prospective
not increase the incidence of spontaneous closure (81%
versus 85%) but decreased the mean time to closure
studies comparing the results for fistula patients
treated with nutrition support, primarily PN, with from 20.4 to 13.9 days in one study 18; other studies
results for historical controls suggested significant have shown no beneficial effect. 19 Some studies suggest
benefits from PN.12-15 Reber et al 16 reviewed results of that PN itself may decrease upper gastrointestinal
fistulae treated between 1968 and 1971 when 35% of tract secretions. 8,20
the patients received PN with results from 1972 to High output intestinal fistulae may result in exces-
1977 when 71% received PN. Neither mortality nor sive losses of some nutrients, especially protein, zinc,
spontaneous closure rates differed between the two copper, and several vitamins. Therefore, although
there are no controlled studies to support the practice,
groups.
Soeters et al6 reviewed records of all 247 gastro- it is appropriate for the nutrient prescription for such
intestinal-cutaneous fistula patients seen at Massa- patients to include 1.5 to 2.0 g of protein/kg/per day in
chusetts General Hospital from 1960 to 1975. Com- the absence of renal or liver failure and 10 to 15 mg of
zinc/liter of fistula fluid lost. Some have recommended
pared with the results obtained by Edmunds2 from the that patients with high output fistulae receive two
same institution from 1946 to 1959 (43% mortality),
overall mortality was 15% for the period 1960 to 1970 times the recommended daily allowance (RDA) for vita-
when technology had improved but SNS was seldom mins and trace minerals and 5 to 10 times the RDA for
used. Mortality remained 21% in the period 1970 to vitamin C,l,l1 but there are no data to support this
1975 when 57% of the patients received PN. Mortality practice.
was 25% among those receiving PN and 16% among
EN is often the preferred method of SNS in patients
those not receiving PN in this retrospective, nonran- with gastrointestinal fistulae. Patients with fistulas
domized study. Significant malnutrition, defined as involving the esophagus, stomach, or duodenum can be
fed into the jejunum using a tube, gastroje-
serum protein less than 6 g/100 mL and/or weight loss nasoiejunal
junal tube, or a jejunostomy.3,21, Patients with fistu-
greater than 7 kg was present in 87% of the 119 lae at least 4 feet distal to the ligament of Treitz have
patients seen in 1960 to 1970 and 51% of the 128 been supported with gastric feeding.21 It is not clear
patients seen in 1970 to 1975. There were significant whether monomeric or low-fat products are better tol-
correlations between malnutrition, sepsis, and mortal-
erated than polymeric. In a dog model, a monomeric
ity. Because the decrease in mortality occurred prior diet produced significantly less output from an ileal
to the frequent use of PN, it cannot be attributed
to PN. fistula than a regular diet but significantly more than
Studies have shown a correlation between intake of parenteral nutrition. 23 Patients with gastrointestinal
fistulae in association with recent complicated abdom-
greater than 1600 kcal/d and decreased mortality. 3,17 inal surgery, marked malnutrition or other serious
Such correlations may or may not indicate that nutri-
tion support improves outcome. The correlations could comorbid conditions may benefit from several months
occur as a result of difficulty achieving calorie goals in
of SNS, given at home if possible.24
the sickest patients, so that the ability to achieve ade-
Practice Guidelines
.

quate nutrient intake by the enteral or parenteral

route may be a marker for less severe disease. Alter- Gastrointestinal t

natively, physicians who are most diligent about pro-

viding nutrition support for patients may provide bet- 1. Patients with enterocutaneous fistulae are at
ter management in other ways. nutrition risk and should undergo formal nutri-
Currently, uncontrolled infection is the major cause tion assessment and development of a nutrition
of mortality among patients with gastrointestinal fis- care plan. (B)
tulae and should be a primary focus of attention. Star- 2. EN, proximal or distal to the fistula, should be
78S A

used in patients who cannot meet their nutri- RENAL DISEASE

tional needs by oral intake and who are malnour-
ished or expected to have inadequate oral intake
Background
for 7 to 14 days or more. (B) Renal failure patients experience a variety of clinical
3. When SNS is required, PN should be reserved for and metabolic abnormalities that can affect their
those patients in whom enteral intake must be nutrition status. The degree of nutritional impairment
restricted. (C) is dependent on the concurrent stress, degree and
duration (chronic or acute) of renal impairment, and
REFERENCES
the treatment modality. In chronic renal failure (CRF),
1. Dudrick SJ, Maharaj AR, McKelvey AA: Artificial nutritional altered taste sensation, anorexia, nausea, and unpal-
support in patients with gastrointestinal fistulas. World J Surg atable diets all lead to decreased nutrient intake. CRF
23:570-576, 1999 has also been associated with a state of chronic inflam-
2. Edmunds LH Jr, Williams GM, Welch CE: External fistulas
arising from the gastro-intestinal tract. Ann Surg 152:445-470, mation that promotes catabolism and anorexia.1 In
1960 acute renal failure (ARF), hypermetabolism is present,
3. Chapman R, Foran R, Dunphy JE: Management of intestinal protein breakdown is accelerated, and protein synthe-
fistulas. Am J Surg 108:157-164, 1964 sis is impaired.2 Renal replacement therapy (RRT) fur-
4. Halversen RC, Hogle HH, Richards RC: Gastric and small bowel
fistulas. Am J Surg 118:968-972, 1969 ther aggravates protein nutriture by inducing losses of
5. Nassos TP, Broasch JW: External small bowel fistulas: current protein, amino acids and albumin. Other metabolic
treatment and results. Surg Clin N Am 51:687-692, 1971 abnormalities include altered glucose utilization and
Soeters PB, Ebeid AM, Fischer JE: Review of 404 patients with
6.
gastrointestinal fistulas. Impact of parenteral nutrition. Ann
impaired lipid metabolism. These metabolic abnor-
malities result in negative nitrogen balance and abnor-
Surg 190:189-202, 1979
7. Rose D, Yarborough MF, Canizaro PL, et al: One hundred and malities in serum amino acid, glucose and triglyceride
fourteen fistulas of the gastrointestinal tract treated with total levels during nutrition support. As a result, protein-
parenteral nutrition. Surg Gynecol Obstet 163:345-350, 1986 calorie malnutrition (PCM) is a frequent complication
8. Meguid MM, Campos ACL: Nutritional management of patients in renal failure patients.5 The presence of PCM in
with gastrointestinal fistulas. Surg Clin N Am 76:1035-1080,
1996 patients with CRF and end-stage renal disease (ESRD)
9. McIntyre PB, Ritchie JK, Hawley PR, et al: Management of remains one of the strongest predictors of morbidity
enterocutaneous fistulas: a review of 132 cases. Br J Surg and mortality in this cohort.
71:293-296, 1984
10. Benson DW, Fischer JE. Fistulas. IN Total Parenteral Nutrition. Evidence
JE Fischer (ed). Little, Brown and Company, Boston, 1991, pp
253-262 PCM is often identified in renal patients by laboratory
11. Berry SM, Fischer JE: Classification and pathophysiology of
enterocutaneous fistulas. Surg Clin N Am 76:1009-1018, 1996
testing.7 Visceral protein measurements are not well
suited for assessment in renal patients. However, indi-
12. MacFadyen BV, Dudrick SJ, Ruberg RL: Management of gastro- viduals with low serum albumin levels and a serum pre-
intestinal fistulas with parenteral hyperalimentation. Surgery
74:100-105, 1973 albumin level <30 mg/dL are at risk for PCM.&dquo;,9 Serum
13. Himal HS, Allard JR, Nadeau JE, et al: The importance of albumin is also a predictor of mortality in renal failure.
adequate nutrition in closure of small intestinal fistulas. Br J The relative risk of death is five times greater when
Surg 61:724-726, 1974 serum albumin is low (below 3 to 3.4 g/dL).lo
14. Deitel M: Nutritional management of external gastrointestinal
fistulas. Can J Surg 19:505-511, 1976 Dietary protein restriction offers several theoretic
15. Thomas RJS, Rosalion A: The use of parenteral nutrition in the benefits for patients with progressive CRF. Motivated,
management of external gastrointestinal tract fistulae. Aust N Z closely monitored patients with CRF not on dialysis
J Surg 48:535-539, 1978
16. Reber HA, Roberts C, Way LW, et al: Management of external
placed on low protein diets (0.6 g/kg per day) and very
low protein diets (0.3 g/kg per day) supplemented with
gastrointestinal fistulas. Ann Surg 188:460-467, 1978
17. Sheldon GF, Gardiner BN, Way LW, et al: Management of gas- essential amino acids have been shown to be capable of
trointestinal fistulas. Surg Gynecol Obstet 133:385-389, 1971 maintaining their nutritional status.ll The modifica-
18. Torres AJ, Landa JI, Moreno-Azcoita M, et al: Somatostatin in tion of diet in a major renal disease (MDRD) study
the management of gastrointestinal fistulas. A multicenter trial. showed no improvement resulting from protein restric-
Arch Surg 127:97-100, 1992
19. Hodin RA, Matthews JB: Small intestine. IN Surgery: Basic tion in CRF patients except for those with advanced
Science and Clinical Evidence. Norton JA, Bollinger RR, Chang CRF. It should be noted that patients with diabetes
AE, et al (eds). Springer-Verlag, New York, 2001, pp. 617-646 mellitus were excluded from the MDRD study and may
20. Hamilton RF, Davis WC, Stephenson DV, et al: Effects of par- have benefited from protein restriction. 12 At present,
enteral hyperalimentation on upper gastrointestinal tract secre-
tions. Arch Surg 102:348-352, 1971
the conventional recommendation for protein intake in
21. Garden OJ, Dykes EH, Carter DC: Surgical and nutritional CRF is 0.6 to 0.8 g/kg per day. 13
management of postoperative duodenal fistulas. Dig Dis Sci Loss of amino acids (approximately 10 to 12 g per
33:30-35, 1988 hemodialysis therapy) occurs with high efficiency dial-
22. Rocchio MA, Mochar C-J, Hass KF, et al: Use of chemically
defined diets in the management of patient with high output YSIS. 14 Protein losses during peritoneal dialysis can be
even higher, often accounting for up to 15 g of protein
gastrointestinal cutaneous fistulas. Am J Surg 127:148-156,
1984 losses during episodes of peritonitis.l~ Hence, intake of
23. Wolfe B, Keltner RM, Willman VL: Intestinal fistula output in 1.2 g/kg per day of protein for maintenance hemodial-
regular, elemental, and intravenous alimentation. Am J Surg ysis patients and 1.2 to 1.3 g/kg per day for patients
124:803-806, 1972
24. Oakley JR, Steiger E, Lavery IC, et al: Catastrophic enterocuta- receiving chronic ambulatory peritoneal dialysis
neous fistulae. The role of home hyperalimentation. Cleve Clin (CAPD) is recommended. 16 In ARF patients undergo-
Quart 46:133-136, 1979 ing continuous hemofiltration, control of azotemia is
 79SA

possible while providing more than 1 g/kg per day of ]phorus restriction, calcium supplementation, and con-
protein. There continues to be controversy whether isideration of dihydroxy-vitamin-D3 supplementation is
increased protein intakes are associated with increas- recommended.21
ing urea nitrogen appearance (UNA). However, Macias
et al showed that ARF patients who received 1 g/kg per Practice Guidelines.

day or greater of protein achieved positive nitrogen Renal Disease

balance and had lower UNA. Conversely, patients

receiving nutrition at levels less than 1 g/kg per day of 1. Renal failure patients are at nutrition risk and
protein had significantly greater nitrogen deficits. i7 should undergo nutrition screening to identify
An early clinical study of PN in patients with ARF those who require formal nutrition assessment
showed improved survival in patients receiving small with development of a nutrition care plan. (B)
doses of essential amino acids dextrose, when
plus
compared with dextrose alone. However, a subse-
2. Well-monitored patients with advanced chronic
renal insufficiency but not on dialysis should
quent prospective, randomized, controlled trial com- receive diets restricted to 0.6 to 0.8 g of protein/kg
paring essential amino acid administration to a bal- per day. (A)
anced mixture of general amino acids (essential and 3. Patients with CRF on hemodialysis or peritoneal
nonessential amino acids) demonstrated no difference
in the formulations effect on mortality, nitrogen bal-
dialysis should receive 1.2 to 1.3 g of protein/kg per
day. (B)
ance, or BUN.19 Further data suggest that there may 4. Patients undergoing continuous hemofiltration
be an increased complication rate with development should receive at least 1.0 g of protein/kg per
of hyperammonemia and metabolic encephalopathy
when only essential amino acids are used for longer
day. (B)
5. Patients with ARF receiving SNS should be given
than 2 to 3 weeks .20 In renal failure patients, nones- a balanced mixture of both essential and nones-
sential amino acids including, arginine, ornithine, and sential amino acids. (A)
citrulline should be supplied to enable detoxification of 6. Patients with ARF who are severely malnour-
ammonia via the Krebs urea cycle.20 As such, caution ished or hypercatabolic should receive 1.5 to 1.8 g
should be used when very low protein diets (0.3 to 0.5 of protein/kg per day. (B)
g essential amino acids per day) are prescribed for 7. Intradialytic parenteral nutrition should only be
nonhypermetabolic ARF patients. considered in situations of gut failure or other
It is generally believed that negative nitrogen bal- unusual circumstances where EN and PN are not
ance in hypermetabolic patients cannot be reversed
feasible. (C)
solely with SNS. However, the results from Macias et 8. Water-soluble vitamin supplementation is required
al 17 suggest that achievement of positive nitrogen bal- for patients treated with dialysis. (A)
ance in patients with ARF requires between 1.5 and
9. Vitamin A status should be carefully monitored in
1.8 g protein/kg per day. Although such levels of pro-
tein support have also been associated with increasing
patients with CRF. (A)
protein catabolic rates, the magnitude of the increase REFERENCES
can be diminished by providing adequate energy sub-
1. Docci D, Bilancioni R, Baldrati L, et al: Elevated acute phase
strates (25 to 35 kcal/kg per day). reactants in hemodialysis patients. Clin Nephrol 34:88-91, 1990
2. Druml W: Protein metabolism in acute renal failure. Miner Elec-
trolyte Metab 24:47-54, 1998
Special Considerations 3. Riella MC: Nutrition in acute renal failure. Renal Failure
19:237-252, 1997
Intradialytic parenteral nutrition (IDPN) has been 4. Druml W, Fischer M, Sertl S, et al: Fat elimination in acute renal
used as a supplement to protein and calorie intake for failure: long-chain vs medium-chain triglycerides. Am J Clin
malnourished patients receiving maintenance hemodi- Nutr 55:468-472, 1992
5. Ahmed KR, Kopple JD: Nutrition in maintenance hemodialysis
alysis. Disadvantages of this modality are that it can
only supplement nutrition provided by other means, it patients. IN Nutritional Management of Renal Disease. Kopple
JD (ed). Baltimore, Williams & Wilkins, 1996, pp 563-560
is expensive, and it does not improve the patients oral 6. Barrett BJ, Parfrey PF, Morgan J, et al: Prediction of early death
intake. As such, IDPN should be reserved for patients in end-stage renal disease patients starting dialysis. Am J Kid-
who cannot meet their nutrient needs orally and who ney Dis 29:214-222, 1997
are not candidates for EN or PN because of gastroin-
7. Brivet FG, Kleinknecht DJ, Loirat P, at al: Acute renal failure in
intensive care units&mdash;causes, outcome, and prognostic factors of
testinal intolerance, venous access problems, or other
hospital mortality; a prospective, multicenter study. French
reasons. 13 Study Group on Acute Renal Failure. Crit Care Med 24:192-198,
Supplementation of water-soluble vitamins (thia- 1996
8. Kaysen GA, Rathore V, Shearer GC, et al: Mechanisms of
mine, riboflavin, pyridoxine, cyanobalamin, folic acid,
biotin, niacin, pantothenic acid, and ascorbic acid) hypoalbuminemia in hemodialysis patients. Kidney Int 48:510-
516, 1995
should be provided to patients receiving dialysis due to 9. Sreedhara R, Avram MM. Blanco M, et al: Prealbumin is the best
intradialytic losses. Caution should be exercised with nutritional predictor of survival in hemodialysis and peritoneal
supplementation of vitamin A (Retinol) as hypervita- dialysis. Am J Kidney Dis 28:937-942, 1996
10. Lowrie EG, Lew NL: Death risk in hemodialysis patients: the
minosis A is often noted in patients with ESRD.
Patients with advanced renal failure (GFR < 25 predictive value of commonly measured variables and an evalu-
ation of death rate differences between facilities. Am J Kidney
mL/min/1.73 m2) have disordered bone metabolism and Dis 15:458-482, 1990
are at significant risk for renal osteodystrophy. Phos- 11. Kasiske BL, Lakatua JD, Ma JZ, et al: A meta-analysis of the
80SA

effects of dietary protein restriction on the rate of decline in renal Metabolic homeostasis is further altered as evi-
function. Am J Kidney Dis 31:954-961, 1998 denced by marked hyperglycemia, altered gastrointes-
12. Levey AS, Adler S, Caggiula AW, et al: Effects of dietary protein tinal function, and depressed immune status markers.
restriction on the progression of advanced renal disease in the
modification of diet in renal disease study. Am J Kidney Dis The degree of hyperglycemia is linked to the severity of
27:652-663, 1996 injury and poorer clinical outcome; however, more
13. K/DOQI, National Kidney Foundation: Clinical practice guide- research is needed to determine if prevention of hyper-
lines for nutrition in chronic renal failure. Am J Kidney Dis
35(Suppl 2):S1-S140, 2000 glycemia actually improves patient outcome.~ Delayed
14. Ikizler TA, Flakoll PJ, Parker RA, et al: Amino acid and albumin gastric emptying can be an impediment to early gut
losses during hemodialysis. Kidney Int 46:830-837, 1994 feeding. Although the exact mechanism is unknown,
15. Blumenkrantz MJ, Gahl GM, Kopple JD, et al: Protein losses increased intracranial pressure, cytokines, and phar-
during peritoneal dialysis. Kidney Int 19:593-602, 1981 macologic agents may play a role. Small bowel feed-
16. Ambler C, Kopple J: Nutrition support for patients with renal
failure. IN A.S.P.E.N. Nutrition Support Practice Manual. Klein ings with concurrent stomach decompression and pro-
S (ed). American Society for Parenteral and Enteral Nutrition, kinetic agents may promote tolerance of EN. Zinc
Silver Spring, MD, 1998, pp 16.1-16.12 losses, due to the acute-phase response, are also seen
17. Macias WL, Alaka KJ, Murphy MH, et al: Impact of the nutri- in head injury; hypozincemia, and increased urinary
tional regimen on protein catabolism and nitrogen balance in
zinc excretion can depress immune status, which may
patients with acute renal failure. JPEN 20:56-62, 1996
18. Abel RM, Beck CH, Abbott WM, et al: Improved survival from impair or slow neurological recovery.2 Zinc supplemen-
acute renal failure after treatment with intravenous L-amino tation may be beneficial in head-injured patients.3
acids and glucose. N Engl J Med 288:695-699, 1973 Unlike patients with TBI, spinal cord-injured
19. Mirtallo JM, Schneider PJ, Mavko K, et al: A comparison of
essential and general amino acid infusions in the nutrition sup- patients are hypometabolic, depending on the severity
of injury, with energy expenditure approximately
port of patients with compromised renal function. JPEN 6:109-
113, 1982 94% of predicted by the Harris-Benedict equation.
20. Nakasaki H, Katayama T, Yokoyama S, et al: Complication of Decreased resting energy expenditure is correlated
parenteral nutrition composed of essential amino acids and his- with the degree of lean body mass loss.7 It is common
tidine in adults with renal failure. JPEN 17:86-90, 1993
21. Maroni BJ: Nutrition in renal disease. IN Primer on Kidney
for patients to experience an approximate 10% weight
Diseases, 2nd ed. Greenberg A (ed). Academy Press, San Diego, loss in the immediate postinjury phase.3 Predictive
1998, pp 440-447 equations must be used with caution as overfeeding
may occur in an attempt to reverse foreseeable nega-
NEUROLOGIC IMPAIRMENT tive nitrogen balance.7 Serial indirect calorimetry mea-
surements are the most accurate predictors of fluctu-
Background ating metabolic requirements.7 These patients are also
Neurologic impairment may occur acutely as a result plagued with gastrointestinal and metabolic complica-
of traumatic brain injury (TBI), cerebral vascular acci- tions, which may result in nutritional compromise over
dent (CVA), or infection or may occur as a result of time. These include gastritis, ileus, hypercalcemia and
chronic, degenerative processes. hypercalciura due to immobilization, osteoporosis, neu-
Acute neurologic injury, such as severe TBI rogenic bowel and bladder (often associated with fecal
(described as a Glascow Coma Scale < 8), can result in impaction and urinary tract infections), development
3
of
a complex cascade of metabolic, physiologic, and func- pressure ulcers, anemia, and hypoalbuminemia.3
tional alterations. Nutrition assessment must take Degenerative neurological diseases (eg, Parkinsons
into consideration the significant hypermetabolism, disease, multiple sclerosis, amylotrophic lateral sclero-
hypercatabolism, and nitrogen wasting followed by sis) as well as CVA differ in that most of the meta-
rapid lean body mass wasting and visceral protein bolic and physiologic changes occur in the chronic stage
depletion seen with TBL23 Nonsedated patients with of disease instead of the acute phase. CVAs are
TBI have mean resting metabolic expenditures 140% strongly associated with dysphagia, although a
to 200% above predicted.4 This may be attributed, in large percentage of patients recover swallowing
part, to the cytokine response, counter-regulatory hor- function over time.8 Screening for dysphagia, before
mones released postinsult, and/or steroid therapy. 2,4 the initiation of an oral feeding regimen, has been
Brain death and the use of barbiturates or neuromus- shown to decrease length of stay and incidence
cular blockers decrease energy expenditure.2 Predic- of aspiration pneumonia in patients with a CVA.9
tive equations have been inconsistent in determining Patients with progressive Parkinsons disease are
caloric needs; research supports the routine use of indi- plagued with gastrointestinal symptoms such as
rect calorimetry in this population.1 anorexia, dysphagia, excessive salivation, drooling,
Nitrogen losses mimic that of patients with 20% to constipation and delayed gastric emptying.3 Persis-
40% body surface area burns with an average nitrogen tent weight loss and dysphagia are hallmark symp-
excretion of 20 g/d during the acute injury phase.4 toms of amylotrophic lateral sclerosis and may
Steroid therapy may further exacerbate nitrogen result in the need for long-term nutrition support,
losses; the degree is dependent on dose and duration of preferably, EN via a percutaneous endoscopic gas-
therapy. Increased exogenous protein administration trostomy tube.lo
in the early injury phase cannot replete the losses, Despite the unique nuances of neurologic dis-
which peak approximately 7 to 10 days postinjury.22 eases, feeding challenges are a prevalent cause of
Despite adequate nutrition support, restoration of malnutrition. Impaired oral feeding may result in
nitrogen balance is often not realized until 2 to 3 weeks the need for nutrition support due to dysphagia,
postinjury. 4 risk of aspiration due to an inability to protect the
 81SA

airway, respiratory muscle weakness, gastroparesis 5. Indirect calorimetry should be utilized, if avail-
or gastrointestinal reflux, and/or impaired appetite able, to accurately determine nutrient require-
control centers in the brain. 11 Nutrition assessment ments in patients with TBI and CVAs. (B)
must be individualized to address the distinct prob- 6. Swallowing function should be evaluated to deter-
lems. mine the safety of oral feedings and risk of aspi-
ration before the initiation of an oral diet. (B)
Evidence
Early nutrition support is important in the acutely REFERENCES
injured neurologically impaired patient. Studies sup-
port early initiation of SNS, ideally, within 48 hours.l2 1. Sunderland PM, Heilbrun MP: Estimating energy expenditure
Early administration of SNS has been shown to be in traumatic brain injury: comparison of indirect calorimetry
with predictive formulas. Neurosurgery 31:246-253, 1992
predictive of a lower risk of infections and has trended 2. Young B, Ott L, Phillips R, et al: Metabolic management of
toward improved survival and reduced disability.-2 EN
the patient with head injury. Neurosurg Clin N Am 2:301-
initiated within 72 hours of a CVA is associated with a
320, 1991
decreased length of stay.l3 More studies are needed to 3. Varella L, Jastremski CA: Neurological impairment. IN The
confirm these relationships. PN can be initiated early Science and Practice of Nutrition Support, A Case Based Core
in the postinjury phase, whereas impaired gastric emp- Curriculum. Gottschlich M (ed). Kendell/Hunt Publishing Com-
pany, Dubuque, IA, 2001
tying occasionally delays the initiation of EN via the 4. Clifton GL, Robertson CS, Grossman RG, et al: The metabolic
gastric route. 14,15 Achievement of nutritional require-5 response to severe head injury. J Neurosurg 60:687-696,
ments may be delayed with EN for 10 to 14 days.5 1984
Although some studies suggest a trend toward 5. Wilson RF, Tyburski JG: Metabolic responses and nutritional
improved outcomes with PN versus EN as assessed by therapy in patients with severe head injuries. J Head Trauma
survival and incidence of septic complications, this Rehabil 13:11-27, 1998
6. Weekes E, Elia M: Observations on the patterns of 24-hour
finding is not universal and may merely reflect the energy expenditure changes in body composition and gastric
ability to administer target quantities of nutrients ear- emptying in head-injured patients receiving nasogastric tube
lier with PN in some patients.14-16 feeding. JPEN 20:31-37, 1996
Several studies support the use of small .bowel feed- 7. Rodriguez DJ, Benzel EC, Clevenger FW: The metabolic
ing as a means to promote more timely, adequate, and response to spinal cord injury. Spinal Cord 35:599-604, 1997
8. Dray TG, Hillel AD, Miller RM: Dysphagia caused by neurolog-
well-tolerated EN.17,18 These studies suggest improved ical deficits. Oryngol Clin N Am 31:507-524, 1998
nitrogen retention, reduced incidence of infections, and 9. Odderson IR, Keaton JC, McKenna BS: Swallow management in
decreased days in the intensive care unit.17,18 Estab- patients on an acute stroke pathway: quality is cost effective.
lishing and maintaining placement of nasoenteric feed- Arch Phys Med Rehabil 76:1130-1133, 1995
10. Mazzini L, Corra T, Zacala M, et al: Percutaneous endoscopic
ing tubes remains a clinical challenge. 17 Other studies
have succeeded with gastric feeding and show no dif- gastrostomy and enteral nutrition in amyotrophic lateral sclero-
sis. J Neurol 242:695-698, 1995
ferences in feeding tolerance or rates of aspiration.19, 20 11. Groher ME: Dysphagia Diagnosis and Management, 3rd ed.
Taylor and colleagues were able to administer full Butterworth-Heinemann, Boston, 1997
nutritional requirements day 1 postinjury via the gas- 12. Yanagawa T, Bunn F, Roberts I, et al: Nutritional support for
tric or intestinal routes. 20 head-injured patients (Cochrane Review). IN The Cochrane
EN remains the preferred method of SNS for neuro- Library, Update Software, Oxford, 2001, pp 1-20
13. Nyswonger GD, Helmchen RH: Early enteral nutrition and
logically impaired patients because of relative ease of length of stay in stroke patients. J Neurosci Nurs 24:220-223,
use and lower cost. However, adjunct or exclusive PN 1992
should be administered to achieve nutrition goals if 14. Rapp RP, Young B, Twyman D, et al: The favorable effect of early

gastrointestinal function is impaired or aspiration is parenteral feeding on survival in head-injured patients. J Neu-
rosurg 58:906-911, 1987
problematic. 5,21 15. Young B, Ott L, Twyman D, et al: The effect of nutritional
support on outcome from severe head injury. J Neurosurg
practice Guidelines
.
67:668-676, 1983
16. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in
Neurologic Impairment clinical practice: Review of published data and recommendations
for future research directions. JPEN 21:133-156, 1997
1. Patients with neurologic impairment are at nutri- 17. Ott L, Annis K, Hatton J, et al: Postpyloric enteral feeding costs
tion risk and should undergo nutrition screening for patients with severe head injury: blind placement, endoscopy,
and PEG/J versus TPN. J Neurotrauma 16:233-242, 1999
to identify those who require formal nutrition 18. Grahm TW, Zadrozny DB, Harrington T: The benefits of early
assessment with development of a nutrition care jejunal hyperalimentation in the head-injured patient. Neuro-
plan. (B) surgery 25:729-735, 1989
2. SNS should be initiated early in patients with 19. Klodell CT, Carroll M, Carrillo EH, et al: Routine intragastric

moderate or severe TBI. (B) feeding following traumatic brain injury is safe and well toler-
ated. Am J Surg 179:168-171, 2000
3. When SNS is required, EN is preferred if it is 20. Taylor SJ, Fettes SB, Jewkes C, et al: Prospective, randomized,
tolerated. (C) controlled trial to determine the effect of early enhanced enteral
nutrition on clinical outcome in mechanically ventilated patients
4. PN should be administered to patients with TBI if
suffering head injury. Crit Care Med 27:2525-2531, 1999
SNS is indicated and EN does not meet the nutri- 21. Twyman D: Nutritional management of the critically ill neuro-
tional requirements. (C) logic patient. Crit Care Clin 1:39-49, 1997
82SA

CANCER tumor growth and metastasis. There are few relevant

clinical studies.11-13 Absent any overt effects, it is rea-
Background sonable to ignore these theoretical considerations
Nutrition status has an important effect on quality of when contemplating the use of SNS in patients.
life and sense of well-being in cancer patients. Malnu- Extensive data are available concerning the use of
trition and weight loss often contribute to the death of SNS in cancer patients and have been summarized
cancer patients. elsewhere.l4,15
Cancer cachexia is syndrome characterized by pro-
a Routine use of SNS in patients undergoing major
gressive, involuntary weight loss. Clinical features cancer operations does not improve surgical outcomes
include host tissue wasting, anorexia, skeletal muscle when either morbidity or mortality are used as end-
atrophy, anergy, fatigue, anemia, and hypoalbumin- points. Preoperative SNS may be beneficial in moder-
emia. Causes of cancer cachexia include anorexia, ately or severely malnourished patients if adminis-
mechanical factors in the gastrointestinal tract related tered for 7 to 14 days preoperatively. In this situation,
to tumor, side effects of surgery, chemotherapy, and/or the potential benefits of nutrition support must be
radiation therapy, alterations in intermediary and weighed against the potential risks of the SNS itself
energy metabolism, and changes in the host cytokine and of delaying the operation. 14,15
and hormonal millieu. The cancer cachexia syndrome There is no benefit to the routine use of SNS as an
(CCS), which is observed in approximately 50% of can- adjunct to chemotherapy. 16 Chemotherapy toxicity is
cer patients,2 involves a heterogeneous medley of phys- not reduced; tumor responses and patient survival are
iologic and metabolic derangements resulting in poten- not improved. Because of an increased risk of infection
tially life-threatening malnutrition.3 Although often associated with the use of TPN, routine adjunctive use
seen in patients with advanced malignancies, CCS in patients receiving chemotherapy is actually delete-
may be present in the early stages of tumor growth. rious. Specialized nutrition support is appropriate in
Weight loss in cancer patients is of prognostic signif- patients receiving active anticancer treatment who are
icance. For any given tumor type, survival is shorter in malnourished and who will be unable to absorb ade-
patients who experience pretreatment weight loss.2 quate nutrients for a prolonged period of time.
Furthermore, CCS is a problematic cause of symptom There are few clinical trials investigating the routine
distress in cancer patients. 4,5 Early recognition and use of SNS as an adjunct to radiation therapy in cancer
intervention to prevent worsening of CCS may afford patients. 17 There is no clearly defined role for routine
the best opportunity to prevent its debilitating conse- EN, TPN, or oral supplements during head and neck,
quences.4 abdominal, or pelvic irradiation.
Nutrition assessment of cancer patients is accom-
plished by taking a nutrition history and conducting a Considerations
complete physical exam guided by the subjective global Special
assessment or a modified version. 6,7 Diagnosis, stage of Some nutrients have specific biologic effects on
cancer, weight loss history, and changes in diet are tumor and host. Use of specific substances for effects
especially informative in cancer patients. Serum albu- beyond their nutritional role may be referred to as

min may also be helpful, as it has been shown to be of nutritional pharmacology. Four nutrients have been
prognostic significance.8 Despite the important role of the subject of recent research: glutamine; arginine;
malnutrition in the pathogenesis of cancer, nutrition nucleic acids; and essential fatty acids. 15 There are no
care is often overlooked in this patient population.8 clinical trial data to support the use of these substrates
Evidence individually in cancer patients, with the possible
exception of the use of glutamine in patients undergo-
Pharmacologic interventions play only a limited role ing allogeneic bone marrow transplantation. 18,19 Clin-
in overcoming the anorexia and metabolic derange- ical trials have investigated nutritional pharmacologic

ments seen in CCS. Research has focused on the use of interventions in perioperative cancer patients using a
specialized nutrition support (SNS), bypassing oral mixture of &dquo;immune enhancing&dquo; substrates in an
intake to overcome CCS related anorexia. enteral formula containing supplemental arginine,
Numerous studies, as summarized by Boseki, have RNA, and n-3 fatty acids. Biomarkers such as immune
looked at the effect of SNS on nutritional parameters status and nitrogen balance may be favorably affected
in cancer patients.9 Parenteral nutrition (TPN) consis- by these specific nutrients, but the effect on clinical
tently causes weight gain, increases body fat, and endpoints is inconclusive. Currently, there is no proven
improves nitrogen balance. The effect of TPN on lean role for combined specific nutrient supplementation in
body mass is minimal. The effects of enteral nutrition the care of cancer patents. 15
(EN) on body composition are less consistent; EN usu- The palliative use of SNS in cancer patients is rarely
ally causes weight gain and improves nitrogen balance. appropriate, although this issue remains controversial
Neither EN nor TPN, when administered for 7 to 49 and is emotionally charged. In carefully selected
days, have demonstrably beneficial effects on serum patients, however, home TPN may lengthen survival
proteins. Specialized nutrition support has less of an and improve quality of life. 20-22 If patients are to ben-
.

effect on nutritional indices in cancer patients than in efit from this complex, intrusive, and expensive ther-
noncancer patients.9,10 Enthusiasm for the use of SNS apy they (1) must be physically and emotionally capa-
in cancer patients has historically been tempered by ble of participating in their own care; (2) should have
.

concern that provision of nutrients may stimulate an estimated life expectancy of greater than 40 to 60
.
 83SA

days; (3) require strong social and financial support at 14. Klein S, Koretz RL: Nutrition support in patients with cancer:
What do the data really show? Nutr Clin Pract 9:91-100, 1994
home, including a dedicated in home lay care provider;
and (4) fail trials of less invasive medical therapies. 23
15. August DA: Nutritional care of cancer patients. IN Surgery:
Scientific Basis and Current Practice. Norton JA (ed). Springer
Those patients with a life expectancy of less than 40 Verlag, New York, 2001, pp 1841-1861
days may be palliated with home intravenous fluid 16. Anonymous: Parenteral nutrition in patients receiving cancer
therapy, although this is also controversial.2o,24 chemotherapy. American College of Physicians. Ann Intern Med
110:734-736, 1989
17. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in
Practice Guidelines clinical practice: Review of published data and recommendations
cancer for future research directions. JPEN 21:133-156, 1997
18. Szeluga DJ, Stuart RK, Brookmeyer R, et al: Nutritional support
of bone marrow transplant recipients: A prospective randomized
1. Patients with cancer are at nutrition risk and clinical trial comparing total parenteral nutrition to an enteral
should undergo nutrition screening to identify feeding program. Cancer Res 47:3309-3316, 1987
19. Schloerb PR, Amare M: Total parenteral nutrition with glu-
those who require formal nutrition assessment tamine in bone marrow transplantation and other clinical appli-
with development of a nutrition care plan. (B) cations (a randomized, double-blind study). JPEN 17:407-413,
2. SNS should not be used routinely in patients 1993
undergoing major cancer operations. (A) 20. August DA, Thorn D, Fisher RL, et al: Home parenteral nutri-
tion for patients with inoperable malignant bowel obstruction.
3. Preoperative SNS may be beneficial in moder- JPEN 15:323-327, 1991
ately or severely malnourished patients if admin- 21. King LA, Carson LF, Konstantinides RN, et al: Outcome assess-
istered for 7 to 14 days preoperatively, but the ment of home parenteral nutrition in patients with gynecologic
potential benefits of nutrition support must be malignancies: What have we learned in a decade of experience?
weighed against the potential risks of the SNS Gynecologic Oncol 51:377-382, 1993
itself and of delaying the operation. (A)
22. Cozzaglio L, Balzola F, Cosentino F, et al: Outcome of cancer
patients receiving home parenteral nutrition. JPEN 21:339-342,
4. SNS should not be used routinely as an adjunct to 1997
chemotherapy. (A) 23. Baines M, Oliver DJ, Carter RI: Medical management of intes-
5. SNS should not be used routinely in patients tinal obstruction in patients with advanced malignant disease: A
clinical and pathological study. Lancet 2:990-993, 1985
undergoing head and neck, abdominal, or pelvic 24. Welk T: Clinical and ethical considerations of fluid and electro-
irradiation. (B) lyte management in the terminally ill client. J Intravenous
6. SNS is appropriate in patients receiving active Nursing 22:43-47, 1999
antic,ancer treatment who are malnourished and
who are anticipated to be unable to ingest and/or
CANCER: HEMATOPOETIC CELL
absorb adequate nutrients for a prolonged period
TRANSPLANTATION
of time. (C)
7. The palliative use of SNS in terminally ill cancer Background
patients is rarely indicated. (B) Hematopoetic cell transplantation (HCT) refers to an
array of therapies whose short- and long-term out-
REFERENCES comes are affected by diagnosis, disease stage, trans-

1. Inagaki J, Rodriguez V, Bodey GP: Causes of death in cancer plant type (autologous, family related allogeneic, unre-
patients. Cancer 33:568-573, 1974 lated allogeneic), degree of donor histocompatibility,
2. DeWys WD, Begg D, Lavin PT, et al: Prognostic effect of weight preparative regimen (myeloablative vs nonmyeloabla-
loss prior to chemotherapy in cancer patients. Am J Med 69:491- tive), stem cell source (bone marrow, peripheral blood,
497, 1980 placental cord blood), age, prior therapy, and nutri-
3. Kern KA, Norton JA: Cancer cachexia. JPEN 12:286-298, 1988
tional status. 1,2 Conventional HCT applies high-dose
4. Ottery FD: Supportive nutrition to prevent cachexia and
improve quality of life. Semin Oncol 22(Suppl 13):98-111, 1995 chemotherapy with or without irradiation to eradicate
5. Puccio M, Nathanson L: The cancer cachexia syndrome. Semin tumor in patients with malignancy. In allograft recip-
Oncol 24:277-287, 1997
ients, the patients own immune system is also ablated
6. Detsky AS, McLaughlin JR, Baker JP, et al: What is subjective to prevent graft rejection. Such marrc-w ablative regi-
global assessment of nutritional status? JPEN 11:8-13, 1987
7. Ottery FD: Definition of standardized nutritional assessment mens are among the most intensive therapies used in
and interventional pathways in oncology. Nutrition 12:S15-S, oncology. Lower intensity cytoreduction may also be
19, 1996 used to establish a mixed chimera, with preservation 01
8. Delmore G: Assessment of nutritional status in cancer patients: host T-cell-mediated immunity.33 Gastrointestinal
Widely neglected? Support Care Cancer 5:376-380, 1997 tract or liver complications are almost always the dose-
9. Bozzetti F: Effects of artificial nutrition on the nutritional status
of cancer patients. JPEN 13:406-420, 1989 limiting toxicities for these therapies.4 The disruption
10. Goldstein AS, Elwun DH, Askanazi J: Functional and metabolic of the mucosal barrier contributes to the pathogenesis
changes during feeding in gastrointestinal cancer. J Am Coll of infection and fevers of unknown origin in the period
Nutr 8:530-536, 1989 of neutropenia that lasts 2 to 6 weeks. Patients expe-
11. Baron PL, Lawrence W, Chan WMY, et al: Effects of parenteral
nutrition on cell cycle kinetics of head and neck cancer. Arch rience a prolonged period of minimal oral intake, ofter
Surg 121:1282-1286, 1986 lasting well beyond stem cell engraftment owing to thE
12. Frank JL, Lawrence W Jr, Banks WL Jr, et al: Modulation of cell delayed effects of cytoreductive therapy on appetite
cycle kinetics in human cancer with total parenteral nutrition. taste, salivary function, gastric emptying, and intesti
Cancer 69:1858-1864, 1992
13. Franchi F, Rossi-Fanelli F, Seminara P, et al: Cell kinetics of
nal function.5
gastrointestinal tumors after different nutritional regimens. A Autologous HCT is associated with low transplant
preliminary report. J Clin Gastroenterol 13:313-315, 1991 related mortality, but less favorable cure rates thar
84SA

allogeneic HCT, which benefits from a graft-versus- sues have healed, tube feeding is feasible as a transi-
tumor effect. Recipients of allografts, however, suffer tion step from TPN to oral diet or when nutrition
high transplant-related mortality as a result of donor support is indicated for late complications such as
T-lymphocyte-mediated graft-versus-host disease GVHD. ~6
(GVHD). Acute GVHD occurs in the first few months
post transplant and targets the skin, liver and gastro- Special Considerations
intestinal tract. A chronic form resembling collagen-
Two randomized, double-blind trials examined the
like immune disorders may develop several months to
benefits of intravenous glutamine and found mixed
years post transplant and involve single or multiple results in terms of clinical infection17,18; the relevance
organs (skin, liver, oral mucosa, eyes, muscolskeletal of these data with current antimicrobial regimens is
system, lung, esophagus, and vagina). Moderate to unclear. The shorter length of hospital stay observed in
severe GVHD and the multidrug regimens used in its

prevention and treatment result in profound and pro- glutamine-treated patients in both these trials is con-
founded by mixed patient types, failure to analyze as
longed immunosuppression. Despite advances in man- intent to treat, and lack of objective criteria for hospital
agement, GVHD remains a significant problem
because of the expanding use of unrelated and partially discharge. Neither intravenous nor oral glutamine has
reduced severity of oral mucositis or dependence on
histocompatible related donors. Patients frequently TPN17-21 with the exception of a subset of autologous
have elevated nutrient requirements, altered carbohy-
drate, lipid and protein metabolism, experience diffi- patients in one trial.~2 In this same trial glutamine
culty eating for a variety of reasons dependent on appeared to worsen mucositis in recipients of alloge-
neic HCT.22 Studies with sufficient power to assess any
organ involvement, and require modified diets, oral effect of glutamine on relapse, survival, and incidence,
supplements, or SNS to prevent malnutrition. 4,6 and severity of GVHD have not been reported.
Significantly higher mortality occurs in underweight
patients undergoing HCT, even amongst those with Practice Guidelines
only mildly deficits. 1,7 Obesity also appears to have a Cancer: Hematopoetic ,
negative influence on outcome.7-9 The role, if any, for
pretransplant intervention, has not been investigated. Transplantation
1. All patients undergoing conventional HCT with
Evidence
myeloablative conditioning regimens are at nutri-
Mixingtypes of transplant, a variety of diagnoses, tion risk and should undergo nutrition screening
and other variables known to be associated with dif- to identify those who require formal nutrition
ferent short- and long-term outcomes have weakened assessment with development of a nutrition care
clinical trials of nutrition support in HCT. TPN plan. (B)
may improve long-term survival in allogeneic HCT 2. When PN is used, it should be discontinued as
patients,10 but no randomized trials of sufficient size soon as conditioning-related toxicities have
have been carried out in autologous HCT to establish resolved after stem cell engraftment. (A)
its efficacy. A few small trials failed to demonstrate a 3. When gastrointestinal function returns post
benefit of TPN compared with no nutrition support&dquo; or engraftment, EN should be used in patients in
an aggressive enteral feeding program,12 but these whom oral intake is inadequate to meet nutri-
studies were not large enough to rule out Type II tional requirements. (B)
errors. Another approach has been to establish the 4. Pharmacologic doses of glutamine should not be
characteristics of HCT patients who require TPN. By used in patients undergoing HCT. (A)
setting standard criteria for weight loss and number of 5. Patients should receive dietary counseling
days with minimal oral intake, TPN is used with regarding high risk foods and safe food handling
increasing frequency for patients with TBI versus during the period of immunocompromise. (B)
chemotherapy only, allogeneic versus autolgous do- 6. SNS is appropriate for patients undergoing HCT
nors, and histoincompatible versus histocompatible who develop moderate to severe 3GVHD accompa-
donors. 13 Increased incidence of infections,10-12 appe- nied by poor oral intake. (C)
tite suppression and delayed refeeding posttrans-
plant, 14 inability to maintain lean body mass,4 and REFERENCES
hepatobiliary complications are all associated with the 1. Thomas ED, Blume KG, Forman SJ (eds). Hematopoietic Cell
provision of TPN in HCT. Transplantation, 2nd ed. Blackwell Science, Malden, MA, 1999
Early peri-transplant enteral tube feeding after con- 2. Deeg HJ, Seidel K, Bruemmer B, et al: Impact of patient weight
ventional conditioning regimens is associated with a on non-relapse mortality after marrow transplantation. Bone
Marrow Transplant 15:461-468, 1995
high rate of failure based on the limited published 3. McSweeney PA, Storb R: Hematology, 2nd ed. Mixed chimerism.
experience. 12, &dquo; The challenges of establishing a safe Preclinical studies and clinical applications. Biol Blood Marrow
enteral route after marrow ablative preparative regi- Transplant 5:192-203, 1999
mens are formidable owing to bleeding, the risk of 4. Bensinger WI, Buckner CD: Preparative regimens. IN Hemato-
aspiration pneumonia, sinusitis, diarrhea, ileus and/or poietic Cell Transplantation, 2nd ed. Thomas ED, Blume KG,
Forman SJ (eds). Blackwell Science, Malden, MA, 1999, pp 123-
abdominal pain, delayed gastric emptying, and vomit- 134
ing. Once a well-functioning white cell and platelet 5. Aker SN, Lenssen P: Nutritional support in hematological malig-
graft is established and oral and gastrointestinal tis- nancies. IN Hemotology: Basic Principles and Practice, 3rd ed.
 85SA

Hoffman R, Benz EJ, Shattil SJ, et al (eds). Churchill Living- AIDS wasting syndrome (AWS) is defined by the
stone, New York, 2000, pp 1501-1514 CDC as an involuntary weight loss greater than 10% of
6. Lenssen P, Sherry ME, Stern J, et al: Prevalence of nutrition-
related problems among long-term survivors of allogeneic mar- baseline body weight plus either chronic diarrhea (at
row transplantation. J Am Diet Assoc 90:835-842, 1990 least two loose stools per day for 30 days or more) or
7. Dickson TM, Kusnierz-Glaz CR, Blume KG, et al: Impact of chronic weakness and documented fever (for 30 days or
admission body weight and chemotherapy dose adjustment on
more, intermittent or constant) in the absence of con-
the outcome of autologous bone marrow transplantation. Biol
current illness or any condition other than HIV infec-
Blood Marrow Transplant 5:290-305, 1999
8. Morton AJ, Gooley T, Hansen JA, et al: Association between tion that could explain the findings.
pretransplant interferon-alpha and outcome after unrelated This definition is based on total weight rather than
donor marrow transplantation for chronic myelogenous leuke- body composition and does not take into consideration
mia in chronic phase. Blood 92:394-401, 1998 the rate at which weight loss occurs. Disproportionate
9. Fleming DR, Rayens MK, Garrison J: Impact of obesity on allo- loss of lean body mass (LBM) has been correlated with
geneic stem cell transplant patients: A matched case-controlled
study. Am J Med 102:265-268, 1997 an increased risk of adverse outcomes.2 Significant loss
10. Weisdorf SA, Lysne J, Wind D, et al: Positive effect of prophy- of LBM may occur with total body weight loss less than
lactic total parenteral nutrition on long-term outcome of bone 10% baseline and may herald the onset of infection.
marrow transplantation. Transplantation 43:833-838, 1987 Loss of LBM may occur early in the course of HIV
11. Lough M, Watkins R, Campbell M, et al: Parenteral nutrition in
bone marrow transplantation. Clin Nutr 9:97-101, 1990 disease.3 A sexual dimorphism in the patterns of wast-
12. Szeluga DJ, Stuart RK, Brookmeyer R, et al: Nutritional support ing may exist with women losing more fat early on due
of bone marrow transplant recipients: A prospective, randomized to higher baseline fat stores, whereas LBM loss that
clinical trial comparing total parenteral nutrition to an enteral occurs later in the course of AWS seems to be compa-
feeding program. Cancer Res 47:3309-3316, 1987 rable in both genders.4 Men with higher fat stores
13. Iestra JA, Fibbe WE, Zwinderman AH, et al: Parenteral nutri-
tion following intensive cytotoxic therapy: an exploratory study seem to lose more fat and less LBM compared with
on the need for parenteral nutrition after various treatment other men with lower fat stores.~5
approaches for haematological malignancies. Bone Marrow The causes of AWS are multifactorial and relate to
Transplant 23:933-939, 1999 food intake, nutrient absorption in the gut, and meta-
14. Charuhas PM, Fosberg KL, Bruemmer B, et al: A double-blind
randomized trial comparing outpatient parenteral nutrition bolic alterations in energy expenditure.
with intravenous hydration: Effect on resumption of oral intake Decreased food intake is multifactorial in etiology.
after marrow transplantation. JPEN 21:157-161, 1997 Oral and esophageal abnormalities, altered smell and
15. Lenssen P, Bruemmer B, Aker SN, et al: Nutrient support in taste sensation, and depression all contribute to the
hematopoietic cell transplantation. JPEN 25:219-228, 2001
16. Roberts SR, Miller JE: Success using PEG tubes in marrow development of food aversion and anorexia. In addi-
transplant recipients. Nutr Clin Pract 13:74-78, 1998 tion, secondary anorexia occurs due to infection and
17. Ziegler TR, Young LS, Benfell K, et al: Clinical and metabolic release of pro-inflammatory cytokines. Malabsorption
efficiency of glutamine-supplemented parenteral nutrition after also affects food intake. Social isolation and decline in
bone marrow transplantation: A randomized, double-blind, con-
trolled study. Ann Intern Med 116:821-828, 1992
socioeconomic status often result in reduced access to
18. Schloerb PR, Amare M: Total parenteral nutrition with glu- proper nutrition.
tamine in bone marrow transplantation and other clinical appli- AIDS patients are susceptible to infection with a
cations (a randomized, double-blind study). JPEN 17:407-413, variety of small bowel pathogens resulting in enterop-
1993
19. Jebb SA, Marcus R, Elia M: A pilot study of oral glutamine
athy and malabsorption. Even with aggressive work-
supplementation in patients receiving bone marrow transplants. up, a specific cause of diarrhea is not identified in a
Clin Nutr 14:162-165, 1995 substantial number of patients. The pathogenesis of
20. Schloerb PR, Skikne BS: Oral and parenteral glutamine in bone malabsorption is multifactorial and includes primary
marrow transplantation: A randomized, double-blind study.
JPEN 23:117-122, 1999
enterocyte injury with partial villous atrophy and crypt
21. Dickson TMC, Wong RM, Negrin RS, et al: Effect of oral glu- hyperplasia, ileal dysfunction with bile salt wasting
tamine supplementation during bone marrow transplantation. and fat malabsorption, and oxidative enteropathy. The
JPEN 24:61-66, 2000 consequences of malabsorption include decreased
22. Anderson PM, Ramsay NKC, Shu XO, et al: Effect of low-dose appetite, and &dquo;enterogastrone&dquo; effects including dry
oral glutamine on painful stomatitis during bone marrow trans-
mouth, decreased gastric acid secretion, decreased rate
plantation. Bone Marrow Transplant 22:339, 1998 of gastric emptying, and slowed intestinal transit.6
Metabolic dysfunction in AWS is similar to other
HIV/ACQUIRED IMMUNO-DEFICIENCY conditions associated with cachexia such as cancer and
SYNDROME COPD. When increased protein turnover is present,
Background resting energy expenditure is raised, but total energy
expenditure is not. Plasma pro-inflammatory cytokines
Nutrition plays a pivotal role in the course, quality of (interleukin-1, interleukin-6, tumor necrosis Factor
life, and outcomes of patients with the acquired immu- alpha) are increased and regulatory cytokines such as
nodeficiency syndrome (AIDS). Protein-calorie malnu- interleukin-12 are decreased. These findings are not
trition is common in HIV-infected patients. The advent uniform. Evidence suggests that decreased energy
of highly active antiretroviral therapy (HAART) has intake rather than elevated energy expenditure, is the
markedly reduced the incidence of malnutrition. How- prime determinant of weight loss in AWS.8 Hypogo-
ever, an emerging syndrome of subcutaneous fat deple- nadism is also a contributor to loss of muscle mass. The
tion and visceral fat accumulation has been recognized prevalence of hypogonadism in AWS patients is high
and is associated with a variety of metabolic abnormal- and the important anabolic effects of testosterone are
ities, including hyperlipidemia and insulin resistance. uncontested.
 86SA

The severity of AWS is of prognostic importance irre- weight that was accompanied by an even greater
spective of the underlying cause of wasting and increase in LBM and a decrease in fat, plus improve-
immune status. Body composition studies have shown ment in treadmill work output. 14 Concerning issues
that LBM loss, decline in quality of life and total body include the development of hyperglycemia and diabe-
weight depletion occur predictably as patients near tes with long-term use. Long-term rhGH therapy is
death.2 This pattern is similar to previous reports of considerably more expensive than other therapies.
starvation with or without associated infections. Nutri- Thalidomide, a drug known for its anti-inflammatory
tion assessment in AIDS is similar to other entities and properties, has shown benefit in increasing weight. In
should include a detailed nutrition history (including one double blind placebo-controlled study using thalid-
current, usual, and ideal body weights), a complete omide at 100 or 200 mg orally for 8 weeks, over one-half
physical examination, assessment of LBM using of the weight gain was fat-free mass.15 Longer courses
anthropometric tools, routine laboratory markers, and and higher doses may be limited by drug side effects.
(when available) either bioelectrical impedance analy- Access to thalidomide is strictly controlled to avoid
sis (BIA) or dual energy X-ray absorptiometry potential teratogenic effects.
(DEXA).9 The value of testosterone in the treatment of AWS
remains under scrutiny, with placebo-controlled stud-
ies showing sustained increases in LBM at doses of 300
Evidence
mg IM every 3 weeks in hypogonadal men.l6 Some
It seems logical that early intervention to prevent encouraging results were found in women with AWS
LBM depletion and successful repletion of lost meta- who had transdermal testosterone administered in a
bolically active tissue would improve outcomes and pilot study. 17 Treatment was well tolerated.
enhance quality of life in patients with AIDS. There Resistance training has been evaluated as a safe
are few supportive data. alternative to pharmacologic therapy. A short-term
Before the introduction of HAART, an estimated two course of high-intensity progressive resistance training
thirds of all HIV patients satisfied CDC criteria for has been shown to increase lean body mass in HIV-
AWS.1 Although the prevalence of AWS has signifi- infected patients, including a few AWS patients. Resis-
cantly declined, numerous reports suggest that malnu- tance training in one observational study looking at
trition is still common. The use, compliance, and eugonadal men with AWS increased LBM without the
response to HAART is variable and the impact on body adverse effects on metabolic variables of anabolic ther-
cell mass is uncertain. Although it is not clear what the apies. 18
numbers are 4 years into the HAART era, the impact The combination of pharmacological doses of nan-
on reduction of infections and improvement of immune drolone decanoate with progressive resistance training
function and survival is undeniable. The restoration of in one randomized, open-label study, yielded signifi-
total body weight may, however, be mainly related to a cant gains in total weight, lean body mass, body cell
gain in fat and some reports have suggested persistent mass, muscle size, and strength when compared with
body cell mass loss.&dquo; anabolic therapy alone. 19 Interestingly, the combina-
A randomized, controlled study has shown that tion of testosterone and resistance training in hypogo-
nutrition counseling in combination with caloric sup- nadal men did not show any additive effects compared
plements may have a beneficial effect on fat free mass with each intervention alone in one randomized, pla-
and may retard protein catabolism in AIDS patients. 11 cebo-controlled study. 20
Therapeutic interventions specifically targeting wast-
ing include appetite stimulants (eg, dronabinol, meges- Special Considerations
trol acetate), cytokine inhibitors (eg, thalidomide,
cyproheptadine, ketotifen, pentoxifylline, fish oil, In a double-blind, randomized, placebo-controlled
N-acetylcysteine), and anabolic agents (eg, testoster- study, the combination of three nutrients, consisting
one, nandrolone, oxandrolone, recombinant human of beta-hydroxy-beta-methylbutyrate (HMB), L-gluta-
growth hormone). A randomized, placebo-controlled mine (Gln) and L-arginine (Arg), was shown to slow the
study showed that megestrol in doses of 400 to 800 course of lean tissue loss in patients with AWS.21 The
mg/d promotes appetite and weight gain, but with a combination of L-glutamine (40 g/d) and antioxidants
predominance of fat gain. Concerning side effects increased weight and body cell mass in another pla-
include a diabetogenic effect as well as Cushingoid cebo-controlled study.22 In the setting of malabsorption,
symptoms and potential for adrenal insufficiency if semi-elemental diets were shown to result in weight and
discontinued precipitously. 12 Short-term dronabinol LBM gain in a randomized, open-label study.23
use in doses of 2.5 mg twice a day has not been dem- PN has been evaluated in both home and inpatient
onstrated to increase lean body mass, and effect on settings. Although central venous access clearly
total body weight is minimal. A positive effect on appe- results in an increased risk for bloodstream infections,
tite has been observed in a placebo-controlled study, a transient impact on weight and LBM has been shown
although food intake was not measured.13 Dronabinol in certain studies.24 No clear effect on survival was
was associated with significant CNS side effects. demonstrated. PN is also markedly more expensive
In a randomized, placebo-controlled trial, treatment than other modes of feeding.
with recombinant human growth hormone (rhGH) at Few studies have looked at the outcomes of EN in
doses of 0.1 mg/kg subcutaneously for 12 weeks AWS. Transient increases in total body weight have
resulted in a significant and sustained increase in been demonstrated in small, randomized studies, at
 87SA

the expense of a higher rate of procedure-related com- 6. Kotler DP: Human immunodeficiency virus-related wasting:
plications.25 The effect on survival remains controver- malabsorption syndromes. Semin Oncol 25(2 Suppl 6):70-75,
1998
sial, although extensive data from other illnesses asso- 7. Baronzio G, Zambelli A, Comi D, et al: Proinflammatory and
ciated with wasting has shown no survival benefit in regulatory cytokine levels in AIDS cachexia. In Vivo 13(6):499-
the absence of treatment of the underlying illness. 502, 1999
Few studies have evaluated the outcomes of surgery 8. Macallan DC, Noble C, Baldwin C: Energy expenditure and
as a function of nutrition status in AIDS patients. wasting in human immunodeficiency virus infection. N Engl
J Med 333(2):83-88, 1995
Expert opinion is that HIV infection is not a signifi- 9. Suttmann U, Ockenga J, Selberg O: Incidence and prognostic
cant, independent risk factor for major surgical proce- value of malnutrition and wasting in human immunodeficiency
dures and the risk of major surgery in this population virus-infected outpatients. J Acquir Immune Defic Syndr Hum
is not unlike that for other immunocompromised or Retrovirol 8(3):239-246, 1995
10. Corcoran C, Grinspoon S: Treatments for wasting in patients
malnourished patients.26 with the acquired immunodeficiency syndrome. N Engl J Med
An alarming observation in the HAART era has been 340(22):1740-1750, 1999
the development of HIV-associated lipodystrophy. 11. Schwenk A, Steuck H, Kremer G: Oral supplements as adjunc-
Reported prevalence rates vary considerably, due at tive treatment to nutritional counseling in malnourished HIV-
least in part to the lack of a case definition, the impre- infected patients: randomized controlled trial. Clin Nutr 18(6):
cision of self-report and physician perceptions, and 371-374, 1999
12. Von Roenn JH, Armstrong D, Kotler DP: Megestrol acetate in
varying durations of follow-up. The morphologic man- patients with AIDS-related cachexia. Ann Intern Med 121(6):
ifestations of lipodystrophy differ by sex and race. The 393-399, 1994
various body composition and metabolic complications 13. Beal JE, Olson R, Laubenstein L: Dronabinol as a treatment for
are multifactorial in their etiologies. Initial analyses anorexia associated with weight loss in patients with AIDS. J
suggest there is little or no short-term increase in Pain Symptom Manage 10(2):89-97, 1995
cardiac risk, but do not settle the question of long-term 14. Schambelan M, Mulligan K, Grunfeld C: Recombinant human
risk. growth hormone in patients with HIV-associated wasting. A
randomized, placebo-controlled trial. Serostim Study Group.
Ann Intern Med 125(11):873-882, 1996
Practice Guidelines 15. Kaplan G, Thomas S, Fierer DS: Thalidomide for the treatment
H I V lacquired of AIDS-associated wasting. AIDS Res Hum Retroviruses 16(14):
Immuno-Deficiency Syndrome , 1345-1355, 2000
16. Grinspoon S, Corcoran C, Anderson E: Sustained anabolic effects
of long-term androgen administration in men with AIDS wast-
1. Patients with HIV are at nutrition risk and ing. Clin Infect Dis 28(3):634-636, 1999
should undergo nutrition screening to identify 17. Miller K, Corcoran C, Armstrong C: Transdermal testosterone
administration in women with acquired immunodeficiency syn-
those who require formal nutrition assessment
drome wasting: a pilot study. J Clin Endocrinol Metab 83(8):
with development of a nutrition care plan. (B) 2717-225, 1998
2. Nutrition assessment of patients with HIV should 18. Roubenoff R, McDermott A, Weiss L: Short-term progressive
include quantitative measurement of LBM using resistance training increases strength and lean body mass in
DEXA or BIA. (B) adults infected with human immunodeficiency virus. AIDS
3. Patients with AWS should receive specific AWS 13(2):231-239, 1999
19. Sattler FR, Jaque SV, Schroeder ET: Effects of pharmacological
directed therapy, including anabolic agents doses of nandrolone decanoate and progressive resistance train-
and/or resistance training, testosterone in hypo- ing in immunodeficient patients infected with human immuno-
gonadal men, and appetite stimulants for those deficiency virus. J Clin Endocrinol Metab 84(4):1268-1276, 1999
20. Bhasin S, Storer TW, Javanbakht M: Testosterone replacement
with decreased appetite. (A)
and resistance exercise in HIV-infected men with weight loss
4. SNS has a very limited role in AWS and should be and low testosterone levels. JAMA 9;283(6):763-770, 2000
reserved for patients receiving active, disease 21. Clark RH, Feleke G, Din M: Nutritional treatment for acquired
directed treatment who are unable to meet their immunodeficiency virus-associated wasting using beta-hydroxy
nutrient requirements by oral feeding (B) beta-methylbutyrate, glutamine, and arginine: a randomized,
double-blind, placebo-controlled study. JPEN 24(3):133&mdash;139,
2000
REFERENCES 22. Shabert JK, Winslow C, Lacey JM: Glutamine-antioxidant sup-
plementation increases body cell mass in AIDS patients with
1. Revision of the CDC surveillance case definition for acquired weight loss: a randomized, double-blind controlled trial. Nutri-
immunodeficiency syndrome. Morbid Mortal Weekly Rep 36:3- tion 15(11-12):860-864, 1999
15, 1987 23. Kotler DP, Fogleman L, Tierney AR: Comparison of total paren-
2. Kotler DP, Tierney AR, Wang J, et al: Magnitude of body-cell- teral nutrition and an oral, semielemental diet on body compo-
mass depletion timing of death from wasting in AIDS.
and the sition, physical function, and nutrition-related costs in patients
Am J Clin Nutr 50(3):444-447, 1989 withmalabsorption due to acquired immunodeficiency syn-
3. Ott M, Lembcke B, Fischer H: Early changes of body composition drome. JPEN 22(3):120-126, 1998
in human immunodeficiency virus-infected patients: tetrapolar 24. Melchior JC, Chastang C, Gelas P: Efficacy of 2-month total
body impedance analysis indicates significant malnutrition. parenteral nutrition in AIDS patients: A controlled randomized
Am J Clin Nutr 57(1):15-19, 1993 prospective trial. The French Multicenter Total Parenteral
4. Kotler DP, Thea DM, Heo M: Relative influences of sex, race, Nutrition Cooperative Group Study. AIDS 10(4):379&mdash;384, 1996
environment, and HIV infection on body composition in adults. 25. Cappell MS, Godil A: A multicenter case-controlled study of
Am J Clin Nutr 69(3):432-439, 1999 percutaneous endoscopic gastrostomy in HIV-seropositive
5. Mulligan K, Tai VW, Schambelan M: Cross-sectional and longi- patients. Am J Gastroenterol. 88(12):2059&mdash;2066, 1993
tudinal evaluation of body composition in men with HIV infec- 26. Harris HW, Schecter WP: Surgical risk assessment and manage-
tion. J Acquir Immune Defic Syndr Hum Retrovirol 15(1):43-48, ment in patients with HIV disease. Gastroenterol Clin N Am
1997 26(2):377-391, 1997
88SA

CRITICAL CARE: BURNS A number of clinical investigations document

increased protein needs postburn. 25-27 The classic
Background
study by Alexander and colleagues showed that
The stress response to burn injury is associated with severely burned children receiving 20% to 23% of total
a spectrum of hormonal, metabolic, immunologic, and calories from protein (calorie to nitrogen ratio of 110:1)
nutrition abnormalities that are generally commensu- had better immune function, higher survival rates,
rate with the depth and size of the burn.-6 Recovery fewer bacteremic days, and fewer days on systemic
from burns has been classified into (1) a shock or resus- antibiotics compared with a control group receiving
citation phase, (2) the acute catabolic phase, and (3) only 17% of total calories as protein (calorie to nitrogen
the adaptive anabolic phase. Particularly relevant to ratio of 150:1).25
nutrition support is the loss of heat, water, protein, and Nutrition support of the burn patient is best accom-
micronutrients through open wound, along with systemic plished enterally. Not uncommonly, a high-calorie,
manifestations of increased energy expenditure and high-protein oral diet is sufficient to maintain small
accelerated protein degradation. Complex endocrine and burns (<20% surface area) not complicated by facial
cytokine alterations likely contribute to postburn hyper- injury, inhalation injury, psychological difficulties, or
metabolism and hypercatabolism, although other effec- preburn malnutrition. Patients with larger surface
tors play a role as well. 3-5 area burns generally have difficulty consuming suffi-
The destructive consequences of prolonged, un- cient calories and protein by mouth. Consequently, EN
treated catabolism in the burn patient have long been should be initiated as soon as practical,
documented.1,2,7,8 Clinically, patients who withstand preferably
within the first 24 hours postburn.4,6,3 -37 Burn
the ravages of postburn hypermetabolism and catabo- patients are normally tube-fed nasogastrically36,37 or
lism become debilitated with weight IOSS1-3,7-10 and nasoenterically. 16,35,38,39 Burn severity generally dic-
erosion of lean body mass.11,12 Children are especially tates which enteral route is indicated. Gastric ileus,
vulnerable because they are still growing. A large burn which limits use of the stomach for EN, is common and
can retard linear growth and decrease growth velocity often resurfaces during operative procedures, septic
for several years. 9,13,14 Parameters such as weight,33 episodes, major dressing changes or other complicating
caloric balance, 15,16 serum transferrin, 17,18 and pre- events. It is therefore standard procedure in many
albumin 19-20 are correlated with risk of infection and burn units to routinely use transpyloric feeding meth-
delayed wound healing, which are complications of ods in an effort to negate the necessity for tube feeding
malnutrition. interruptions.5,16,28,35,38,39
Evidence PN is associated with complications (intestinal dys-
motility, hepatic steatosis, septic morbidity, and cath-
SNS is a significant positive effector of outcome and eter-related infection). In several prospective trials,
should receive priority consideration postburn. An Herndon and associates have demonstrated that PN
aggressive nutrition approach is required to address was associated with increased mortality in severely
burn-induced hypermetabolism, enhance nitrogen burned patients. 40,41 Hence, the use of PN is reserved
retention, and maximize conditions conducive to anab- for those patients where gastrointestinal support is
olism, immunocompetence, and healing. anticipated to be impossible for a prolonged period.42,~3
Assessment of nutrition status (with an emphasis on
energy and protein needs) is required on admission,
and ongoing reassessment should occur until the Special Considerations
patient is no longer at risk. 4,5 Nutritional require- Pharmacologic nutritional modulation of metabo-
ments may be determined either by direct measure- lism, prostaglandins, and cytokines and the adjunctive
ment or estimated using generally accepted tools.4-6 In role of anabolic agents such as hormones and growth
either case, interpretation of nutrition parameters factors represent potential modalities for further
must include recognition of relevant limitations. 5,21
enhancing wound healing and immunocompetence
It is undisputed that energy 1-3,5-8,11,15,22-24 and postburn. Among the specific nutrients most fre-
protein needs4,5,25,26 are heightened postburn and quently used in the pharmacologic support of
that adequate, but not excessive, calories should burn patients are arginine, glutamine, omega-3 fatty
be provided. 4-6,23 Nevertheless, there is no consen- acids, zinc, and vitamins A and C. Although the results
sus regarding an optimal method for defining macro- of preliminary clinical trials involving arginine,44 glu-
nutrient goals. At least 30 mathematical equations tamine45 and omega-3 fatty acids44 look promising,
have been developed for estimating the energy needs of considerable controversy remains.38,39 Even less well
burn patients, incorporating various demographic data understood are the requirements and pharmacologic
such as weight, body surface area, and body surface effects of specific micronutrients, 46,47 although supple-
area burned .4-6,24,27-29 The validity and reliability of mentation with a number of vitamins and trace ele-
such formulae have been questioned by many. 22,29,31 ments has become standard practice. 6,28,48-53
When feasible, indirect calorimetry is recommended to The combination of various nutrient modulators into
assess and reassess caloric needs. 4,5,23,24 A factor of purported &dquo;immune enhancing&dquo; formulations has been
20% to 30% above the measured energy expenditure is evaluated with dubious results. Burn patients receiv-
commonly recommended to account for increased ing the Shriners diet (eg, high protein, low fat and
caloric demands from physical therapy along with the linoleic acid, and fortified with omega-3 fatty acids,
stresses of wound care. 4,22,32 arginine, cysteine, histidine, vitamins A and C, and
 89SA

zinc) experienced fewer wound and general infections 10. Newsome TW, Mason AD, Pruitt BA: Weight loss following ther-
mal injury. Ann Surg 179:215-217, 1973
along with a shortened length of hospital stay.44 On the 11. Gore DC, Rutan RL, Hildreth MA, et al: Comparison of resting
other hand, Saffle et a139 found no advantage of an
energy expenditures and caloric intake in children with severe
immune enhancing substrate (containing omega-3 burns. J Burn Care Rehabil 11:400-404, 1990
fatty acids, nucleotides, and arginine) when compared 12. Bessy PQ, Jiang ZM, Johnson DJ, et al: Post-traumatic skeletal
with a simple high-protein enteral formula. Additional muscle proteolysis: the role of the ormonal environment. World
studies are required to determine the efficacy of phar- J Surg 13:465-470, 1989
13. Prelack K, Petras L, Antoon A, et al: Measures of height and
macologic nutrient enrichment. weight in children recovering from severe burn injury. J Burn
Care Rehabil 18:S171, 1997
Practice Guidelines 14. Rutan RL, Herndon DN: Growth delay in postburn pediatric
e > : ,
patients. Arch Surg 125:392-395, 1990
15. Mancusi-Ungaro HR, Van Way CW, McCool C: Caloric and nitro-
gen balances as predictors of nutritional outcome in patients
1. Patients with second or third degree burns are at with burns. J Burn Care Rehabil 13:695-702, 1992
nutrition risk and should undergo nutrition 16. Jenkins M, Gottschlich MM, Mayes T, et al: Enteral feeding
screening to identify those who require formal during operative procedures. J Burn Care Rehabil 15:199-205,
nutrition assessment with development of a 1994
nutrition care plan. (B) 17. Jensen TG, Long JM, Dudrich SJ, et al: Nutritional assessment
indications of postburn complications. J Am Diet Assoc 85:68-
2. Adequate calories must be provided to address the 72, 1985
hypermetabolism associated with acute burn 18. Ogle CK, Alexander JW: The relationship of bacteremia to levels
injury. (A) of transferrin, albumin and total serum protein in burn patients.
3. When possible, the energy requirements of burn Burns 8:32&mdash;38, 1981
patients should be measured using indirect calo- 19. Gottschlich MM, Baumer T, Jenkins M, et al: The prognostic
value of nutritional and inflammatory indices in patients with
rimetry. (B) burns. J Burn Care Rehabil 13:105-113, 1992
4. Severely burned patients require increased 20. Morath MA, Miller SF, Finley RK, et al: Interpretation of nutri-
intake of protein until significant wound healing tional parameters in burn patients. J Burn Care Rehabil 4:361&mdash;
is achieved. (A) 366, 1984
5. There is no current role for the routine use of 21. Cynober L, Prugnaud O, Lioret N, et al: Serum transthyretin
specific nutrients and anabolic agents (eg, argi- levels in patients with burn injury. Surgery 109:640-644, 1991
nine, glutamine, omega-3 fatty acids, vitamins, 22. Saffle JR, Medina E, Raymond J, et al: Use of indirect calorim-
trace minerals, antioxidants, growth hormone, etry in the nutritional management of burned patients.
J Trauma 25:32-39, 1985
oxandrolone, etc) in burn patients. (B) 23. Saffle JR, Larson CM, Sullivan J: A randomized trail of indirect
6. EN should be used in preference to PN in burn calorimetry-based feedings in thermal injury. J Trauma 30:776-
patients requiring SNS. (A) 782, 1990
7. EN should be initiated as soon as possible in 24. Curreri PW, Richmond D, Marvin J, et al: Dietary requirements
of patients with major burns. J Am Diet Assoc 65:415&mdash;417, 1974
patients with moderate/severe burns. (A) 25. Alexander JW, MacMillan BC, Stinnett JP, et al: Beneficial
8. PN should be reserved for patients who require effects of aggressive protein feeding in severely burned children.
SNS and in whom EN is contraindicated or is Ann Surg 192:505-517, 1980
nutritional requirements within
unlikely to meet 26. Matsuda T, Kagan RJ, Hanumadass M, et al: The importance of
4 to 5 days. (B) burn wound size in determining the optimal calorie: nitrogen
ratio. Surgery 94:562-568, 1983
27. Cunningham JJ, Lydon MK, Russell WE: Calorie and protein
REFERENCES provision for recovery from severe burns in infants and young
children. Am J Clin Nutr 51:553-557, 1990
1. Wilmore DW: Nutrition and metabolism following thermal 28. Williamson J: Actual burn nutrition care practices. A national
injury. Clin Plast Surg 1:603-606, 1974 survey (part II). J Burn Care Rehabil 10:185-194, 1989
2. Wilmore DW, Curreri PW, Spitzer KW, et al: Supranormal 29. Mayes T, Gottschlich MM, Khoury J, et al: Evaluation of pre-
dietary intake in thermally injured hypermetabolic patients. dicted and measured energy requirements in burned children.
Surg Gynecol Obstet 132:881&mdash;886, 1971 J Am Diet Assoc 96:24-29, 1996
3. Wilmore DW, Kinney JM: Panel Report on nutritional support of 30. Hildreth MA, Herndon DN, Parks DH, et al: Evaluation of a
patients with trauma or infection. Am J Clin Nutr 34:1213-1222, caloric requirement formula in burned children treated with
1981 early excision. J Trauma 27:188-189, 1987
4. Mayes T, Gottschlich MM: Burns and wound healing. IN The 31. Turner WW, Ireton CS, Hunt JL, et al: Predicting energy expen-
Science and Practice of Nutrition Support. A Case-Based Core diture in burned patients. J Trauma 25:11-16, 1985
Curriculum. Gottschlich MM (ed). Kendall Hunt Publishing Co., 32. Goran MI, Peters EJ, Herndon DN, et al: Total energy expendi-
Dubuque, IN, 2001, pp 391-420 ture in burned children using the doubly labeled water tech-
5. Mayes T, Gottschlich MM. Burns. IN Contemporary Nutrition nique. Am J Physiol 259:E576-E585, 1990
Support Practice. Matarese L, Gottschlich M (eds). WB Saunders 33. Taylor SJ: Early enhanced enteral nutrition in burned patients
Co, Philadelphia, PA, 1998, pp 590-610 is associated with fewer infective complications and shorter hos-
6. Peck M: American Burn Association Clinical Guidelines. Initial pital stay. J Hum Nutr Dietet 12:85-91, 1999
nutrition support of burn patients. J Burn Care Rehabil 22:595&mdash; 34. Gottschlich MM, Warden GD, Michel M, et al: Diarrhea in tube-
665, 2001 fed burn patients: incidence, etiology, nutritional impact and
7. Gump FE, Kinney JM: Energy balance and weight loss in burned prevention. JPEN 12:338-345, 1988
patients. Arch Surg 103:442-448, 1971 35. Jenkins M, Gottschlich MM, Alexander JW, et al: Effect of imme-
8. Guber EV, Zimina EP: Variations of energy metabolism in burns. diate enteral feeding on the hypermetabolic response following
Fed Proc 23:441-443, 1964 severe burn injury. JPEN 13:12, 1989
9. Childs C, Hall T, Davenport PJ, et al: Failure of TPN supple- 36. McDonald WS, Sharp CW, Deitch EA: Immediate enteral feed-
mentation to improve liver function, immunity and mortality in ing in burn patients is safe and effective. Ann Surg 213:177-183,
thermally injured patients. J Trauma 27:195&mdash;204, 1987 1991
 90SA

37. Raff T, Hartmann B, Germann G: Early intragastric feeding of and net protein catabolism. 3,5,6 The combined impact
seriously burned and long-term ventilated patients: a review of of these metabolic alterations, bed rest, and lack of
55 patients. Burns 23:19-25, 1997
38. Garrel DR, Razi M, Lariviere F, et al: Improved clinical status nutritional intake can lead to rapid and severe deple-
and length of care with low fat nutrition support in burn tion of lean body mass. Nutrition support cannot fully
patients. JPEN 19:482-491, 1995 prevent or reverse the metabolic alterations and dis-
39. Saffle JR, Wiebke G, Jennings K, et al: Randomized trial of
immune-enhancing enteral nutrition in burn patients. J Trauma
ruptions in body composition associated with critical
42:73-802, 1997
illness. 5,7 Nutrition support in these patients is sup-
40. Herndon DN, Stein MD, Rutan TC, et al: Failure of TPN sup- portive (as opposed to therapeutic) in that it can slow
plementation to improve liver function, immunity and mortality the rate of net protein catabolism. 5,7
in thermally injured patients. J Trauma 27:195-204, 1987 It has been proposed that atrophy of the gastrointes-
41. Herndon DN, Barrow RE, Stein MD, et al: Increased mortality
tinal tract resulting from disuse contributes to morbid-
with intravenous supplemental feeding in severely burned
patients. J Burn Care Rehabil 10:309-313, 1989 ity and mortality in critically ill patients by facilitating
42. Gottschlich MM, Warden GD: Parenteral nutrition in the burned or permitting the translocation of enteric bacteria or
patient. IN Total Parenteral Nutrition. Fischer JE (ed). Little, their metabolic products into the circulation.8 How-
Brown and Co, Boston, 1991, pp 279-298
ever, a clear path of evidence linking fasting, gut atro-
43. Goodwin CW: Parenteral nutrition in thermal injuries. IN Clin-
ical Nutrition: Parenteral Nutrition. Rombeau JL, Caldwell MD phy, bacterial translocation, and the development of
(eds). WB Saunders Co, Philadelphia, 1993, pp 566-584 sepsis or SIRS in humans has not been established.9,10
44. Gottschlich MM, Jenkins M, Warden GD, et al: Differential A corollary of the gut atrophy-bacterial translocation
effects of three enteral dietary regimens on selected outcome
variables in burn patients. JPEN 14:225-236, 1990
hypothesis is that, by virtue of its intravenous delivery,
PN leads to gut atrophy, and therefore increases the
45. Ogle CK, Ogle JD, Mao JX, et al: Effect of glutamine on phago-
cytosis and bacterial killing by normal and pediatric burn risk of bacterial translocation. Such a connection has
patient neutrophils. JPEN 18:128-133, 1994 not been confirmed to date. 10-12 Moreover, several
46. Berger MM, Spertini F, Spertini F, et al: Trace element supple- reports have documented abnormal intestinal struc-
mentation modulates pulmonary infection rates after major ture and function in patients receiving EN, thus bring-
burns: a double-blind, placebo-controlled study. Am J Clin Nutr
68:365-371, 1998 ing into question the putative &dquo;protective&dquo; effect of
47. Rock CL, Dechert DE, Khilnani R, et al: Carotenoids and anti- enteral feedings.11,13 In addition, in some studies EN is
no better than PN in preventing the of
oxidant vitamins in patients after burn injury. J Burn Care
Rehabil 18:269-278, 1997 development
multisystem organ failure in septic patients, nor does
48. Gottschlich MM, Warden GD: Vitamin supplementation in the
it prevent increases in gastrointestinal permeability (a
patient with burns. J Burn Care Rehabil 11:275-279, 1990 measure frequently used as a surrogate for bacte-
49. Manning AJ, Meyer N, Klein GL: Vitamin and trace element
homeostasis following burn injury. IN Total Burn Care. Herndon rial translocation) after upper gastrointestinal sur-
DN (ed). WB Saunders Co, Philadelphia, PA, 1996, pp 251-258
50. Gamlier Z, DeBiasse MA, Demling RJ: Essential microminerals
gery. 15,16
Edema and nonspecific changes in plasma protein
and their response to burn injury. J Burn Care Rehabil 17:264-
concentrations frequently hamper nutrition assess-
272, 1996
51. King N, Goodwin CW: Use of vitamin supplements for burned ment during critical illness. Premorbid nutrition sta-
patients: a national survey. J Am Diet Assoc 84:923-925, 1984 tus, severity of disease, and clinically sound predic-
52. Shippee RL, Wilson SW, King N: Trace mineral supplementation tions of future clinical course should help identify those
of burn patients: a national survey. J Am Diet Assoc 87:300-303,
1987 patients at both ends of the spectrum of nutrition risk.
Multiple investigators have examined the alter-
ations in energy expenditure associated with critical
CRITICAL CARE: CRITICAL ILLNESS illness, most frequently in septic and posttrauma
Background patients .5,17-21 These and other studies have docu-
mented substantial increases in resting energy expen-
Critical illness refers to a wide spectrum of life- diture during critical illness and the inaccuracy of
threatening medical or surgical conditions usually predictive equations in the assessment of energy
requiring intensive care unit (ICU) level care. Most expenditure in these subjects.22-24 Recent publications
critically ill patients exhibit at least severe single demonstrate increased non-resting energy expenditure
organ system dysfunction necessitating active thera- (ie, activity) after the first week of critical illness.19
peutic support. Sepsip or the systemic inflammatory Total energy expenditure in septic patients was 25 5
response syndrome (SIRS) is present in a substantial kcal/kg per day during the first week of illness and
number of cases. Sepsis is the systemic response to closely correlated with the measured resting energy
infection and is thought to result from the activation of expenditure rate. Energy expenditure increased to
a series of endogenous mediators, including classical 47 6 kcal/kg per day during the second week of
hormones, cytokines, coagulation factors, eicosanoids, illness and was markedly higher than the measured
and others.l-4 The systemic inflammatory response resting expenditure.9 It remains to be determined if
syndrome is clinically indistinguishable from the septic feeding at rates greater than 25 to 30 kcal/kg per day is
syndrome, thought to result from the same endogenous of benefit to these patients. It appears, in addition, that
mediators, and can occur in patients with severe pan- provision of 1 g/kg per day protein suffices to minimize
creatitis, hemorrhage, burns,1 ischemia, and other loss of body protein during the initial 2 weeks of critical
severenoninfectious diseases. illness.25 There is little information regarding require-
The most prominent metabolic alterations character- ments for minerals, trace elements and vitamins dur-
izing sepsis and SIRS include hypermetabolism, hyper- ing critical illness.26,27 Although low serum concentra-
glycemia with insulin resistance, accelerated lipolysis, tions of some antioxidants have been documented, 2,1
 91SA

there is no information regarding requirements, bio- found in practice with the use of enteral feedings.55 In
availability, or efficacy of replacement in the critically this study, only 53% of patients were able to tolerate
ill patient. sufficient enteral support to avoid the need for supple-
mental PN, caloric intake through the enteral route
Evidence averaged only 77 2% of prescription, most patients
required more than one feeding tube insertion (mean of
It is not known how long critically ill patients can 2.2 z- 0.2 tubes per patient), 11% evidenced severe
survive without food. It appears obvious that denying gastrointestinal symptoms, and 14% of the patients
nutrition support will, over an unknown but finite suffered aspiration pneumonia. This study is the only
period of time aggravate pre-existing nutritional defi- one to report on the cost of the surgical, endoscopic, or
cits or establish malnutrition as a co-morbidity in crit- radiologic placement of postpyloric feeding tubes. In
ically ill patients. If results from patients recovering this regard, there appears to be no advantage in deliv-
from major surgery can be cautiously extrapolated to ering feedings beyond the pylorus (nasoduodenal
other critically ill patients, morbidity and mortality tubes, feeding jejunostomies) in reducing the risk of
increase significantly after 2 weeks of glucose infusion aspiration.35
(at rates of 250 to 300 g/d) when compared with nutri-
tionally complete PN.29 Most importantly, initiating Special Considerations
PN after 2 weeks of glucose infusion does not improve
outcome.29 It appears reasonable to recommend that The effects of supplementing enteral or parenteral
some form of SNS be started after 5 to 10 days of diets with a variety of nutrients at pharmacologic
fasting in patients who are likely to remain unable to doses has been explored in multiple trials, mostly
eat for an additional week or more. including trauma and surgical patients. Studies have
A meta-analysis was conducted of studies comparing investigated the effects of supplemental branched-
PN to &dquo;standard care&dquo; (intravenous dextrose plus oral chained amino acids, glutamine, arginine, omega-3
diet when tolerated) in a heterogeneous group of well- fatty acids, RNA, and others. For the most part, studies
nourished and malnourished critically ill patients. have used diets supplemented with more than one of
Twenty-six clinical trials met the criteria for inclusion these nutrients, thus making assessment of efficacy of
in the meta-analysis. However, only three of these specific supplements impossible. A recent meta-analy-
trials did not involve elective surgical patients. Of the sis suggests these so-called immuno-enhancing for-
three, one addressed patients with acute neurologic mulas may reduce the incidence of infectious com-
injury, one subjects with pancreatitis, and the remain- plications in critically ill patients but do not alter mor-
ing study involved major burns. The meta-analysis tality. In some subgroups, mortality may actually be
showed no effect of therapy on mortality and a modest increased.34
decrease in complications in patients receiving PN only A recent review of the use of supplemental branched-
in studies that required that patients be malnourished chain amino acids in critically ill patients failed to
at time of enrollment.3o There is no comparable anal- identify specific benefit from these compounds.36 One
ysis of the efficacy of EN in comparison to &dquo;standard
&dquo;
study investigated the use of glutamine supplementa-
therapy.&dquo; tion during PN in critically ill patients and reported
EN has emerged as the preferred manner of nutri- improved survival at 6 months in the supplemented
tion support in patients requiring SNS. Rationales for group.37 These findings were not duplicated when glu-
this preference have included its lower cost and pre- tamine was supplemented enterally.38 A randomized
sumed increased safety over PN. Although often trial comparing glutamine-supplemented enteral feed-
repeated, these perceived advantages have been chal- ings to isocaloric, isonitrogenous, nonsupplemented
lenged.ll,16 Studies of patients after major trauma in feeds in severe trauma documented reductions in the
which PN was compared with a variety of EN protocols incidence of pneumonia, bacteremia, and sepsis in
using standard polymeric diets, elemental diets, or patients receiving the supplemented diets .39 Oral sup-
diets supplemented with a variety of specific nutrients plementation with glutamine at high doses (30 g/d) had
including glutamine, branched-chain amino acids, no effects on several outcome measures after bone mar-

omega-3 fatty acids, arginine, and nucleotides, gener- row transplantation when compared with placebo. 40

ally report improvements in some measures of outcome Recent meta-analyses of trials of &dquo;immune enhanc-
(ie, infectious complications) in the enterally fed ing&dquo; enteral diets containing supplemental arginine,
patients.31-33 These findings are supported by the glutamine, branched-chain amino acids, omega-3 fatty
results of a recent meta-analysis that pooled the acids, RNA, and trace elements in critical illness con-
results of 22 randomized trials of the use of immune- cluded that the use of the aforementioned diets
enhancing EN formulas (containing some combination reduced the risk of infection, ventilator days, and hos-
of arginine, glutamine, nucleotides, and omega-3 fatty pital length of stay without influencing mortality. 41,12
acids) in critically ill and perioperative patients.34 These results have not been confirmed by others.43 One
Immune-enhancing EN appears to effect a modest study documented increased mortality in patients
reduction in infectious complications, especially in receiving &dquo;immune enhancing&dquo; diets.44
perioperative patients, but has no apparent effect on A recent study provided evidence for improved out-
mortality. A recent report on the use of EN in a specific come in acute respiratory distress syndrome patients
group of critically ill patients (those suffering from fed low carbohydrate diets supplemented with specific
severe head trauma) well illustrates the problems fatty acids (eicosapentanoid acid and gamma-linolenic
92SA

acid) and antioxidants.45 The specific role of the differ- 17. Moriyama S, Okamoto K, Tabira Y, et al: Evaluation of oxygen
ent supplemented nutrients was not established. consumption and resting energy expenditure in critically ill
patients with systemic inflammatory response syndrome. Crit
Care Med 27:2133-2136, 1999
Practice ,. 18. Monk DN, Plank LD, Franch-Arca G, et al: Sequential changes
i Care: Critical illness
, in the metabolic response in critically injured patients during
the first 25 days after blunt trauma. Ann Surg 223:395-405,
1996
1. Patients with critical illnesses are at nutrition 19. Uehara M, Plank LD, Hill GL: Components of energy expendi-
risk and should undergo nutrition screening to ture in patients with severe sepsis and major trauma: A basis for
clinical care. Crit Care Med 27:1295-1302, 1999
identify those who require formal nutrition &20.
dquo; Koea JB, Wolfe RR, Shaw JHF: Total energy expenditure during
assessment with development of a nutrition care
total parenteral nutrition: Ambulatory patients at home versus
plan. (B) patients with sepsis in surgical intensive care. Surgery 118:54-
2. SNS should be initiated when it is anticipated 62, 1995
that critically ill patients will be unable to meet :21.
I Khorram-Sefat R, Behrendt W, Heiden A, et al: Long-term mea-
their nutrient needs orally for a period of 5-10 surements of energy expenditure in severe burn injury. World
J Surg 23:115-122, 1999
days. (B) ,
22. Epstein CD, Peerless JR, Martin JE, et al: Comparison of meth-

3. EN is the preferred route of feeding in critically ill ods of measurements of oxygen consumption in mechanically
patients requiring SNS. (B) ventilated patients with multiple trauma: The Fick method ver-
4. PN should be reserved for those patients requir- sus indirect calorimetry. Crit Care Med 28:1363-1369, 2000

SNS r
23. Weissman C, Kemper M, Askanazi J, et al: Resting metabolic
ing in whom EN is not possible. (C)
rate of the critically ill patient: measured versus predicted. Anes-
thesiology 64:673-679, 1986
REFERENCES 24.
Weissman C, Kemper M, Damask MC, et al: Effect of routine
intensive care interactions on metabolic rate. Chest 86:815-818,
1. American College of Chest Physicians/Society of Critical Care 1984
Medicine Consensus Conference: Definitions for sepsis and organ 25. Ishibashi N, Plank LD, Sando K, et al: Optimal protein require-
failure and guidelines for the use of innovative therapies in ments during the first 2 weeks after the onset of critical illness.
sepsis. Crit Care Med 20:864-874, 1992 Crit Care Med 26:1529-1535, 1998
2. Vrees MD Albina JE: Metabolic response to illness and its medi- 26. Story DA, Ronco C, Bellomo R: Trace element and vitamin con-
ators. IN Clinical Nutrition: Parenteral Nutrition, Rombeau JL, centrations and losses in critically ill patients treated with con-
Rolandelli RH (eds). WB Saunders, Philadelphia, 2000, pp 21-34 tinuous venovenous hemofiltration. Crit Care Med 27:220-223,
3. Plank, LD Hill, GL: Sequential metabolic changes following 1999
induction of systemic inflammatory response in patients with 27. Elia M: Changing concepts of nutrient requirements in disease:
severe sepsis or major blunt trauma. World J Surg 24:630&mdash;638, implications for artificial nutritional support. Lancet 345:1279-
2000 1284, 1995
4. Hill AG: Initiators and propagators of the metabolic response to 28. Schorah CJ, Downing C, Piripitsi A, et al: Total vitamin C,
injury. World J Surg 24:624-629, 2000 ascorbic acid, and dehydroascorbic acid concentrations in plasma
5. Shaw JHF, Wolfe RR: An integrated analysis of glucose, fat, and of critically ill patients. Am J Clin Nutr 63:760-765, 1996
protein metabolism in severely traumatized patients. Studies in 29. Sandstr&ouml;m R, Drott C, Hyltander A, et al: The effect of postop-
the basal state and the response to total parenteral nutrition. erative intravenous feeding (TPN) on outcome following major
Ann Surg 209:63-72, 1987 surgery evaluated in a randomized study. Ann Surg 217:185-
6. Wolfe RR Martini WZ: Changes in intermediary metabolism in 195, 1993
severe surgical illness. World J Surg 24:639-647, 2000
30. Heyland DK, MacDonald S, Keefe L, et al: Total parenteral
nutrition in the critically ill patient. A meta-analysis. JAMA
7. Streat SJ, Beddoe AH, Hill GL: Aggressive nutritional support
does not prevent protein loss despite fat gain in septic intensive 280:2013-2019, 1998
care patients. J Trauma 27:262-266, 1987
31. Heyland DK: Nutritional support in the critically ill patient. A
critical review of the evidence. Critical Care Clin 14:423-440,
8. Wilmore DW, Smith RJ, ODwyer ST, et al: The gut: A central 1998
organ after surgical stress. Surgery 104:917-923, 1988 32. Moore FA, Moore EE, Kudsk KA, et al: Clinical benefits of an
9. Klein S, Alpers DH, Grand RJ, et al: Advances in nutrition and immune-enhancing diet for early postinjury enteral feeding.
gastroenterology: Summary of the 1997 A.S.P.E.N. Research J Trauma 37:607-615, 1994
Workshop. JPEN 22:3-13, 1998 33. Moore FA, Moore EE, Jones TN, et al: TEN versus TPN following
10. Lipman TO: Bacterial translocation and enteral nutrition in major abdominal trauma-reduced septic morbidity. J Trauma
humans: An outsider looks in. JPEN 19:156-165, 1995 29:916-923, 1989
11. Lipman TO: Grains or veins: Is enteral nutrition really better 34. Heyland DK, Novak F, Drover JW, et al: Should immunonutri-
than parenteral nutrition? A look at the evidence. JPEN 22:167- tion become routine in critically ill patients? A systematic review
182, 1998 of the evidence. JAMA 286:944-953, 2001
12. Sedman PC, MacFie J, Sagar P, et al: The prevalence of gut 35. Ott L, Annis K, Hatton J, et al: Postpyloric enteral feeding costs
translocation in humans. Gastroenterology 107:643-649, 1994 for patients with severe head injury: Blind placement, endos-
13. Cummins A, Chu G, Faust L, et al: Malabsorption and villous copy, and PEG/J versus TPN. J Neurotrauma 16:233-242, 1999
atrophy in patients receiving enteral feeding. JPEN 19:193-198, 36. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in
1995 clinical practice: Review of published data and recommendations
14. Cerra FB, McPerson JP, Konstantinides FN, et al: Enteral nutri- for future research directions. JPEN 21:133-156, 1997
tion does not prevent multiple organ failure syndrome (MOFS) 37. Griffiths RD, Jones C, Palmer TEA: Six-month outcome of crit-
after sepsis. Surgery 104:727-733, 1988 ically ill patients given glutamine-supplemented parenteral
15. Brooks AD, Hochwald SN, Heslin MJ, et al: Intestinal perme- nutrition. Nutrition 13:295-302, 1997
ability after early postoperative enteral nutrition in patients 38. Jones C, Palmer TEA, Griffiths RD: Randomized clinical out-
with upper gastrointestinal malignancy. JPEN 23:75-79, 1999 come study of critically ill patients given glutamine-supple-
16. Reynolds JV, Kanwar S, Welsh FKS, et al: Does the route of mented enteral nutrition. Nutrition 15:108-115, 1999
feeding modify gut barrier function and clinical outcome in 39. Houdijk APJ, Rijnsburger ER, Jansen J, et al: Randomised trial
patients after major upper gastrointestinal surgery? JPEN of glutamine-enriched enteral nutrition on infectious morbidity
21:196-201, 1997 in patients with multiple trauma. Lancet 352:772-776, 1998
 93SA

40. Dickson TMC, Wong RM, Negrin RS, et al: Effect of oral glu- Special Considerations
tamine supplementation during bone marrow transplantation.
JPEN 24:61-66, 2000 The initiation of SNS in patients with significant
41. Beale RJ, Bryg DJ, Bihari DJ: Immunonutrition in the critically malnutrition may result in refeeding syndrome.
ill: A systematic review of clinical outcome. Crit Care Med
Refeeding syndrome is a serious metabolic derange-
27:2799-2805, 1999 ment manifested by hypophosphatomeia, hypokale-
42. Heys SD, Walker LG, Smith I, et al: Enteral nutritional supple-
mentation with key nutrients in patients with critical illness and mia, hypomagnesemia, and edema in response to reiniti-
cancer. A meta-analysis of randomized controlled clinical trials. ating nutrient intake in malnourished individuals. 5,6
Ann Surg 229:467-477, 1999 Women with HG resulting in malnutrition should be
43. Heslin MJ, Latkany L, Leung D, et al: A prospective, randomized considered at risk for developing refeeding syndrome.
trial of early enteral feeding after resection of upper gastroin- Decreased thiamine levels, frequently seen in patients
testinal malignancy. Ann of Surg 226:567-580, 1997
with HG,7 increases the risk for Wemickes encephalop-
44. Bower RH, Cerra FB, Bershadsky B, et al: Early enteral admin-
istration of a formula (Impact&reg;) supplemented with arginine, athy, a potentially fatal neurologic syndrome.8-~ Thi-
nucleotides, and fish oil in intensive care unit patients: Results amine supplementation should be considered with
of a multicenter, prospective, randomized, clinical trial. Crit initiation of dextrose-containing fluids in patients
Care Med 23:436-449, 1995
with HG.
45. Gadek JE, DeMichele SJ, Karlstad MD, et al: Effect of enteral
feeding with eicosapentaenoic acid, g-linolenic acid, and antioxi-
dants in patients with acute respiratory distress syndrome. Crit Practice Guidelines
.

Care Med 27:1409-1420, 1999

Hyperemesis i i

HYPEREMESIS GRAVIDARUM 1. Pregnant women are at nutrition risk and should

undergo nutrition screening to identify those who
Background require formal nutrition assessment with devel-
Nausea and vomiting occur commonly within the opment of a nutrition care plan. (B)
first trimester of pregnancy, generally without detri- 2. SNS is indicated in women with hyperemesis
mental effect on mother and fetus. Nausea and vomit- gravidarum who are unable to achieve appropri-
ing affects 50 to 90% of women in early pregnancy. ate weight gain despite the use of noninvasive
Known as &dquo;morning sickness&dquo; the symptoms generally therapies. (B)
begin between the 4th and 7th week and peak by the 3. When SNS is indicated, EN should be initiated as
12th week of pregnancy. Weight loss and nutritional a slow, continuous, isotonic EN infusion to mini-

deficiencies are uncommon in this situation and nutri- mize nausea and vomiting and establish adequate
tional intervention is not necessary.1 Hyperemesis calorie intake. (B)
gravidarum (HG) is a severe form of nausea and vom- 4. PN should be used to treat hyperemesis gravida-
iting that occurs in up to 1% of pregnancies. It is rum when EN is not tolerated. (B)
manifested by persistent vomiting that occurs for the 5. When SNS is started in malnourished women
first time before the 20th week of gestation, weight loss with hyperemesis gravidarum, thiamin supple-
greater than 5% of prepregnancy weight, fluid and mentation and careful monitoring for signs of
electrolyte alterations, acid-base disturbances, and development of refeeding syndrome should be
ketonuria.2 HG can have deleterious effects on mother instituted. (B)
and fetus. The etiology of HG remains unclear but may
be associated with elevated levels of gestational hor- REFERENCES
mones, gastrointestinal dysfunction, or thyroid abnor-
malities. When conventional management using anti- 1. Gadsby R, Barnie-Achdead AM, Jagger C: A prospective study of
nauseaand vomiting during pregnancy. Br J Gen Pract 43:245-
emetic therapy, intravenous- therapy, and oral nutrient 248, 1993
modification are unsuccessful in achieving adequate 2. Wagner BA, Worthington P, Russo-Stieglitz KE, et al: Nutri-
weight gain, patients with HG become candidates for tional management of hyperemesis gravidarum. Nutr Clin Pract
SNS. 15:65-76, 2000
3. Hsu JJ, Clark-Glena R, Nelson DK, et al: Nasogastric enteral
feeding in the management of hyperemesis gravidarum. Obstet
Evidence Gynecol 88(3):343-346, 1996
4. Gulley RM, Pleog NV, Gulley J: Treatment of hyperemesis gravi-
Patients who are unable to attain appropriate darum with nasogastric feeding. Nutr Clin Pract 8(1):33-35,
1993
weight gain despite conservative measures of diet mod- 5. Solomon SM, Kirby DF: The refeeding syndrome: a review.
ification, intravenous hydration, and antiemetic ther- JPEN 14(1):90-97, 1990
apy are candidates for EN or PN. Hsu et al3 reported 6. Havala T, Shronts E: Managing the complications associated
effective relief of intractable nausea and vomiting by with refeeding. Nutr Clin Pract 5:23-29, 1990
7. Van Stuijevenberg ME, Schabort I, Labadarios D, et al: The
provision of EN using an 8-F nasogastric tube in seven nutritional status and treatment of patients with hyperemesis
patients with HG. In a study of 30 patients, Gulley et gravidarum. Am J Obstet Gynecol 172(5):1585-1591, 1995
a14 described better control of nausea and vomiting 8. Omer SM, al Kawi MZ, al Watban J, et al: Acute Wernickes
with small-bore nasogastric tube feeding than they encephalopathy associated with hyperemesis gravidarum: mag-
obtained with traditional measures using intravenous netic resonance imaging findings. J Neuroimag 5(4):252-253,
1995
hydration and antiemetic therapy. PN is indicated in 9. Lavin PJ, Smith D, Kori SH, et al: Wernickes encephalopathy: a
cases of HG when enteral feeding cannot be tolerated.
predictable complication of hyperemesis gravidarum. Obstet
PN is safe and effective in this setting.2 Gynecol 63(suppl):13S-15S, 1983
94SA

10. Wood P, Murray A, Sinha B, et al: Wernickes encephalopathy interventions may not be easily initiated, because a
induced by hyperemesis gravidarum: Case reports. Br J Obstet
person with anorexia nervosa typically presents as
Gynecol 90:583-586, 1983
bright, well-versed in nutrition, and desirous of mak-
PSYCHIATRIC DISORDERS: ing dietary changes to enhance nutrition status. She
may honestly believe that she can, and will, eat more
EATING DISORDERS tomorrow.
Background It is important to recognize that the biobehavioral
disruptions that malnutrition has caused may make it
Eating disorders involve a complex blend of physio- for the individual to carry intent through to
logical disruption, behavioral dysfunction, and envi- impossible
actual behaviors. In addition, the perfectionistic ten-
ronmental susceptibility. Of the three eating disorders
dencies typical of anorexia nervosa create a perception
listed in the Diagnostic and Statistical Manual-IV
on the part of the patient that nutrition support is a
(anorexia nervosa, bulimia nervosa, and binge eating
disorder), the diagnostic standards for anorexia ner- punitive measure or an indication of treatment failure.
Much energy may be devoted to bargaining, delaying
vosa are the only ones that include measurable malnu-
the use of this treatment option, and focusing on any-
trition (weight 85% of ideal).11
Although the incidence of malnutrition in anorexia thing but the task at hand-restoring adequate nutri-
tion status. The proactive practitioner needs to develop
nervosa is 100%, its presentation can vary. Some of the
the ability to recognize early in treatment when a
more common medical complications include arrhyth-
mias, bradycardia, hypercholesterolemia, amenorrhea, patient is likely to be able to implement desired behav-
ior changes and when it is appropriate to use nutrition
muscle loss, reduced gastrointestinal motility, consti-
pation, impaired kidney function, immune system dys- support without a prolonged waiting period.
2 It is important that the interdisciplinary treatment
function, hypothermia, and impaired taste.2 team develop standard criteria and procedures for the
Malnutrition is also associated with numerous neu-
use of SNS. A decision tree with strict deadlines may
roendocrine aberrations. For example, compromised
nutrition status has been associated with increased be helpful to keep the team focused on what is best for
the patients recovery and to limit their susceptibility
physical activity, alterations in appetite, and impaired to patient bargaining and treatment delays. A unified
memory and learning ability.3-5 Normal feeding behav-
front is important, as the dissenting practitioner who
ior is dependent on a nervous system that can engage
even nonverbally communicates disagreement with
activities that support this goal. It is important to
the team decision is likely to be targeted by the patient
improve nutrition status in an expedient fashion so as the one who can change the team decision and who
that neuroendocrine-based behaviors related to malnu-
can dilute the effectiveness of the team as a whole.
trition do not impair the individuals ability to respond
to behavioral psychotherapy.
Nutrition assessment in anorexia should include
total weight, but should be complemented with other
In many cases, an additional psychiatric diagnosis
exists in conjunction with the eating disorder (eg, anthropometric measures that are not as sensitive to
depression, anxiety disorder, obsessive-compulsive dis- manipulation by the patient and that are reflective of
order), and recovery may depend on response to psy- long-term nutrition trends (eg, percentage body fa.t,
midarm muscle circumference). It is important to note
choactive medications. Evidence suggests that these
that many of the standard nutrition assessment mea-
drugs are not as active in malnourished patients.6 surements used in other medical diagnoses are often
Nutrition support can be an important component of
normal in anorexia nervosa. Typical findings in mal-
eating disorder treatment, as it can accelerate the indi- nourished patients with anorexia nervosa include
viduals response to therapeutic interventions.
severe weight loss (20% to 30% or more of usual body
It is not uncommon for an individual to experience a
hypermetabolic period when treatment is initiated. weight), constipation, cold intolerance, fatigue, yellow
skin secondary to hypercarotinemia, knuckle scarring
This calorie level can be 10 times what the person was
and enamel erosion secondary to self-inducement of
eating before seeking treatment; introduced into a mal- vomiting, hirsutism, iron deficiency anemia, hypokale-
nourished gastrointestinal tract, it can create severe
bloating, cramping and constipation. Complicating this mia, and hyponatremia.8 Visceral protein measure-
ments that have been found to be helpful include C-3
scenario is the malnourished patient that may inter-
pret these changes not as short-term issues but as complement level, serum ferritin, serum iron, and
transferrin saturation.9
weight gain that needs to be acted upon. The anxiety
that these early refeeding events creates, compounded Although the purpose of nutrition support is to
restore body mass and optimal function, the long-term
with an already fragile state, can create a spiral that is
difficult to break. Nutrition support can reduce total goal of treatment in anorexia nervosa is to restore
caloric volume as well as total oral food volume and normal, orally based food behaviors. Unless there is a
help to ease the discomfort of early refeeding. complicating medical condition that precludes oral
intake, nutrition support in anorexia nervosa should
Evidence always be an adjunct to, not a replacement for, oral
nutrition therapy. Occasionally, a patient becomes
Because prolonged malnutrition related to
eating dependent on nutrition support as it provides a means
disorders may permanently alter brain structure, of avoiding contact with food. This behavior should be
early recognition and intervention are important for discouraged. Joining peers at mealtime and developing
improving the long-term outcome of treatment. These comfort with food by sitting at a table with friends or
 95SA

family is an important step toward recovery and should than 65% of ideal body weight) who are unable or
not be eliminated because nutrition support is part of unwilling ingest adequate nutrition. (B)
to
the treatment plan. 3. Upon initiation of SNS in patients with anorexia
Indications for SNS in patients with anorexia ner- nervosa, frequent fluid, electrolyte, and acid-base
vosa include severe malnutrition (greater than 30% monitoring must be undertaken to avoid sequelae
recent weight loss or current weight less than 65% of of the refeeding syndrome. (A)
ideal body weight) in patients who are unable or
unwilling to ingest adequate nutrition. EN is generally REFERENCES
sufficient, with only rare patients requiring PN. These 1. Diagnostic and Statistical Manual of Mental Disorders, 4th ed.
patients are at high risk for developing refeeding syn- American Psychiatric Association, Washington, DC, 1994
drome. SNS should be initiated at no more than 70% of 2. Alexander T: Medical Complications in Eating Disorders. IN
Eating Disorders: Putting It All Together. Woolsey M (ed). Amer-
predicted resting energy expenditure. Monitoring for ican Dietetic Association, Chicago, 2000
possibly fatal manifestations of refeeding syndrome 3. Wyrwicka W: Anorexia nervosa as a case of complex instrumen-
should include initial frequent monitoring of serum tal conditioning. Exp Neurol 83(3):579-599, 1984
4. Jiang JC, Gietzen DW: Anorectic response to amino acid imbal-
electrolytes, calcium, magnesium, phosphate, and acid- ance: a selective serotonin3 effect? Pharmacol Biochem Behav
base status. The short-term goal of SNS should be to
47(1):59-63, 1994
safely restore the patients nutrition status to a level 5. Castro CA, Tracy M, Rudy JW: Early-life undernutrition impairs
compatible with stable health (greater than 80% of the development of the learning and short-term memory pro-
ideal body weight).88 cesses mediating performance in a conditional-spatial discrimi-
nation task. Behav Brain Res 32(3):255-264, 1989
6. Walsh BT, Devlin MJ. The pharmacologic treatment of eating
Special Considerations disorders. Psychiatr Clin N Am 15(1):149-160, 1992
7. Lambe EK, Katzman DK, Mikulis DJ, et al: Cerebral gray mat-
In anorexia nervosa, nutrition support is as much a ter volume deficits after weight recovery from anorexia nervosa.
psychological treatment as it is a medical one. If the Arch Gen Psychiatry 54(6):537-542, 1997
patients unique perception and response style is not 8. Russell M, Cromer M, Grant J. Complications of enteral nutri-
taken into account in the nutrition support treatment tion therapy. IN The Science and Practice of Nutrition Support.
Gottschlich MM (ed). Kendall/Hunt, Dubuque, IA, 2001:189-209
plan, the feeding is likely to be sabotaged. 9. Keddy D, Lyon TJ: Assessing Nutritional Status. Eating Disor-
An individual whose intentional behaviors have ders Rev 9(5): 5-7, 1998
brought her weight to a level where nutrition support 10. Kratina K: Sexual Abuse, Dissociative Disorders and the Eating
is necessary has been engaged in her eating disorder Disorders: Nutrition Therapy as a Healing Tool. IN Eating Dis-
for a significant period of time. During that time, she orders: Putting It All Together. Woolsey M (ed). American Die-
tetic Association, Chicago, 2000
has experienced the frustration of family members,
friends, and caregivers who were unable to help her PERIOPERATIVE NUTRITION SUPPORT
regain her health. It is not uncommon for loved ones, in
a moment of frustration, to threaten a tube feeding as Background
punishment for not complying with the recommended Malnourished patients undergoing surgical procedures
course of treatment. When nutrition support actually are at increased risk for postoperative morbidity and
1
becomes a necessity, it can be perceived by the individ- mortality when compared with well-nourished patients.
ual as a personal failure. It is important that when However, it is difficult to definitively demonstrate a
such an intervention is decided upon, that time is pro- causal relationship between malnutrition and surgical
vided in therapy to process those feelings and to facil- outcome. Malnutrition may, in many cases, serve as a
itate a perspective of nutrition support as a positive, surrogate marker of severity of disease.
nurturing decision.
Sexual abuse is common in eating disorders.l For Evidence
the individual who has been a victim of abuse, espe- trials have looked at the effi-
Multiple prospective
cially oral sexual abuse, the sensations experienced cacy of SNS given preoperative and postopera-
in the
during placement of the tube feeding may provoke tive periods to prevent complications and effect out-
memories that are frightening and retraumatizing. It come. 2,3 The trials that have been done however, are
is important to prepare the individual for the proce- difficult to compare due in part to variability in (1) the
dure by discussing what to expect. Personnel perform- definitions of and incidence of malnutrition and other
ing tube placement also need to be aware of the comorbidities; (2) the route of admission and duration
patients psychological presentation. Verbal and phys- of nutrition support; (3) the amount and composition of
ical language should be gentle. the nutrition support; and (4) the incidence of nutrition

Practice Guidelines
support-related complications.
In most of the prospective, randomized, controlled
Psychiatric Disorders: EatingDisorders trials (PRCT) performed, preoperative PN has been
shown to decrease the incidence of postoperative com-
1. All patients with anorexia nervosa are malnour- plications by an absolute rate of approximately l0~1e.2~3
ished and should undergo formal nutrition assess- Most patients in these studies had gastrointestinal
ment with development of a nutrition care plan. (B) cancer and were categorized as moderately malnour-
2. SNS should be initiated in patients with anorexia ished. The benefits were seen mostly in patients who
nervosa with severe malnutrition (greater than were severely malnourished. Improvements in patient
30% recent weight loss or current weight less selection and avoidance of overfeeding and hyperglyce-
96SA

mia may allow these moderate benefits to be achieved going major gastrointestinal surgery for 7 to 14
in other patient populations. The use of preoperative days if the operation can be safely postponed. (A)
EN has been compared with an ad libitum oral diet, 2. PN should not routinely be given in the immedi-
mostly in patients who had cancer. 5,6 The overall inci- ate postoperative period to patients undergoing
dence of postoperative complications was lower in the major gastrointestinal procedures. (A)
EN fed patients. 3. Postoperative SNS should be administered to
The routine use of early postoperative PN has been
studied in multiple PRCTs. Many of the patients in
patients whom it is anticipated will be unable to
meet their nutrient needs orally for a period of 7 to
these studies were moderately malnourished. The 10 days. (B)
absolute rate of complications in these studies was
approximately 10% higher in the PN-fed groups.2 Four
PRCTs have compared the use of early postoperative REFERENCES
EN with routine postoperative diet advancement. Most 1. Mullen GL, Buzby GP, Waldman MT, et al: Prediction of opera-
of these patients had gastrointestinal tract cancers. tive morbidity and mortality by preoperative nutritional assess-
There were no obvious differences between the groups ment. Surg Forum 30:80-82, 1979
in operative morbidity or mortality.2 Postoperative EN 2. Klein S, Kinney J, Jeejeebhoy K, et al: Nutrition support in
has been compared with PN as well. Generally, the clinical practice: Review of published data and recommendations
for future research directions. JPEN 21:133-157, 1997
incidence of complications was higher in the PN
3. Torosian MJ: Perioperative nutrition support for patients under-
groUPS.7-9 going gastrointestinal surgery: Critical analysis and recommen-
The use of &dquo;immune-enhancing&dquo; EN, specifically, dations. World J Surgery 23:565-569, 1999
enteral diets supplemented with L-arginine, w-3 fatty 4. VA TPN Cooperative Study: Perioperative total parenteral nutri-
acids, and ribonucleic acids has been studied in post- tion in surgical patients. N Engl J. Med 325:525-532, 1991
5. Von Meyenfeldt M, Meijerink W, Rouflart M, et al: Perioperative
operative gastrointestinal cancer patients and in crit- nutritional support: Randomized clinical trial. Clin Nutr
ical illness. Biomarkers such as immune status and
11:180-186, 1992
nitrogen balance may be favorably affected by these 6. Shukla HS, Rao PR, Banu N, et al: Enteral hyperalimentation in
specific nutrients. A recent meta-analysis that malnourished surgical patients. Indian J Med Res 80:339-346,
included nine randomized trials that studied the use of 1984
perioperative immune-enhancing EN in elective surgi- 7. Baigrie RJ, Devitt PG, Watkins S: Enteral versus parenteral
cal patients suggested a favorable impact on the rate of nutrition after esophagogastric surgery; a prospective random-
ized comparison. Aust NZ J Surg 66:668-670, 1996
post-operative infectious complications and on length 8. Reynolds JV, Kanwar S, Welsh FKS, et al: Does the route of
of hospital stay.10 Oral supplements have been used in
feeding modify gut barrier function and clinical outcome in
the postoperative period, and one PRCT showed a sig- patients after major upper gastrointestinal surgery? JPEN
nificant decrease in complications in the supplemented 21:196-201, 1997
9. Braga M, Gianotti L, Vignoli A, et al: Artificial nutrition after
groups. 11 major abdominal surgery: Impact of route of administration and
composition of the diet. Crit Care Med 26(1):24-30, 1998
.. 10. Heyland DK, Novak F, Drover JW, et al: Should immunonutri-
Perioperative Nutrition Support tion become routine in crtically ill patients? A systematic review
of the evidence. JAMA 286:944-953, 2001
11. Kiele AM, Barry MJ, Emery PW, et al: Two phase randomized
1. Preoperative SNS should be administered to mod- controlled clinical trial of prospective oral dietary supplements
erately or severely malnourished patients under- in surgical patients. Gut 40(3):343-349, 1997
 Section XII: Administration of Specialized Nutrition Support-
Issues Unique to Pediatrics

INDICATIONS, TYPES, AND ROUTES OF children

< who were treated for iron deficiency in infancy
ADMINISTR,ATION: ENTERAL NUTRITION continue
< to have developmental and learning problems
Indications
at age 10.4
Soy formulas are both milk-free and lactose-free. Soy
Background. The most common indication for EN in protein, glucose polymers (and sometimes sucrose),
the Neonatal Intensive Care Unit (NICU) is immatu- and vegetable oils are the energy-providing nutrients
rity. The ability to suck, swallow, and breathe in a in soy formulas. Indications and contraindications for
well-coordinated fashion occurs at approximately 32 to use of soy formulas have recently been reviewed by the

34 weeks gestational age. Infants less mature than this AAP1 and are shown in Table I.
are tube-fed. Preterm or term infants who are too sick Casein hydrolysate formulas contain extensively
to nipple-feed or who are mechanically ventilated are hydrolyzed protein. They generally do not elicit an
tube-fed. Infants whose nutrient and/or calorie needs immunologic response in infants with allergies to
cannot be met by oral feeding may benefit from EN. intact cow milk or soy protein. Casein hydrolysates are
Conditions under which enteral feeding may be consid- also recommended for infants with significant malab-
ered include chronic lung disease, cystic fibrosis, con- sorption secondary to gastrointestinal or hepatobiliary
disease.l These formulas are lactose-free and may con-
genital heart disease, alimentary tract disease or dys- tain medium-chain triglycerides to facilitate fat
function, renal disease, hypermetabolic states, 1 severe absorption.
trauma, and neurologic disease, among others. Special considerations are required to meet the
Human milk is considered the ideal food for healthy nutritional needs of preterm infants. Milk of mothers
and most sick infants.l2 If the infant is too sick, imma- who deliver preterm is higher in protein and electro-
ture, or weak to directly breastfeed, milk can be lytes and more suited to the preterm infants needs
pumped and fed to the baby by tube. Protocols exist for3 than is the milk of mothers who deliver at term. Even
collecting, storing, and feeding pumped human milk.3 preterm human milk, however, is suboptimal in nutri-
Generally, donor milk (from a mother other than the ent content to meet the needs of small preterm
infants own) is not used because human milk may be a infants. Commercial human milk fortifiers have been
vehicle for transmission of infectious diseases includ- developed to supplement nutrient intake. Special for-
ing HIV-1. mulas are available for preterm infants not receiving
If human milk is not available or indicated, iron- human milk. In-hospital preterm formula differs qual-
fortified infant formula is recommended for the first itatively (in blends of carbohydrates and fats) and
year of life. Standards for nutrient content of infant quantitatively (in higher amounts of many nutrients)
formulas have been established by the American Acad- from term formula. Preterm discharge formulas have a
emy of Pediatrics (AAP) and the Infant Formula Act.1 nutrient content intermediate to that of an in-hospital
Clinical trials demonstrating weight gain, normal preterm formula and a standard term formula.
serum chemical indices, and normal nutrient balance Human milk and infant formulas are 20 calories ,per
in healthy infants must precede the marketing of new fluid ounce (callfl oz) at standard dilution. Feedings are
infant formulas in the United States. Although most generally started at 20 cal/fl oz since no clear benefit to
infants can be successfully fed with human milk or starting with dilute formula has been shown. Tube-fed
standard cow milk-based formula, a variety of infants who are fluid-sensitive may benefit from con-
formulas for different indications is available (see centrated feedings at 24 to 30 callfl oz.~ The increased
Table I). renal solute load and osmolality in concentrated for-
The AAP recommends that all formulas fed to mulas must be considered. Caloric supplements may be
infants be fortified with iron at 10 to 12 mg/L (greater used with or instead of formula concentration as the
than 6.7 mg/100 kcal). Iron is important for normal individual case warrants.6
mental and motor development. Low-iron formulas Additional detailed information about infant formu-
remain on the US market, partly because iron is per- las is published elsewhere7 and is available directly
ceived to cause gastrointestinal and behavioral prob- from the manufacturers.
lems. Preventing iron-deficiency is paramount because Evidence. Although breastfeeding is recommended in

97SA
98SA

TABLE I
Enteral feeding products for infants

most situations, a large prospective, randomized con- mental outcomes when fed fortified human milk or
trolled trial (PRCT) concluded that the use of infant preterm formula as opposed to term formula during the
formula for infants whose mothers are HIV-1 positive neonatal period. 15,16 When controlled for other vari-
helps prevent infant infections and is associated with ables, these effects of early nutrition persist up to age
improved HIV-1-free survival. 8 8 years.17 Thus, choice of early nourishment for pre-
Commercial cow milk-based infant formulas have terms is of long-term importance.
been tested extensively in controlled and field condi- After hospital discharge, use of preterm discharge
tions ; they meet the nutrient needs of infants when formulas (as opposed to term formulas) results in
used as the sole source of nutrition for the first 6 improved growth and bone mineralization in former
months of life and as the primary source of nutrition preterm infants.18,19 The AAP recommends use of pre-
for the second 6 months.1 term discharge formulas for former preterm infants to
In three PRCTs, no difference in gastrointestinal the age of 9 months.1
intolerance or behavioral abnormalities was seen in
infants on iron-fortified formulas compared with those
Routes of Enteral Nutrition
on low-iron formulas.
Soy formulas have been shown to promote growth Background. Infants who are greater than 32 to 34
and bone mineralization in healthy, term infants sim- weeks gestational age and free from respiratory dis-
ilar to that seen in br-ast-fed and cow milk-based ease are generally nipple fed. Enteral feeding (by naso-
formula-fed infants.1,10 gastric or orogastric tube) is most commonly used in
Infants who are allergic to intact proteins do not the NICU for infants who are preterm (less than 32 to
react on double-blind, placebo-controlled challenge to 34 weeks gestational age), weak, or critically ill.
casein hydrolysate formulas.&dquo; Infants who are exquis- Transpyloric feedings may be used for infants who
itely allergic to intact or even hydrolyzed proteins show have delayed gastric emptying.2 Continuous feedings
symptom resolution and normal growth on amino acid- are used when the gastric reservoir function and the
based formulas. 12 regulatory function of the pylorus are bypassed with
PRCTs have shown that multinutrient fortifica- transpyloric tube placement.
tion of human milk improves growth in preterm A gastrostomy tube should be considered for infants
infants.13,14 Preterm formulas promote growth and who will be unable to orally feed for 2 to 3 months. ~>20
bone mineralization at an intrauterine rate. In con- Infants with either neurological problems precluding
trolled trials, preterm infants had improved develop- nipple feedings or anatomical alimentary tract malfor-
 99SA

mations above the level of the stomach are good can- 8. Infants with nasogastric, orogastric, or gastros-
didates for gastrostomy feedings. tomy tubes may be fed by either bolus or contin-
Evidence. Tubes may either be left indwelling for up uous method. (A)
to 3 days or removed and replaced for each feeding
without affecting the infants weight gain or cardiore- REFERENCES
spiratory status.21 1. American Academy of Pediatrics Committee on Nutrition: Pedi-
In PRCTs, gastrointestinal (GI) priming (eg, tube atric Nutrition Handbook, 4th ed. AAP, Elk Grove Village, IL, 1998
feeding 20 slag per day for 10 days) is associated 2. Position of the American Dietetic Association: Promotion of
with enhanced gut motility22,23 and better mineral breast-feeding. J Am Dietet Assoc 97:662-666, 1997
3. Hurst NM, Myatt A, Schanler RJ: Growth and development of a
retention23 in comparison with enteral starvation after hospital-based lactation program and mothers own milk bank.
preterm birth. Necrotizing entercolitis (NEC) rates are JOGNN 27:503-510, 1998
not increased with GI priming, even when an umbilical 4. Lozoff B, Jimenez E, Hagen J, et al: Poorer behavioral and
arterial catheter is in place.24 Several retrospective developmental outcome more than 10 years after treatment for
iron deficiency in infancy. Pediatrics 105(4):e51, 2000
studies have shown that NEC rates are higher in at- 5. Davis A: Indications and techniques for enteral feeds. IN Pedi-
risk infants whose feedings are advanced at a rate atric Enteral Nutrition. Baker SB, Baker RD Jr, Davis A (eds).
greater than 20 mlJkg per day. Increasing at a rate of Chapman & Hall, New York, 1994
20 mL/kg per day allows the infant to reach approxi- 6. Davis A, Baker SB: The use of modular nutrients in pediatrics.
JPEN 20:228-236, 1996
mately 150 mL/kg per day (and approximately 100 7. Sapsford AL: Human milk and enteral nutrition products. IN
Cal/kg per day at 20 Cal/fl oz) in 1 week of progressive Nutritional Care for High-Risk Newborns. Groh-Wargo S,
feeding advancement. Feedings can then be adjusted Thompson M, Cox JH (eds). Precept Press, Chicago, IL, 2000
as fluid, calorie, and nutrient needs dictate. 8. Nduati R, John G, Mbori-Hgacha D, et al: Effect of breastfeeding
Two PRCTs in preterm infants have shown that both and formula feeding on transmission of HIV-1. A randomized
clinical trial. JAMA 283:1167-1174, 2000
continuous and bolus feeding methods result in similar 9. American Academy of Pediatrics Committee on Nutrition: Iron
outcomes of growth, macronutrient retention, of
length
hospitalization, and days to reach full feedings. 25,26 A
fortification of infant formulas. Pediatrics 104:119-123, 1999
10. Lasekan JB, Ostrom KM, Jacobs JR, et al: Growth of newborn,
term infants fed soy formulas for 1 year. Clin Pediatr 38:563-
third, large PRCT showed improved feeding tolerance 571, 1999
(less gastric residual volume) with bolus feedings.23 In 11. Sampson HA, Bernhisel-Broadbent J, Yang E, et al: Safety of
practice, continuous feedings may be better tolerated casein hydrolysate formula in children with cow milk allergy.
than bolus feedings by infants with malabsorption J Pediatr 118:520-525, 1991
12. Hill DJ, Heine RG, Cameron DJS, et al: The natural history of
problems. However, the continuous feeding method is intolerance to soy and extensively hydrolyzed formula in infants
associated with reduced nutrient delivery when com-
1 with multiple food protein intolerance. J Pediatr 135:118-121,
pared with the bolus feeding method. 1999
13. Wauben IP, Atkinson SA, Grad TL, et al: Moderate nutrient
practice Guidelines
.
supplementation of mothers milk for preterm infants supports
adequate bone mass and short-term growth: A randomized, con-
I I l Types, I Routes trolled trial. Am J Clin Nutr 67:465-472, 1998
I Administration: 14. Barrett Reis B, Hall RT, Schanler RJ, et al: Enhanced growth of
Enteral Nutrition preterm infants fed a new powdered human milk fortifier: A
randomized controlled trial. Pediatrics 106:581, 2000
15. Lucas A, Morley R, Cole TJ, et al: Early diet in preterm babies
1. Preterm and ill newborns are at nutrition risk and developmental status at 18 months. Lancet 335:1477-1481,
and should undergo nutrition screening to iden- 1990
16. Lucas A, Morley R, Cole TJ, et al: A randomised multicentre
tify those who require formal nutrition assess- study of human milk versus formula and later development in
ment with development of a nutrition care plan. (B)
preterm infants. Arch Dis Child 70:F141-F146, 1994
2. Infants who are greater than 32 to 34 weeks ges- 17. Lucas A, Morley R, Cole TJ: Randomised trial of early diet in
tational age and free from respiratory disease preterm babies and later intelligence quotient. Br Med J 317:
should be nipple-fed. (B) 1481-1487, 1998
3. EN should be administered to infants through a 18. Lucas A, Bishop NJ, King FJ, et al: Randomised trial of nutrition
for preterm infants after discharge. Arch Dis Child 67:324-327,
nasogastric or orogastric tube that can either be 1992
left in for up to 3 days or placed before and 19. Bishop NJ, King FJ, Lucas A: Increased bone mineral content of
removed after each feeding. (A) preterm infants fed with a nutrient enriched formula after dis-
4. Human milk or iron-fortified, cow milk-based charge from hospital. Arch Dis Child 68:573-578, 1993
20. Wessel JJ: Feeding methodologies. IN Nutritional Care for High-
infant formula should be used for most term Risk Newborns. Groh-Wargo S, Thompson M, Cox JH (eds).
infants. (B) Precept Press, Chicago, IL 2000, pp 321-340
5. Fortified human milk or preterm formula should 21. Symington A, Ballantyne M, Pinelli J, et al: Indwelling versus
be used for preterm infants. (B) intermittent feeding tubes in premature neonates. JOGNN
6. Feedings for sick or preterm infants should be 24:321-326, 1995
22. McClure RJ, Newell SJ: Randomised controlled trial of trophic
started within the first few days of life at 20 Cal/fl feeding and gut motility. Arch Dis Child Fetal Neonatal Ed
oz and at 20 mL/kg per day and advanced at 20 80:F54-F58, 1999
mL/kg per day according to the infants clinical 23. Schanler RJ, Shulman RJ, Lau C, et al: Feeding strategies for
condition. (B) premature infants: Randomized trial of gastrointestinal priming
and tube-feeding method. Pediatrics 103:434-439, 1999
7. A gastrostomy should be considered for infants 24. Davey AM, Wagner CL, Cox C, et al: Feeding premature infants
who will require tube feeding for longer than 2 to while low umbilical artery catheters are in place: A prospective,
3 months. (C) randomized trial. J Pediatr 124:795-799, 1994
 100SA

25. Silvestre MAA, Morbach CA, Brans YW, et al: A prospective against the benefits of nutrition support prior to the
randomized trial comparing continuous versus intermittent initiation of therapy in each individual patient. More-
feeding methods in very low birth weight neonates. J Pediatr
128:748-752, 1996 over, a systematic schedule of metabolic monitoring is
26. Akintorin SM, Kamat M, Pildes RS, et al: A prospective random- mandated.
ized trial of feeding methods in very low birth weight infants.
Pediatrics 100(4):e4, 1997
Evidence

INDICATIONS, TYPES, AND The optimal time for initiating PN is dependent on

ROUTES OF ADMINISTRATION: the childs baseline nutrition status, disease acuity,
PARENTERAL NUTRITION and age.l3 Strong evidence exists that many hospital-
ized pediatric patients are undernourished. Seminal
Background work by Koop reported that 18% to 40% of hospitalized
PN is indicated in infants and children who are pediatric surgical patients suffer acute protein calorie
unable to tolerate adequate enteral feedings to sustain malnutrition.5 Periera et al6 demonstrated that prema-
their nutritional requirements. This may occur in chil- ture infants have energy stores that last 4 to 12 days.
dren who suffer from chronic malnutrition (failure to They reported that depletion of nutritional stores may
thrive) or who are at high risk for developing malnu- occur as early as 4 days in high-risk infants. Therefore,
trition as a result of acute medical illness or prolonged PN may be indicated within 48 hours of surgery in
post-operative recovery. This commonly includes (1) premature infants or children with significant premor-
premature infants, due to immaturity of their gastro- bid nutrition risk factors.66 Because of their more
intestinal tracts, (2) infants/children in whom pro- replete energy reserves, older children usually do not
longed starvation is anticipated, ie, necrotizing entero- require PN unless undernutrition is anticipated to
colitis, pancreatitis, graft-versus-host disease or extend beyond 7 days. Several studies reviewed by
postoperatively, and (3) pediatric patients with inade- Levy et al cite improved outcomes in patients whose7
quate intestinal nutrient absorption (short-bowel SNS was started early in the setting of acute illness.~
syndrome, intestinal pseudoobstruction, postchemo- Numerous studies reviewed by Leonberg et al confirm
therapy, etc). The maximum period of tolerable under- the ability of long-term PN with regard to maintaining
nutrition depends on the patients age, baseline nutri- growth and weight gain.
tion status, and underlying medical conditions. Catheter selection is based on patient factors and the
The -therapeutic goal of PN in children is both to anticipated duration of PN therapy. Two principle cat-
maintain nutrition status and to achieve balanced egories of devices are available for achieving venous
somatic growth. Various components in PN may induce access: temporary (percutaneous) or permanent (tun-

major metabolic disturbances, end organ dysfunction, neled or implantable). Temporary percutaneous cathe-
and drug interactions that mandate periodic monitor- ters may be used when PN duration will be less than 3
1
ing, and meticulous surveillance. weeks, whereas tunneled devices should be used for
The administration of PN requires the placement of longer periods of therapy.2 Placement of an implant-
an appropriate venous access device to safely deliver able subcutaneous titanium or plastic port is also an
the hyperosmotic fluid. Peripheral infusion of paren- option. Several prospective, nonrandomized studies
teral formulations is limited to dextrose concentrations have demonstrated a lower rate of catheter sepsis
of less than 12.5%.1 Because supraphysiologic fluid when subcutaneous ports are used.9,10 However, these
volumes would be necessary to meet the high caloric devices have not been used widely in young children
demand of infants and children using these concentra- requiring chronic PN because they require a needle
tions, peripheral parenteral nutrition (PPN) is rarely stick for each port access.2 Several studies are ongoing
indicated. PPN is useful only for partial nutrition sup- to delineate the incidence of complications according to
plementation or as bridge therapy for patients await- the type of venous access device used.&dquo;
ing central access. Consequently, full PN support in The principal factor influencing the selection of the
children typically requires central venous access. This route of venous access is the caloric requirement. The
may pose significant technical challenges and compli- poor tolerance of peripheral veins of hyperosmotic solu-
cations in the pediatric population. Moreover, the care tions limits their utility to supply adequate calories.
and maintenance of these indwelling venous catheters Gazitua et al demonstrated a 100% incidence of periph-
is associated with infectious and mechanical complica- eral phlebitis with infusion of PN solutions of >600
tions that may create significant morbidities and, mOsm (a typical infusion of 10% dextrose with electro-
rarely, mortality. 2,3 lytes is almost 1000 mOsm).12,13 Either percutaneous
In preparing and planning for a patient to receive venipuncture or a venous cutdown approach must be
PN, the goals should be clearly stated by determining used to obtain central access. The route of access is
the patients (1) nutritional requirements, (2) baseline dependent on the patients size, medical status, avail-
metabolic parameters, (3) anticipated PN duration, able venous access sites, and indicated catheter type.
(4) accessibility of central veins, (5) the most appro- Venous cutdown procedures are favored in small
priate device for placement, and (6) the complications patients (premature infants) and patients with coagu-
of therapy. Despite the obvious benefits of PN, nu- lopathies. This approach essentially eliminates the
merous complications (metabolic, infectious, and insertion risks of pneumothorax and hemothorax.l4
mechanical) may arise as a result of PN use. Conse- The distal end of the vessel is usually ligated using the
quently, the multiple risks of PN should be weighed cutdown approach, preventing its use for future access.
 101SA

Percutaneous venipuncture is often the easiest occurs or along the tunnel. Pocket infec-
at the exit-site
means of achieving central venous access. Excellent tions occuronly with implantable ports. Systemic
technical reviews are available on the subject.15 Alter- infections, formerly called catheter sepsis or bactere-
native sites are necessary for those patients who mia, are defined as a positive culture of the catheter tip
present with multiple sites of central venous thrombo- or a positive pathogen isolated from both blood drawn
sis. Liberal use of duplex ultrasonography or magnetic through the catheter and peripherally.23
resonance imaging to assess venous patency should be Staphylococcus epidermidis, Staphylococcus aureus,
used in these patients. Alternative access sites include and other skin flora are the most common pathogens
the azygous, inferior epigastric, and intercostals veins. isolated in patients with systemic infections. Entero-
As a final resort, a translumbar catheterization of the coccus and enteric flora are the next most frequently
inferior vena cava may achieve reliable access for PN.33 isolated organisms. Although less common, Candida is
Improvements in design over the last two decades an important pathogen because of its virulence and
have led to the development of small caliber catheters resistance to treatment.2
ranging in size from 2F to 4F. PICC lines (peripherally Therapy for catheter infections is dependent on the
inserted central venous catheter) are becoming a com- type of infection and pathogen. Exit site infections are
mon route of PN administration. 2,3 They have recently often cleared with topical measures and systemic anti-
gained popularity because of their ease of bedside biotics, whereas tunnel and pocket infections usually
insertion and good patient tolerance. Numerous pro- require catheter remova1.24-2 Although the &dquo;gold stan-
spective, nonrandomized studies have reported a dard&dquo; therapy for systemic catheter-related infections
decreased incidence of major morbidity relative to sur- is line removal, many lines may be effectively treated
gically placed central venous catheters. Long-term without catheter removal.22 Widmer reported that
morbidities such as risk of catheter-related sepsis and patient factors such as immunocompetence and the
thrombosis are similar to surgically placed lines. 16 The virulence of the pathogen determine the efficacy of
compelling data from these studies and clinical expe- antibiotic therapy. 21 When signs of systemic infection
riences have made PICC lines the catheter of choice for are present, early initiation of empiric intravenous
many hospitalized children requiring extended venous antibiotic therapy is crucial to ensure catheter salvage.
access. 17 There are no studies in the current literature Blood cultures should be obtained both centrally and
on the risks or benefits of these catheters for long-term peripherally prior to the initiation of intravenous anti-
outpatient PN therapy. biotics.23
Treatment protocols vary widely, and there are no
Special Considerations randomized, prospective studies stratifying pediatric
patients by important risk factors like age, disease,
Four major categories of complications exist: (1) acuity, or pathogen to support the appropriate antibi-
mechanical or technical; (2) infectious; (3) metabolic; otic selection or length of therapy. 2,3
and (4) nutritional. Mechanical or technical complica- Existing studies support the institution of anti-
tions are those problems related to catheter placement, staphylococcal therapy given through the catheter
ie, pneumothorax, hemothorax, cardiac tamponade, or for community-acquired infections.3,23,28,29 Antibiotic
equipment malfunction. Catheter thrombosis is a sig- treatment is governed by the sensitivities of the blood
nificant problem with a rate ranging from 0% to 50% of cultures. Therapy is then continued for at least a
all central lines. This may lead to partial catheter 10-day period. The recent increased incidence of methi-
malfunction, infection, or IOSS.2,3 Several reviews cillin-resistant coagulase-negative staphylococcal infec-
report an association between catheter thrombosis and tions in hospitalized or chronically ill patients war-
infection. 18-20 A potential early sign of catheter throm- rants the institution of empiric vancomycin therapy as
bosis is progressively sluggish or absent blood return the initial coverage in these compromised patients. 2,3
on catheter aspiration. Thrombolytic agents are effec- Neonates, short-bowel patients, and hospitalized chil-
tive dissolving catheter thrombi. There are no stan- dren should receive additional coverage for Gram-neg-
dardized protocols for catheter thromblysis, based on a ative organisms. Repeat blood cultures at the end of
multicenter prospective randomized control stud- treatment are indicated to confirm microbial clearance.
i es. 21,22 Deterioration of clinical status during antibiotic ther-
Catheter-related infections are the most common apy or failed catheter sterilization by treatment are
complications associated with central venous access for indications for catheter removal. Infections with S.
PN. The incidence may approach 60% in long-term aureus, Gram-negative bacteria, and Candida may be
devices.1,17-19,22 The diagnosis of catheter infection especially virulent and lethal. Candida, though uncom-
and sepsis requires a high index of suspicion (ie, fever, mon, should be considered with low-grade infections
erythema at catheter site, vague constitutional symp- and when the child has received multiple antibiotics.
toms). Critical evidence-based assessments of thera- The treatment for Candida line sepsis is removal,
pies and clinical outcomes have been plagued by the along with a complete course of antifungal therapy., 30
lack of consistently accepted diagnostic criteria and Various materials, caps, valves and coatings have
classifications. Recently published guidelines by the been proposed to decrease rates of catheter infec-
Centers for Disease Control (CDC) for prevention of tion. Silver-chelated cuffs and antibiotic/antiseptic-
catheter-related infections have standardized the impregnated catheters are two recent technological
nomenclature. Localized infections are defined as ery- developments that show great promise. These cathe-
thema, tenderness, induration, or purulence that ters decrease infection rates in randomized, controlled
102SA

studies, but the effect is short-lived. Despite numer- 13. Shizgal HM, Knowles JB. Peripheral amino acids. IN Parenteral
ous studies on silver chelated cuffed catheters, the Nurtrition, 2nd ed. Fischer JE (ed). Little Brown and Company,
literature supporting their use is limited. 31,32 Boston, 1991:389
14. Chathas MK, Paton JB, Fisher DE: Percutaneous central venous
Use of a valve-tipped catheter has been advocated to catheterization: Three years experience in a neonatal intensive
reduce thrombotic complications, however, in a pro- care unit. Am J Dis Child 144:1246, 1990
15. Cobb LM, Vinocur CD, Wagner CW, et al: The central venous
spective trial in pediatric oncology patients, no benefit anatomy in infants. Surg Gynecol Obstet 165:230, 1987
was shown to support the use of these catheters.33 16. Alhimyary A, Fernandez C, Picard M, et al: Safety and efficacy of
total parenteral nutrition delivered via a peripherally inserted
Practice i central venous catheter. Nutr Clin Pract 11:199, 1996
17. Wiener ES: Catheter sepsis: The central venous line Achilles
Indications, f f, f heel. Semin Pediatr Surg 4:207, 1995
f Administration: 18. Decker MD, Edwards KM: Central venous catheter infections.
Pediatr Clin N Am 35:579, 1988
Parenteral Nutrition 19. Mansfield PF, Hohn DC, Fornage BD, et al: Complications and
failures of subclavian-vein catheterization. N Engl J Med 331:
1. Pediatric patients unable to meet their nutrient 1735, 1994
20. Atkinson JB, Chamberlin K, Boody BA: A prospective random-
requirements orally or with EN should receive ized trial: Urokinase as an adjuvant in the treatment of proven
PN. (B) Hickman catheter sepsis. J Pediatr Surg 33:714, 1988
2. PN should be initiated within 1 day of birth in 21. Kellerman S, Chan J, Jarvis W: Use of urokinase in pediatric
neonates and within 5 to 7 days in pediatric patients hematology/oncology patients. Am J Infect Control 26:502, 1998
22. Tobiasky R, Lui K, Dalton DM, et al: Complications of Central
unable to meet their nutrient requirements orally or Venous access Devices in children with and without Cancer.
with EN. (C) J Pediatr Child Health 33:509-514, 1997
3. Catheter exit site infections should be treated 23. Hospital Infection Control Advisory Committee, Centers for Dis-
ease Control and Prevention: Guidelines for prevention of intra-
topically and with systemic antibiotics. (B) vascular-device related infections. Infect Control Hosp Epide-
4. Tunnel infections should be treated with catheter miol 17:438, 1996
removal. (B) 24. Groeger JS, Lucas AB, Thaler HT, et al: Infectious morbidity
associated with long-term use of venous access devices in
5. Systemic catheter-related infections should be patients with cancer. Ann Intern Med 119:1168-1174, 1993
initially treated with at least a 10-day course of 25. Hiemenz J, Skelton J, Pizzo PA: Perspective on the management
intravenous antibiotics given through the cathe- of catheter-related Infections in cancer patients. Pediatr Surg
ter, adjusting the antibiotics according to the sen- 22:702-707, 1987
26. Whitman E: associated with the use of central
Complications
sitivities of the blood cultures. (B) venous accessdevices. Curr Probl Surg 33:313-378, 1996
6. Clinical deterioration, persistent infection or Can- 27. Widmer AF: Intravenous-related infections. IN Prevention and
dida sepsis should be treated with prompt cathe- Control of Nosocomial Infections. Wenzel RP (ed). Williams &
ter removal. (B) Wilkins, Philadelphia, 1997, p 771
28. Buchanan AL, Moukarzel A, Goodson B, et al: Catheter related
infections associated with home parenteral infections and pre-
dictive factors of catheter removal in their treatment. JPEN
REFERENCES
18:297, 1994
1. Acra SA, Rollins C: Principles and guidelines for parenteral 29. Newman K, Tenney J, Reed W: Infectious and non-infectious
nutrition in children. Pediatric Ann 28:2, 113-120, 1999 complications of Hickman catheters. Microbiol Rev A345:156,
1987
2. Krzywda, EA, Andris DA, Edmiston CE: Catheter infections:
30. Lecciones JA, Lee JW, Navano EE, et al: Vascular catheter
Diagnosis, etiology, treatment and prevention, Nutr Clin Pract associated fungemia: Analysis of 155 episodes. Clin Infect Dis
14:1781999
14:875, 1992
3. Chung DH, Ziegler MM: Central venous catheter access. Nutri-
tion 14:119-123, 1998
31. Pasquale MD, Campbell JM, Magnant CM: Groshong versus
Hickman catheters. Surg Gynecol Obstet 172:408, 1992
4. Meadows, N: Monitoring and complications of parenteral nutri- 32. Beekman SE, Henderson DK. Unfinished business: assessing
tion. Nutrition 14:806-808, 1998 the efficacy of extraluminal silver ions on the prevention of
5. Cooper A, Jakobowski D, Spiker J, et al: Nutrition assessment: microbial colonization and catheter-associated infection. Crit
An integral part of the preoperative pediatric surgical evalua- Care Med 27:456-458, 1999
tion. J Pediatr Surg 16:554, 1982 33. Warner BW, Haygood MM, Davies SL, Hennies GA: A random-
6. Pereira GR, Zeigler MM: Nutritional care of the surgical neo- ized, prospective trial of standard Hickman compared with Gro-
nate. Clin Perinatol 16:233, 1989 shong central venous catheters in pediatric oncology patients.
7. Levy JS, Winter RW, Heird WC: Total parenteral nutrition in J Am Coll Surgeons 183:140, 1996
pediatric patients. Pediatr Rev 2:99, 1980
8. Leonberg BL, Chuang E, Eicher P, et al: Long term growth and
COMPLICATIONS UNIQUE TO NEONATES:
development in children after home parenteral nutrition. J Pedi- ENTERAL NUTRITION
atr 132:461, 1998
9. La Quaglia MP, Lucan A, Thaler HT, et al: A prospective anal- Background
ysis of vascular access device-related infections in children.
J Pediatr Surg 27:840, 1992 EN in the neonate can be associated with a variety of
10. Miller K, Buchanan GR, Zappa S, et al: Implantable venous technical, gastrointestinal, developmental, and meta-
access devices in children with hemophilia: A report of low infec- bolic complications.
tion rates. J Pediatr 132(6):934-938, 1998 Sick neonates (who cannot nipple-feed) are generally
11. Orr ME: Vascular access device selection for parenteral nutri-
tion. Nutr Clin Pract 14:172, 1999
fed using nasogastric or orogastric tubes. Tubes are
12. Gazitua R, Wilbon K, Bistrian BR, et al: Factors determining usually inserted by nurses who check tube placement
peripheral vein tolerance to amino acid infusions. Arch Surg by auscultation and by pH of the fluid aspirated from
114:897, 1979 the tube. Tube malposition can result in delivery of
 103SA

nutrients either upstream or downstream from the reduce the duration of loose stools in older infants with
intended site of infusion (leading to aspiration or moderate-to-severe diarrhea6 and with antibiotic-in-
dumping). Nasogastric tubes may cause nasal conges- duced diarrhea.77
tion or erosion. Careful handling of commercially sterile, ready-to-
Gastrostomy tubes may be used for long-term tube feed bottled formulas using aspectic techinque, reduces
feeding in neonates. A common complication with gas- the risk of formula contamination.8 Non-ready-to-feed
trostomy tubes is migration of the tube. Feeding tubes enteral formulas for infants should be prepared using
may also be occluded by crushed medications. Feeding aseptic technique in a designated hospital formula
pump malfunction can be associated with over- or room (or separate formula preparation area).9 Individ-
under-delivery of feeding substrate. ual formula portions that are removed from floor stock
A serious complication of enteral feedings in neo- (or refrigeration) and opened should be used within 4
nates (particularly preterms) is neonatal necrotizing hours or discarded,9 although commercially sterile
enterocolitis (NEC). Gastrointestinal complications of products may be hung in a closed delivery system for 8
EN in the neonate include emesis, abdominal disten- to 12 hours.4 Hospital-prepared tube feedings or
sion, and diarrhea. Although occurrence of these symp- human milk should not be hung for more than 4
toms may be a harbinger for NEC, they are frequently hours.4 Disposable enteral delivery equipment (tubing,
signs of less severe feeding intolerance. Emesis and/or fasteners, etc) should be changed every 24 hours and
abdominal distension may be an indication of obstruc- should not be reused.4
tion, intolerance of the rate of feeding or impaired Non-nutritive sucking (sucking on a pacifier while
gastric emptying. being tube-fed) facilitates transition from tube to bottle
Diarrhea can be related to hyperosmolality of the feeding in preterm infants and is associated with a
feeding, rate ofdelivery of the feeding, malabsorption, decrease in length of hospital stay.10 Preterm infants
contaminated feedings, and/or gastrointestinal tract are more likely to breastfeed if they receive supple-
infections. mental feedings by nasogastric tube rather than by
Long-term tube feeding without nipple feeding can bottle. 11
result in oral aversion. Early and frequent oral stimu-
lation is necessary to avoid this complication.1 Practice Guidelines
.

Although less frequent with EN than with PN, met- i i i Unique to Neonates: ,

abolic complications may occur. Fluid and/or electro- Enteral i

lyte abnormalities, glucose abnormalities, nutrient
deficiencies, and/or metabolic bone disease (in pre- 1. Feeding tube position should be verified before
terms) are occasionally seen. In severely malnour-
ished infants, overzealous nutritional rehabilitation feeding is initiated. (C)
2. When administered by feeding tube, medications
may be hazardous. Refeeding may result in hypergly- should be given in liquid form. (C)
cemia, hypokalemia, hypophosphatemia, and hypo- 3. Enteral feedings (including human milk) should
magnesemia. be handled and stored using aseptic technique. (B)
4. Nonnutritive sucking during tube feeding should
Evidence be encouraged. (A)
Use of a small, properly anchored soft tube reduces REFERENCES
the risks of nasal congestion or erosion. The risk of
1. American Academy of Pediatrics, Committee on Nutrition: Pedi-
gastric or intestinal perforation (by stiff, nonpliable atric Nutrition Handbook, 4th ed. AAP, Elk Grove Village, IL,
tubes) is reduced by use of tubes made of polyurethane 1998
or silicone rubber, rather than polyvinyl chloride. 2. Armstrong VL: Teaching pediatric tube feeding to caregivers.
Gastrostomy tube migration can be minimized by Ross Products Division, Columbus, OH, 1999, p 30
firmly attaching the tube and placing a mark on the 3. Marchand V, Baker SB, Baker RD: Enteral nutrition in the
tube to facilitate detection of migration. Tube occlu- pediatric population. Gastrointest Endoscop Clin N Amer 8:669-
702, 1998
sion by medications is avoided in neonates by use of 4. Davis A: Indications and techniques for enteral feeds. IN Pedi-
liquid medications. Tube flushing also reduces the risk atric Enteral Nutrition. Baker SB, Baker RD, Davis A (eds).
of occlusion. In neonates, tubes should be flushed with Chapman & Hall, New York, 1994, pp 67-94
1 mL of air instead of water to avoid fluid overload.22 5. Vanderhoof JA, Murray ND, Paule CL, et al: Use of soy fiber in
acute diarrhea in infants and toddlers. Clin Pediatr 36:135-139,
Smaller volume, continuous feedings in neonates are 1997
generally infused by intravenous pumps, which are 6. Brown KH, Perez F, Peerson JM, et al: Effect of dietary fiber (soy
more accurate than enteral pumps. polysaccharide) on the severity, duration and nutritional out-
If gastrointestinal obstruction is ruled out, proki- come of acute, watery diarrhea in children. Pediatrics 92:241-

netic drugs may be helpful in treating abdominal dis- 247, 1993

7. Burks AW, Vanderhoof JA, Mehra S, et al: Randomized clinical
tension and/or emesis. Diarrhea can be minimized trial of soy formula with and without fiber in antibiotic induced
with correct formula selection, concentration, and diarrhea. J Pediatr 139:578, 2001
preparation, and with review of medications. 4 Diar-3 8. Patchell CJ, Anderton A, Holden C, et al: Reducing bacterial
rhea may be managed by decreasing the feeding rate.3 contamination of enteral feeds. Arch Dis Child 78:166-168, 1998
9. American Dietetic Association: Preparation of Formula for
Fiber has not been shown to be efficacious in the treat- Infants: Guidelines for Health Care Facilities. ADA, Chicago, IL,
ment of diarrhea in infants less than 6 months of age.~5 1991, pp 1-100
However, soy formula with fiber has been shown to 10. Pinelli J, Symington A: Non-nutritive sucking for promoting
104SA

physiologic stability and nutrition in preterm infants (Cochrane

Hypocalcemia may be due to hypoalbuminemia,
Review). IN The Cochrane Library, Issue 1, 2000. Oxford:
Update Software
hypoparathyroidism, vitamin D deficiency, hyperphos-
11. phatemia, or medication-induced urinary calcium
Kliethermes PA, Cross ML, Lanese MG, et al: Transitioning
preterm infants with nasogastric tube supplementation: excretion (diuretics, corticosteroids).1,22 Two studies,
including a randomized controlled trial, show that
Increased likelihood of breastfeeding. JOGNN 28:264-273, 1998
hypocalcemia may result from hypercalciuria second-
COMPLICATIONS UNIQUE TO NEONATES: ary to amino acid intake from PN. In this situation,
PARENTERAL-FLUID AND ELECTROLYTES serum phosphate concentrations rise significantly.15,16

Background Pelegano et al 17 studied the effect of PN calcium-to-

phosphate ratio (in mg) in very low birth weight
PN significantly contributes to the patients daily infants. Calcium retention was
higher with a 2:1 ratio,
fluid intake. Electrolyte imbalances in patients receiv- whereas
phosphate retention was higher with a 1.7: 1
ing PN are generally related to the PN, underlying or 1.3:1 ratio. In two studies, supplementation of phos-
clinical conditions, and drug therapy. Changes in
phate in neonates with hypophosphatemia resulted in
intake, losses, redistribution, and physiologic and decreased calciuria and increased calcium reten-
pathophysiologic regulatory mechanisms affect electro- tion. 18,19 Vielisis et al2 showed that a phosphate dose
lyte homeostasis. 1,2 The treatment of electrolyte disor- of 1.34 mmlkg per day (40 mg/kg per day) is necessary
ders relies on the identification of the etiology and is to normalize serum
phosphate concentrations in criti-
guided by the acuity and the presence or absence of cally ill neonates without inducing phosphaturia. Met-
symptoms. PN solutions should not be used primarily astatic calcification may occur. when the serum Ca/P
to manage fluid and electrolyte abnormalities, but
product exceeds 60 to 70 mg2/dL2.21 Based on these
adjustments in PN solutions can avoid and/or amelio- studies, it appears that a 1.7:1 calcium-to-phosphate
rate potential complications. ratio in PN allows for the highest absolute retention of
both minerals and simulates the in utero accretion of
Evidence
calcium and phosphate.
Premature infants lose sodium in the urine because
of the immaturity of the sodium reabsorptive capacity Practice Guidelines
.

of the kidneys and with diuretic therapy. Hyponatre- Complications I to Neonates: ,

mia, due to water retention, is managed by free water Parenteral-Fluid

i I, electrolytes
restriction and gentle diuresis. 3,4 Hyponatremia in
infants may lead to poor tissue growth and adverse
developmental outcomes. Normalizing sodium intake
1. Hyponatremia in premature infants should be
corrected by increasing sodium intake in order to
promotes cell growth and weight gain. 1,6 A general goal promote tissue growth and weight gain. (A)
should be a urine sodium concentration greater than
2. Calcium and phosphate concentrations should be
10 mEq/L. Hypernatremia denotes free water deficit
and is corrected with free water and sodium restric- optimized in PN solutions to promote maximum
bone mineral retention. (A)
tion. Sodium concentrations in PN can be adjusted to a
maximum of 154 mEq/L or the equivalent of normal
saline. REFERENCES

Hypokalemia is more common than hyperkalemia in 1. Schultz NJ, Chitwood-Dagner KK: Body electrolyte homeostasis.
hospitalized patients.7 Hyperkalemia is frequent in IN Pharmacotherapy: A Pathophysiologic Approach. Dipiro JT,
Talbert RL, Yee GC, et al (eds). Appleton & Lange, Stamford,
very low birth weight infants8 and is usually the result
of reduced renal clearance (renal failure, potassium- 1997, pp 1105-1137
2. Dunham B, Marcuard S, Khazanie PG, et al: The solubility of
sparing diuretics), impaired renal drug excretion (tri- calcium and phosphorus in neonatal total parenteral nutrition
methoprim-sulfamethoxazole), excessive potassium solutions. JPEN 15:608-611, 1991
load (hemolysis, blood transfusions), redistribution 3. Modi N: Hyponatraemia in the newborn. Arch Dis Child 78:F81-

(metabolic acidosis), or protein catabolism.9 To avoid F84, 1988

4. Maguire D, Doyle P: Sodium balance in very-low-birth-weight
toxicity, potassium concentrations in PN solutions as infants. Crit Care Nurse 14:61-66, 1994
well as in other intravenous admixtures should be 5. Haycock GB: The influence of sodium on growth in infancy.
carefully watched. Although rare patients may require Pediatr Nephrol 7:871-875, 1993
6. Bower TR, Pringle KC, Soper RT: Sodium deficit causing
more potassium, potassium concentration in PN solu-
decreased weigh gain and metabolic acidosis in infants with
tions is usually limited to 80 mEq/L. ileostomy. J Pediatr Surg 23:567-572, 1988
Hypomagnesemia is usually associated with severe 7. Weiner ID, Wingo CS: Hypokalemia-consequences, causes, and
diarrhea, medications (diuretics, aminoglycosides, correction. J Am Soc Nephrol 8:1179-1188, 1997
8. Shaffer SG, Kilbride HW, Hayen LK, et al: Hyperkalemia in very
Amphotericin B) or maternal diabetes.lo,l1 Hypermag- low birth weight infants. J Pediatr 121:275-279, 1992
nesemia may be seen in infants born to pre-eclamptic 9. Fukuda Y, Kojima T, Ono A, et al: Factors causing hyperkalemia
mothers treated with magnesium sulfate and usually in premature infants. Am J Perinatol 6:76-79, 1989
resolves within 48 to 72 hours. 12,13 Hypermagnesemia 10. Ahsan SK, al-Swoyan S, Hanif M, et al: Hypomagnesemia and
also occurs in the setting of impaired renal function. 14 clinical implications in children and neonates. Indian J Med Sci
Serum calcium concentrations are higher, and serum 52:541-547, 1998
11. Weintrob N, Karp M, Hod M, et al: Short- and long-range com-
parathyroid hormone concentrations lower in hyper- plications in offspring of diabetic mothers. J Diabetes Complica-
magnesemic neonates, perhaps because of suppression tions 10:294-301, 1996
of neonatal parathyroid function. 12. McGuiness GA, Weinstein MM, Cruikshank DP, et al: Effects of
 105SA

magnesium sulfate treatment on perinatal calcium metabolism. aiming for blood glucose concentrations between 100
II. Obstet Gynecol 56:595-600, 1980
and 150 mg/dL. Collins et al,l1 in a prospective ran-
13. Donovan EF, Tsang RC, Steichen JJ, et al: Neonatal hyper-
magnesemia: Effect on parathyroid hormone and calcium domized trial, evaluated the administration of insulin
homeostasis. J Pediatr 96:305-310, 1980 by continuous infusion for an average of 14 days in 24
14. Nadler JL, Rude RK: Disorders of magnesium metabolism.
Endocrinol Metab Clin N Am 24:623-641, 1995
extremely low birth weight infants. They showed
15. Bengoa JM, Sitrin MD, Wood RJ, et al: Amino acid-induced improved glucose tolerance, greater protein and calorie
hypercalciuria in patients on total parenteral nutrition. Am J intake, and greater weight gain in the insulin-treated
Clin Nutr 38:264-269, 1983 group compared with the control group.
16. Prestridge LL, Schanler RJ, Shulman RJ, et al: Effect of paren-
teral calcium and phosphorus therapy on mineral retention and Hypoglycemia develops rapidly in neonates if feed-
bone mineral content in very low birth weight infants. J Pediatr ings are delayed or interrupted, because of the im-
122:761-768, 1993 maturity of homeostatic mechanisms. Additionally, in-
17. Pelegano JF, Rowe JC, Carey DE, et al: Effect of calcium/ fants receiving PN may have high levels of insulin that
phosphorus ratio on mineral retention in parenterally fed pre- suppresses ketogenesis; this may linger after abrupt
mature infants. J Pediatr Gastroenterol Nutr 12:351-355, 1991
18. Chessex P, Pineault M, Zebiche H, et al: Calciuria in parenter- discontinuation ofPN.12,13 Bendorf et al14 showed in a
ally fed preterm infants: Role of phosphorus intake. J Pediatr controlled trial that acute discontinuation of PN lead to
5:794-796, 1985 a greater incidence of hypoglycemia in young infants.
19. Cary DE, Goetz CA, Horak E, et al: Phosphorus wasting during
phosphorus supplementation of human milk feedings in preterm
Older children (more than 2 years of age), 15 however,
infants. J Pediatr 5:790-793, 1985 were not affected by abrupt discontinuation of PN. It is
20. Vileisis RA: Effect of phosphorus intake in total parenteral recommended that PN be tapered over 1 to 2 hours in
nutrition infusates in premature neonates. J Pediatr 110:586-
infants before discontinuation to avoid reactive hypo-
589, 1987
21. Gertner JM: Disorders of calcium and phosphorus homeostasis. glycemia. Although there is no established time period,
Pediatr Clin N Am 37:1441-1465, 1990 significant hypoglycemia can be seen as early as 15 to
30 minutes after stopping PN; this should guide the
COMPLICATIONS UNIQUE TO NEONATES: timing of initial blood glucose sampling for monitoring
these children. 15 Blood glucose concentrations should
HYPERGLYCEMIA AND HYPOGLYCEMIA
be checked within 15 to 60 minutes after discontinua-
Background tion of PN.
Premature infants are at increased risk for hy-
perglycemia possibly due to saturation of insulin re- Practice Guidelines
ceptors or the immaturity of hepatic and pancreatic Complications Unique I Neonates:,

response. 1, Hyperglycemia may also be the result of Hyperglycemia, l, Hypoglycemia,

sepsis, surgery, or respiratory distress and may lead to
derangements in fluid and electrolyte status.34 Hyper- 1. Dextrose infusion rates in infants should not
glycemia in the neonate is defined as plasma glucose exceed 10 to 14 mg/kg per minute. (A)
concentration greater than 150 mg/dL or whole blood 2. Insulin administration by continuous infusion
glucose concentrations greater than 125 mg/dL. Hypo- is safe and effective in controlling parenteral
glycemia is defined as blood glucose concentrations less nutrition-associated hyperglycemia in infants. (A)
than 40 mg/dL.2 In patients receiving PN, hypoglyce- 3. PN should be tapered off over to 2 hours before
mia may be caused by sudden cessation of the PN discontinuation in infants under age 2. (B)
infusion.
REFERENCES
Evidence
1. Pollak A, Cowett RM, Schwartz R, et al: Glucose disposal in
Premature, low-gestational-age, and low-birth-weight low-birth-weight infants during steady-state hyperglycemia:
infants are more likely to develop hyperglycemia. 3,4 effects of exogenous insulin administration. Pediatrics 61:546-
The incidence of hyperglycemia in has been reported 549, 1978
between 43 and 86% in premature infants and in-
2. Farrag HM, Cowett RM: Glucose homeostasis in the micropre-
mie. Clin Perinatol 27:1-22, 2000
creases with increasing prematurity. 4,5 It is also seen 3. Stonestreet BS, Rubin L, Pollak A, et al: Renal functions of low
more frequently in vatients requiring mechanical ven- birth infants with hyperglycemia and glucosuria produced by
tilation.6 Hyperglycemia was found in 43% of prema- glucose infusions. Pediatrics 66:561-567, 1976
4. Zarif M, Pildes RS, Vidyasagar D: Insulin and growth-hormone
ture infants receiving dextrose infusions at a mean rate responses in neonatal hyperglycemia. Diabetes 25:428-433,
of 4.7 to 4.9 mg/kg per minute (range, 3 to 7 mg/kg per 1976
minute). 4,7 In very premature infants, hyperglycemia 6. Dweck HS, Cassady G: Glucose intolerance in infants of very low
will almost invariably occur as the infusion rate increases birth weight. I. Incidence of hyperglycemia in infants of birth
weights 1,100 grams or less. Pediatrics 53:189-195, 1974
beyond 8 mg/kg per minute.~ Because this rate of dex- 7. Binder N, Raschko PK, Benda GI, et al: Insulin infusion with
trose infusion is insufficient to allow full caloric delivery, parenteral nutrition in extremely low birth weight infants with
insulin may needed for additional carbohydrate admin- hyperglycemia. J Pediatr 114:273-280, 1989
istration. 8. Jones MO, Pierro A, Hammond P, et al: Glucose utilization in the
Continuous insulin infusion (0.01-0.1 unit/kg per surgical newborn infant receiving total parenteral nutrition.
J Pediatr Surg 28:1121-1124, 1993
hour) has been shown to be safe and effective in man- 9. Heron P, Bourchier D: Insulin infusions in infants of birthweight
aging hyperglycemia in the neonate.9,10 Glucose con- less than 1250 g and with glucose intolerance. Aust Pediatr J
centrations should be monitored at least every 2 hours, 24:362-365, 1988
106SA

10. Kanarek KS, Santeiro ML, Malone JI: Continuous infusion of cated, adding heparin at a dose of 1 unit/mL of neonatal
insulin in hyperglycemic low-birth weight infants receiving par-
PN solution improves lipid emulsion clearance.
enteral nutrition with and without lipids. JPEN 15:417-420,
1991 Premature infants have low carnitine reserves. Low
11. Collins JW Jr, Hoppe M, Brown K, et al: A controlled trial of carnitine levels can also be seen in full-term neonates
insulin infusion and parenteral nutrition in extremely low birth
receiving long-term PN.2o,21 Carnitine supplementa-
weight infants with glucose intolerance. J Pediatr 118:921-927, tion may increase lipid clearance,22>23 but low plasma
1991
12. Cornblath M, Hawdon JM, Williams AF, et al: Controversies carnitine concentrations do not necessarily correlate
regarding the definition of neonatal hypoglycemia: suggested with elevated serum triglyceride concentrations.24 It
operational thresholds. Pediatrics 105:1141-1145, 2000 has been shown that fatty acid oxidation and improved
13. Dudrick SJ, Macfadyen BV Jr, Van Buren CT, et al. Parenteral
hyperalimentation. Metabolic problems and solutions. Ann Surg triglyceride levels are seen in premature infants
176:259-264, 1972 receiving supplemental intravenous carnitine who are
14. Bendorf K, Friesen CA, Roberts CC: Glucose response to discon- also receiving lipid emulsions.25 Although studies are
tinuation of parenteral nutrition in patients less than 3 years of
somewhat inconclusive, the administration of L-carni-
age. JPEN 20:120-122, 1996
15. Werlin SL, Wyatt D, Camitta B: Effect of abrupt discontinuation tine (at a dose of 10 mg/kg per day) seems to enhance
of high glucose infusion rates during parenteral nutrition. fatty acid oxidation, especially in carnitine-deficient
J Pediatr 124:441-444, 1994 infants. L-carnitine may be useful in infants with
hypertriglyceridemia when other etiologies have been
COMPLICATIONS UNIQUE TO NEONATES: ruled out. Guidelines on monitoring for hypertriglycer-
HYPERTRIGLYCERIDEMIA idemia are predominately empiric.
Background
Practice Guidelines
PN-associated hypertriglyceridemia is usually due to
uncontrolled hyperglycemial or the administration of Complications I I Neonates:
.
,

excessive amounts of lipid emulsion.2 Reduced lipid Hypertriglyceridemia ,

clearance occurs with prematurity, low birth weight,

and sepsis. 1. Lipidemulsion infusions in infants should begin
at 0.5 to 1 g/kg per day and advance at rate of 0.5
Evidence g/kg per day to a maximum of 3 g/kg per day. (A)
2. Lipid emulsion infusion rates should be reduced
Overfeeding of carbohydrates leads to hyperglycemia in premature or septic infants and serum triglyc-
and hypertriglyceridemia. If hypertriglyceridemia eride concentrations should be monitored. (B)
and hyperglycemia coexist, an attempt should be made 3. If serum triglyceride concentrations exceed 200
first to achieve normoglycemia. Lipid clearance in pre-
mature infants is less than half that of mature infants,
mg/dL in the neonate, lipid emulsion infusion
should be suspended and then restarted at a rate
most likely because of limited lipoprotein lipase activ- of 0.5 to 1 g/kg per day. (B)
ity.4 In a prospective study that examined the toler- 4. Intravenous heparin, at a dose of 1 unit/mL of PN
ance of 10% lipid emulsions in 262 infants, a significant
correlation was found between low birth weight and
fluids, should be given to enhance the clearance of
lipid emulsions. (B)
high serum triglyceride concentrations.5 Two studies 5. A trial of carnitine supplementation should be
in low-birth-weight infants reported that sepsis
given to premature infants with unexplained
impairs lipid utilization. 6,7 Increasing the lipid emul- hypertriglyceridemia. (B)
sion dose from 2 to 3 g/kg per day increased serum 6. Infants should receive 20% lipid emulsion to
triglyceride and fatty acid concentrations in septic improve clearance of triglycerides and phospho-
infants more than in nonseptic infants. Lipid dose in
lipids. (B)
premature septic infants may need to be reduced.8
Hypertriglyceridemia may also be seen in acute ill-
ness. Haumont et al reported that the higher phos- REFERENCES
pholipid content found in 10% lipid emulsions in com- 1. Aarsland A, Chinkes D, Wolfe RR: Hepatic and whole-body fat
parison to 20% lipid emulsions is associated with synthesis in humans during carbohydrate overfeeding. Am J
accumulation of cholesterol, triglycerides, and phos- Clin Nutr 65:1774-1782, 1997
2. Andrew F, Chan G, Schiff D: Lipid metabolism in the neonate. I.
pholipids in low-birth-weight infants and can be cor- The effects of Intralipid infusion on plasma triglyceride and free
rected by reverting back to 20% emulsions.69-11 A fatty acid concentrations in the neonate. J Pediatr 88:273-278,
slower rate of lipid emulsion infusion has also been 1976
shown to result in less elevation of serum triglyceride 3. Haumont D, Deckelbaum RJ, Richelle M, et al: Plasma lipid and
levels. 12,13 Lipids can be safely administered on the plasma lipoprotein concentrations in low birth weight infants
first day of life (at a rate of 1 g/kg per day). 14,15 The given parenteral nutrition with twenty or ten percent lipid emul-
sion. J Pediatr 115:787-793, 1989
American Academy of Pediatrics recommends limiting 4. Dhanireddy R, Hamosh M, Sivasubramanian KN, et al: Posthep-
lipid infusion rates to less than 0.25 g/kg per hour in arin lipolytic activity and Intralipid clearance in very low-birth-
low-birth-weight infants, while not exceeding 3 g/kg weight infants. J Pediatr 98:617-622, 1981
5. De Leeuw R, Kok K, De Vries IJ, et al: Tolerance of intravenously
per day. 16 Lipoprotein lipase (LPL) and hepatic lipases administered lipid in newborns. Acta Poediatr Scand 74:52-56,
are needed for lipid clearance. 4,17 Heparin can increase 1985
LPL levels and lipolytic activity, stabilizing triglyceride 6. Park W, Paust H, Schroder H: Lipid infusion in premature
levels.18,19 Unless heparin administration is contraindi- infants suffering from sepsis. JPEN 8:290-292, 1984
 107SA

7. Park W, Paust H, Brosicke H, et al: Impaired fat utilization in serum conjugated bilirubin concentration is one of the
parenterally fed low-birth-weight infants suffering from sepsis.
JPEN 10:627-630, 1986
best established parameters. 3,13,14
8. Dahlstrom KA, Goulet OJ, Roberts RL, et al: Lipid tolerance in
children receiving long-term parenteral nutrition: A biochemical Evidence
an immunological study. J Pediatr 113:985-990, 1988
9. Haumont D, Richelle M, Deckelbaum RJ, et al: Effect of liposo- Reestablishing enteral feedings may lead to a regres-
mal content of lipid emulsions on plasma lipid concentrations in jaundice and normalization of liver function
sion of
low birth weight infants receiving parenteral nutrition. J Pediatr tests (LFTs).15,16
The etiology of PNAC is unknown.
121:759-763, 1992 PNAC may be due to the build-up and toxic effects of
10. Carpentier YA: Intravascular metabolism of fat emulsions. Clin elevated serum and bile levels of lithocholic acid, 17,18 or
Nutr 8:115-125, 1989
11. Griffin E, Breckenridge WC, Kuksis MH, et al: Appearance and a reduction of gastrointestinal hormones blood levels,
characterization of lipoprotein X during continuous Intralipid including cholecystokinin.7,19 Other potential etiolo-
infusion in the neonate. J Clin Invest 64:1703-1712, 1979 gies include amino acid profile changes with PN,2o
12. Kao LC, Cheng MH, Warburton D: Triglycerides, free fatty acids, bacterial overgrowth, and bowel dysfunction due to
free fatty acid/albumin molar ratio, and cholesterol levels in decreased bowel length.10 PNAC is more commonly
serum of neonates receiving long-term lipid infusions: Controlled
seen in children with recurrent sepsis. 6,11,22,23 Treat-
trials of continuous and intermittent regimens. J Pediatr 104:
429-435, 1984 ment or avoidance of sepsis may reduce the risk of
13. Brans WY, Andrew DS, Carrillo DW, et al: Tolerance of fat PNAC,24,25
emulsions in very-low-birth-weight neonates. Am J Dis Child Providing a balanced energy source by altering the
142:145-152, 1988 carbohydrates-to-fat ratio may improve LFTs and
14. Gilbertson N, Kovar IZ, Cox DJ, et al: Introduction of intrave-
reduced PN-associated hepatic complications. 22,26
nous lipid administration on the first day of life in the very low
birth weight neonate. J Pediatr 119:615-623, 1991 Although overfeeding should be avoided,25,29 there is
15. Wells DH, Ferlauto JJ, Forbes DJ, et al: Lipid tolerance in the no convincing evidence that lipid emulsions at normal
very low birth weight infant on intravenous and enteral feed- doses induce cholestasis.27 Limiting lipid emulsion
ings. JPEN 13:263-267, 1989 dose in children to a rate of no more than 3 g/kg per day
17. American Academy of Pediatrics, Committee on Nutrition:
Nutritional needs of low-birth weight infants. Pediatrics 75:976- is recommended to avoid hepatic steatosis. 28
986, 1985 Although animal studies have shown that PN-asso-
18. Zaidan H, Dhanireddy R, Hamosh M, et al: The effect of contin- ciated liver toxicity may be mediated by one or more
uousheparin administration on Intralipid clearing in very low amino acids, particularly methionine, convincing
birth weight infants. J Pediatr 101:599-602, 1982
19. Spear ML, Stahl GE, Hamosh M, et al: Effect of heparin dose and human data are lacking.29,30
infusion rate on lipid clearance and bilirubin binding in prema- No definitive preventive measure is known. Three
ture infants receiving intravenous fat emulsions. J Pediatr 112: studies have shown ursodeoxycholic acid (UDCA) to be
94-98, 1988 safe. It can reduce serum bilirubin levels and, in some
20. Schmidt-Sommerfeld E, Penn D, Wolf H: Carnitine deficiency in
premature infants receiving total parenteral nutrition: Effect of studies, normalize of transaminase levels.31-33 These
L-carnitine supplementation. J Pediatr 931-935, 1983 were retrospective, noncontrolled studies. UDCA is
21. Tibboel D, Delemarre FMC, Przyrembel H, et al: Carnitine defi- only available for oral administration and has limited
ciency in surgical neonates receiving total parenteral nutrition. usage in neonates who cannot absorb oral medications.
J Pediatr Surg 25:418-421, 1990 Intravenous administration of CCK-octapeptide has
22. Larson LE, Olegard R, Ljung ML, et al: Parenteral nutrition in
been reported to have some benefit in conju-
preterm neonates with and without carnitine supplementation.
Acta Anaesthesiol Scand 34:501-505, 1990
reducing
gated bilirubin in some patients with PNAC.34, 5 CCK-
23. Smith RB, Sachan DS, Plattsmier J, et al: Plasma carnitine octapeptide has also been shown to lead to lower con-
alterations in premature infants receiving various nutritional
jugated bilirubin levels if given prophylactically to
regimens. JPEN 12:37-42, 1988
24. Helms RA, Mauer EC, Hay WW Jr et al. Effect of intravenous long-term PN infants.36 These studies were all either
L-carnitine on growth parameters and fat metabolism during retrospective or nonrandomized trials. Antibiotics such
parenteral nutrition in neonates. JPEN 14:448-453, 1990 as metronidazole and oral gentamicin have been used
25. Bonner CM, DeBrie KL, Hug G, et al: Effects of parenteral to prevent bacterial overgrowth. Neonates who
L-carnitine supplementation on fat metabolism and nutrition in received oral gentamicin showed no significan. rise in
premature infants. J Pediatr 126:287-292, 1995
peak or mean direct serum bilirubin concentrations,
compared with a significantly higher mean and peak
COMPLICATIONS UNIQUE TO NEONATES: direct serum bilirubin concentrations in neonates who
HEPATOBILIARY did not receive oral gentamicin.37 Two other studies
showed evidence of a benefit of intravenous metroni-
Background dazole on PNAC.3839 Although phenobarbital has been
PN-associated cholestasis (PNAC) is the most com- used to treat PNAC,4o,41 other studies have shown it to
mon and life-threatening long-term complication of PN worsen the course of PNAC.42,43 Taurine supplemen-
in children. 1-3 About 30% to 60% of children develop tation in premature infants has shown to improve bile
PN-associated hepatic dysfunction during long-term flow and bile acid excretion.44 Levels of taurine are low
PN. The mean time to onset of PNAC was reported to in premature infants and those with short-bowel syn-
be 42 days. 2,5 Factors that correlate with PNAC drome.45 Cooke et a146 evaluated the role of taurine
include prematurity, low birth weight, 6 deficiency in the pathogenesis of PNAC in 20 prema-
lack of enteral feeding,,8 long duration of PN,s- 0 overfeeding ture infants. Taurine at a dose of 10.8 mg/kg/d for 10
recurrent sepsis, 6,11 and short-bowel syndrome.10,12 days did not alter hepatocellular function. Forchielli et
Although several markers indicate PNAC, elevated al4 compared the effects of two different taurine-sup-
108SA

amino acid formulations on PNAC in 11. Manginello FP, Javitt NB: Parenteral nutrition and neonatal
plemented cholestasis. J Pediatr 94:296-298, 1979
infants less than 1 year of age. The overall incidence of
12. Ito Y, Shils ME: Liver dysfunction associated with long-term
cholestasis was 43%, but PNAC was judged by the
total parenteral nutrition in patients with massive bowel resec-
authors as the cause in only 21.4% of infants. The tion. JPEN 15:271-276, 1991
effects of taurine supplementation on reversing or pro- 13. Black DD, Whitington PF, Korones SD: The effect of short-term
tecting against PNAC are inconclusive. Carnitine is total parenteral nutrition on hepatic function in the human
not a routine constituent of PN formulas and carnitine neonate: A prospective randomized study demonstrating alter-
ation of hepatic canalicular function. J Pediatr 99:445-449, 1981
deficiency in PN patients has been suggested as a 14. Beath SV, Needham SJ, Kelly DA, et al: Clinical features and
predisposing factor to liver dysfunction. Two case prognosis of children assessed for isolated small bowel or com-
reports of adults with hepatocyte fatty infiltration bined small bowel and liver transplantation. J Pediatr Surg
showed improvement in LFTs and normalized biliru- 32:459-461, 1997
bin concentrations with carnitine supplementation. 48,49 15. Pereira GR, Sherman MS, DiGiacomo J, et al: Hyperalimenta-
Another report in four adults showed no change in liver tion-induced cholestasis: increased incidence and severity in pre-
mature infants. Am J Dis Chil 135:842-845, 1981
morphology with carnitine, 50 and declines in carnitine 16. Barbier J, Gineste D, Kraimps JL, et al: Complications hepato-
levels probably have little adverse effect.51 Cyclic infu-
biliaires de la nutrition parenterale totale. Chirurgie 118:47-54,
sion of PN over less than 24 hours allows hepatic rest 1992
by reducing continuous and compulsive liver overload- 17. Fouin-Fortunet H, Le Quernec L, Erlinger S, et al: Hepatic
ing and may reduce PNAC.52 Although studies have alterations during total parenteral nutrition in patients with
failed to demonstrate a statistically significant reduc- inflammatory bowel disease: A possible consequence of litho-
tion in cholestasis, levels of bilirubin have been cholate toxicity. Gastroenterology 82:932-937, 1982
observed to fall with conversion to a cyclic regimen.52 18. Farrell MK, Balistreri WF, Suchy FJ: Serum-sulfated litho-
cholate as an indicator of cholestasis during parenteral nutrition
in infants and children. JPEN 6:30-33, 1982
Practice Guidelines 19. Jawaheer G, Pierro A, Lloyd DA, et al: Gall bladder contractility
Complications unique to Neonates: ,
in neonates: Effects of parenteral and enteral feeding. Arch Dis
Child 72:F200-F202, 1995
Hepatobiliary 20. Brown MR, Thunberg BG, Golub L, et al: Decreased cholestasis
with enteral instead of intravenous protein in the very-low-birth
1. Avoidance of overfeeding, early initiation of infant. J Pediatr Gastroenterol Nutr 9:21-27, 1989
enteral nutrition, and prevention and aggressive 21. Simmons MG, Georgeson KE, Figueroa R, et al: Liver failure in
treatment of sepsis should be used to minimize parenteral nutrition-dependent children with short bowel syn-
the incidence of PN associated cholestasis. (B) drome. Trans Proc 28:2701, 1996
22. Buchmiller CE, Kleiman-Wexler RL, Ephgrave KS, et al: Liver
2. Administration of ursodeoxycholic acid or chole-
dysfunction and energy source: Results of a randomized clinical
cystokinin should be considered if EN cannot be trial. JPEN 17:301-306, 1993
given. (B) 23. Clark PJ, Bail MJ, Kettlewell MG: Liver associated tests in
3. PN should be administered using a cyclic regimen patients receiving parenteral nutrition. JPEN 15:54-59, 1991
when possible if long-term use is anticipated. (C) 24. Beau P, Barrioz T, Ingrand P: Total parenteral nutrition-related
cholestatic hepatopathy, is it an infectious disease? Gastroen-
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25. Messing B, Colombel JF, Heresbach D, et al: Chronic cholestasis
1. Rodgers BM, Hollenbeck JI, Donnelly WH, et al: Intrahepatic
and macronutrient excess in patients treated with prolonged
cholestasis with parenteral alimentation. Am J Surg 131:149-
155, 1976 parenteral nutrition. Nutrition 8:30-35, 1992
26. Meguid MM, Akahoshi MP, Jeffers S, et al: Amelioration of
2. Hodes JE, Grosfeld JL, Weber TR, et al: Hepatic failure in
infants on total parenteral nutrition (TPN): Clinical and his- metabolic complications of conventional total parenteral nutri-
tion. Arch Surg 119:1294-1298, 1984
topathologic observations. J Pediatr Surg 17:463-468, 1982
3. Benjamin DR: Hepatobiliary dysfunction in infants and children 27. Wagner WH, Lowry AC, Silberman H: Similar liver function
associated with long-term total parenteral nutrition. A clinico- abnormalities occur in patients receiving glucose-based and
pathologic study. Am J Clin Pathol 76:276-283, 1981 lipid-based parenteral nutrition. Am J Gastroenterol 78:199-
4. Suita S, Ikeda K, Nagasaki A, et al: Follow-up studies of children 202, 1983
treated with a long-term intravenous nutrition (IVN) during the 28. Reif S, Tano M, Oliverio R, et al: Total parenteral nutrition-
neonatal period. J Pediatr Surg 17:37-42, 1982 induced steatosis: reversal by parenteral lipid infusions. JPEN
5. Beale E, Nelson R, Bucciarelli R, et al: Intrahepatic cholestasis 15:102-104, 1991
associated with parenteral nutrition in premature infants. Pedi- 29. Vileisis RA, Inwood RJ, Hunt CE: Prospective controlled study of
atrics 64:342-347, 1979 parenteral nutrition-associated cholestatic jaundice: Effect of
6. Beath S, Davies P, Papadpoulou A, et al: Parenteral nutrition- protein intake. J Pediatr 96:893-897, 1980
related cholestasis in postsurgical neonates: Multivariate anal- 30. Moss RL, Haynes AL, Pastuszyn A, et al: Methionine infusion
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8. Colomb V, Goulet O, Rambaud C, et al: Long-term parenteral ursodeoxycholic acid treatment. J Pediatr Endocrinol Metab
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24:1054-1055, 1992 32. Spagnuolo MI, Iorio R, Vegnente A et al: Ursodeoxycholic acid for
9. Drongowski RA, Coran AG: An analysis of factors contributing to the treatment of cholestasis in children on long-term total par-
the development of total parenteral nutrition-induced cholesta- enteral nutrition: A pilot study. Gastroenterology 111:716-719,
sis. JPEN 13:586-589, 1989 1996
10. Cavicchi M, Beau P, Crenn P, et al: Prevalence of liver disease 33. Narkewicz MR, Smith D, Gregory C, et al: Effect of ursodeoxy-
and contributing factors in patients receiving home parenteral cholic acid therapy on hepatic function in children with intrahe-
nutrition for permanent intestinal failure. Ann Intern Med 132: patic cholestatic liver disease. J Pediatr Gastroenterol Nutr
525-532, 2000 26:49-55, 1998
 109SA

34. Rintala RJ, Lindahl H, Pohjavuori M: Total parenteral nutri- mia, hyperphosphatemia, elevated serum alkaline
tion-associated cholestasis in surgical neonates may be reversed
phosphatase, low-normal plasma parathyroid hor-
by intravenous cholecystokinin: A preliminary report. J Pediatr
Surg 30:827-830, 1995 mone, and normal 25-hydroxyvitamin D and low 1,25
35. Teitelbaum DH, Han-Markey T, Schumacher RE: Treatment of hydroxyvitamin D plasma concentrations. 1,5 The etiol-
parenteral nutrition associated cholestasis with cholecystokinin- ogy of bone demineralization or inadequate bone
octapeptide. J Ped Surg 30:1082-1085, 1995 matrix mineralization is multifactorial and often asso-
36. Teitelbaum DH, Han-Markey T, Drongowski R, et al: Use of
ciated with calcium, phosphorus, and vitamin D defi-
cholecystokinin to prevent the development of parenteral nutri-
tion-associated cholestasis. JPEN 20:100-103, 1997 ciencies.6,7 Aluminum accumulation in boneS8 and
37. Kaufman SS, Loseke CA, Lupo JV, et al: Influence of bacterial excessive vitamin D may also contribute. 9
overgrowth and intestinal inflammation on duration of paren-
teral nutrition in children with short bowel syndrome. J Pediatr
131:356-361, 1997 Evidence
38. Spurr SG, Grylack LJ, Mehta NR: Hyperalimentation-associated
neonatal cholestasis: Effect of oral gentamicin. JPEN 13:633- Hypocalcemia in MBD patients may be due to
636, 1989 decreased calcium intake or increased urinary calcium
39. Kubota A, Okada A, Imura K, et al: The effect of metronidazole elimination. Because of solubility limitations, calcium
on TPN-associated liver dysfunction in neonates. J Pediatr Surg
and phosphate in neonatal PN are generally inade-
6:618-621, 1990
40. Capron JP, Gineston JL, Herve MA, et al: Metronidazole in quate to meet the needs for optimal bone growth. There
prevention of cholestasis associated with total parenteral nutri- are few clinical trials investigating MBD in infants and
tion. Lancet 1:446-447, 1983 children and most data are derived from studies in
41. South M, King A, Chir B: Parenteral nutrition-associated cho-
adult patients.
lestasis: recovery following phenobarbitone. JPEN 11:208-209,
1987 Investigators have shown that very low birth weight
42. Gleghorn EE, Merritt RJ, Subramanian N, et al: Phenobarbital infants who received high calcium (1.68 mM/dL) and
does not prevent total parenteral nutrition-associated cholesta- phosphate (2 mM/dL) in their daily PN had greater
sis in noninfected neonates. JPEN 10:282-283, 1986 calcium and phosphate retention and greater bone
43. Nemeth A, Wikstrom SA, Strandvik B: Phenobarbital can aggra-
vate a cholestatic bile acid pattern in infants with obstructive
mineral content.7,lO,11 Hypocalcemia due to hypercal-
cholangiopathy. J Pediatr Gastroenterol Nutr 10:290-297, 1990 ciuria has been consistently reported in patients
44. Okamoto E, Rassin DK, Zucker CL, et al: Role of taurine in receiving PN. Factors known to promote hypercalci-
feeding the low-birth-weight infant. J Pediatr 104:936-940, uria include increased calcium intake, decreased phos-
1984
45. Cooper A, Betts JM, Pereira GR, et al: Taurine deficiency in the phate supplementation, excessive amino acid infusion,
severe hepatic dysfunction complicating total parenteral nutri-
chronic metabolic acidosis, and cyclic PN infusion. A
tion. J Pediatr Surg 19:462-465, 1984 reduction in calciuria and bone pain can be achieved by
46. Cooke RJ, Whitington PF, Kelts D: Effect of taurine supplemen- reducing calcium intake and altering the calcium-to-
tation on hepatic function during short-term parenteral nutri-
tion in the preterm infant. J Pediatr Gastroenterol Nutr 3:234-
phosphate ratio from 1:1.5 to 1:2.12 Several studies
have correlated amino acid intake with hypercalci-
238, 1984
47. Forchielli NL, Gura KM, Sandler R, et al: Aminosyn PF or uria.5,13,14 Chronic metabolic acidosis from excessive
Trophamine: Which provides more protection from cholestasis amounts of amino acids or from D-lactic acidosis can
associated with total parenteral nutrition? J Pediatr Gastroen- lead to MBD by direct loss of bone involving buffering
terol Nutr 21:374-382, 1995 bone systems or impaired vitamin D metabolism. 15,16
48. Palombo JD, Schnure F, Bistrian BR, et al: Improvement of liver
function tests by administration of L-carnitine to a carnitine-
Two studies comparing cycled versus noncycled
deficient patient receiving home parenteral nutrition: A case administration of PN showed that cycling increases
report. JPEN 11:88-92, 1987 bone mineral IOSS.14,17 In one of these studies, mea-
49. Worthley LI, Fishlock RC, Snoswell AM: Carnitine deficiency surement of bone mass by photon absorbtiometry
with hyperbilirubinemia, generalized skeletal muscle weakness
and reactive hypoglycemia in a patient on long-term total par-
showed reduced vertebral bone mass but not wrist
enteral nutrition: treatment with intravenous L-carnitine. JPEN bone mass in long-term (55.2 8.7 months) PN
7:176-180, 1983 patients.
50. Bowyer BA, Miles JM, Haymond MW, et al: L-carnitine therapy Small amounts of aluminum are present in calcium
in home parenteral nutrition patients with abnormal liver tests and phosphate salts, vitamins, heparin, and trace ele-
and low plasma carnitine concentrations. Gastroenterology
ment solutions.18 Aluminum in PN solutions may
94:434-438, 1988
51. Moukarzel AA, Dahlstrom KA, Buchman AL, et al: Carnitine result in a decreased rate of bone formation. 1819 Koo et
status of children receiving long-term total parenteral nutrition: al2 found that aluminum accumulated at the miner-
a longitudinal prospective study. J Pediatr 120:759-762, 1992
alization front of bones in premature infants. Measure-
52. Collier S, Crough J, Hendricks, et al. Use of parenteral nutrition
ment of serum aluminum concentration can help deter-
in infants less than 6 months of age. Nutr Clin Pract 9:65-68,
1994 mine the role of aluminum excess when MBD is
suspected in long-term PN patients. Aluminum toxic-
COMPLICATIONS UNIQUE TO NEONATES: ity may be a particular problem in young infants whose
METABOLIC BONE DISEASE kidneys cannot adequately excrete aluminum com-
Background pared with older children. The FDA has recommended
restriction of aluminum contamination in large volume
Metabolic bone disease (MBD) has been reported in parenterals to a maximum of 25 rLg/L. Patients who
infants and premature neonates receiving PN. 1,2 The have elevated aluminun levels should have parenteral
incidence of MBD is unknown, but it is common in sources of aluminum investigated.21

patients receiving long-term PN. 3,4 Biochemical evi- -

Underlying conditions and concurrent medications

dence of MBD may include hypercalciuria, hypercalce- may also be responsible or predispose to MBD. These
110SA

are especially prevelant in patients with malabsorp- 6. Leape LL, Valaes T: Rickets in low birth weight infants receiving
total parenteral nutrition. J Pediatr Surg 11:665-674, 1976
tion, glucocorticoid administration, and antineoplastic 7. Prestridge LL, Schanler RJ, Shulman R, et al: Effect of paren-
agents.19,21 teral calcium and phosphorus on mineral retention and bone
Several reports of improvement of MBD after vita- mineral content in very low birth weight infants. J Pediatr
min D removal from PN suggest a possible role of 122:761-768, 1993
vitamin D in the development of MBD. 9,22 If this is 8. Vargas JH, Klein GL, Ament ME, et al: Metabolic bone disease of
total parenteral nutrition: Course after changing from casein to
attempted, it is advised that patients have their amino acids in parenteral solutions with reduced aluminum
plasma PTH and 25-hydroxyvitamin D and 1,25 content. Am J Clin Nutr 48:1070-1078, 1988
hydroxyvitamin D concentrations measured. If PTH 9. Shike M, Sturtridge WC, Tam CS, et al: A possible role for
and 1,25 hydroxyvitamin D concentrations are low and vitamin D in the genesis of parenteral nutrition-induced meta-
25 hydroxyvitamin D concentrations are normal, then bolic bone disease. Ann Intern Med 95:560-568, 1981
10. Wood RJ, Sitrin MD, Cusson GJ, et al: Reduction of total paren-
vitamin D should be withdrawn from the PN solution. teral nutrition-induced urinary calcium loss by increasing the
phosphorus in the total parenteral nutrition prescription. JPEN
Practice Guidelines
.
10:188-190, 1986
11. Sloan GM, White DE, Brennan MF: Calcium and phosphorus
Complications Unique to . ,
metabolism during total parenteral nutrition. Ann Surg 197:
Metabolic Bone l , ,

1-6, 1983
12. Larchet M, Garabedian M, Bourdeau A et al: Calcium metabo-
lism in children during long-term total parenteral nutrition: The
1. Calcium and phosphate should be provided in influence of calcium, phosphorus, and vitamin D intakes. J Pedi-
adequate amounts to assure optimal bone miner- atr Gastroenterol Nutr 13:367-375, 1991
alization in long-term PN patients. (A) 13. Bengoa JM, Sitrin MD, Wood RJ, et al: Amino acid-induced
2. Serum aluminum concentrations should be mea- hypercalciuria in patients on total parenteral nutrition. Am J
sured whenever unexplained MBD is present in Clin Nutr 38:264-269, 1983
14. Lipkin EW, Ott SM, Chesnut CH, et al: Mineral loss in the
long-term PN patients. (B) parenteral nutrition patient. Am J Clin Nutr 47:515-523, 1988
3. In patients with low PTH and 1,25 hydroxyvita- 15. Cunningham J, Fraher LJ, Clemens TL, et al: Chronic acidosis
min D concentrations and normal 25 hydroxyvi- with metabolic bone disease. Am J Med 73:199-204, 1982
tamin D concentration with MBD, vitamin D 16. Karton MA, Rettmer R, Lipkin EW, et al: D-Lactate and meta-
bolic bone disease in patients receiving long-term parenteral
should be removed from the PN solution. (B) nutrition. JPEN 13:132-135, 1989
17. Wood RJ, Bengoa JM, Sitrin MD, et al: Calciuric effect of cyclic
versus continuous total parenteral nutrition. Am J Clin Nutr
REFERENCES
41:614-619, 1985
1. The TS, Kollee LA, Boon JM, et al: Rickets in a preterm infant 18. Koo WWK, Kaplan LA, Horn J, et al: Aluminum on parenteral
during intravenous alimentation. Acta Pediatr Scand 72:769-71, nutrition solution-sources and possible alternatives. JPEN
1993 10:591-595, 1986
2. Kien CL, Browning C, Jona J, et al: Rickets in premature infants 19. Klein GL: Metabolic bone disease of total parenteral nutrition.
receiving parenteral nutrition: A case report and review of the Nutrition 14:149-152, 1998
literature. JPEN 6:152-156, 1982 20. Koo WWK, Kaplan LA, Bendon R, et al: Response to aluminum
3. Shike M, Harrison JE, Sturtridge WC, et al: Metabolic bone in parenteral nutrition during infancy. J Pediatr 109:883-887,
disease in patients receiving long-term total parenteral nutri- 1986
tion. Ann Intern Med 92:343-350, 1980 21. Seidner DL, Licata A: Parenteral nutrition associated metabolic
4. Shike M, Shils ME, Heller A. et al: Bone disease in prolonged bone disease: Pathophysiology, evaluation, and treatment. Nutr
parenteral nutrition: Osteopenia without mineralization defect. Clin Pract 15:163-170, 2000
Am J Clin Nutr 44:89-98, 1986 22. Verhage AH, Cheong WK, Allard JP, et al: Increase in lumbar
5. De Vernejoul MC, Messing B, Modrowski D, et al: Multifactorial spine bone mineral content in patients on long-term parenteral
low remodeling bone disease during cyclic total parenteral nutri- nutrition without vitamin D supplementation. JPEN 19:431-
tion. J Clin Endocrinol Metab 60:109, 1985 436, 1995
 Section XIII: Specific Guidelines for Disease-Pediatrics

NECROTIZING ENTEROCOLITIS study subjects. Once NEC develops, enteral feedings

should be stopped and PN initiated.
Background
Necrotizing enterocolitis (NEC) is the most commonL Practice Guidelines
gastrointestinal emergency in the neonatal popula- NecrotizingEnterocolitis
i
tion. It is characterized by abdominal distention and l
tenderness, pneumatosis intestinalis, bloody stools,~ 1. Newborns with NEC are at nutrition risk and
gangrenous or perforated bowel, sepsis, and shock.2 should formal nutrition assessment with
The primary risk factor for NEC is prematurityT undergo
development of a nutrition care plan. (B)
because approximately 90% of all cases occur in this
2. The rate of advancement of EN feeding incre-
population.3 Other risk factors associated with this, ments should be kept to less than 35 cc/kg per day
disease include aggressive enteral feedings, infectious,
to decrease the risk of NEC. (B)
agents, and hypoxic-ischemic insults. 3. Fresh human milk feeding should be encouraged
in neonates. (B)
Evidence 4. PN should be initiated in infants when NEC is

Through retrospective chart review and a case controlj diagnosed. (B)

study, rapid advancement of EN has been associatedl
with development of NEC.4 NEC is associated with feed- .
REFERENCES
ing volume increments greater than 35 cc/kg per day. 1. Neu J, Weiss MD: Necrotizing enterocolitis: Pathophysiology
Recently, a prospective randomized trial examined slow and prevention. JPEN 23:S13-S17, 1999
(15 cc/kg per day) versus fast (35 cc/kg per day) incre- 2. Neu J: Necrotizing enterolcolitis: The search for a unifying
ments in enteral feeding in 185 formula-fed infants with1 pathogenic theory leading to prevention. Pediatr Clin N Am
birth weights ranging from 501 to 1500 g.5 This study 43:409-432, 1996
showed that the incidence of NEC was not significantly 3. Israel EJ: Neonatal necrotizing enterolcolitis, a disease of the
immature intestinal mucosal barrier. Acta Paediatr Suppl 396:
different between the two groups. Of note, the fast group
27-32, 1994
did reach goal feedings and regained their birth weight 4. McKeown RE, Marsh TD, Amaranth W, et al: Role of delayed
sooner than the slow group, but at discharge there were and of feeding increments in necrotizing enterocolitis.
feeding
no significant age differences between the groups. J Pediatr 121:764-770, 1992
Infection is a necessary component of NEC; various 5. Rayyis SF, Ambalavana N, Wright L, et al: Randomized trial of
studies support this assertion. Gram-negative rods, "slow" versus "fast" feed advancements on the incidence of necro-
such as Klebsiella, Escherichia coli, or Enterobacter, tizing enterocolitis in very low birth weight infants. J Pediatr
are frequently isolated from infants with NEC.6
6 134:293-297, 1999
6. Bell MJ, Shackelford RD, Feigin J, et al: Epidemiologic and
Human milk feeding has been shown to decrease the bacteriologic evaluation of neonatal necrotizing enterocolitis.
incidence of NEC, perhaps because of the immune- -
J Pediatr Surg 14:1-4, 1979
7. Lucas A, Cole TJ: Breast milk and neonatal necrotizing entero-
enhancing effects of breast milk, which contains immu- colitis. Lancet 336:1519-1523, 1990
noglobulins, lysozyme, macrophages, and PAF acetyl 8. Nowicki PT, Nankervis CA: The role of the circulation in the
hydrolase. pathogenesis of necrotizing enterocolitis. Clin Perinatol 21:219-
Clinical and physiologic evidence support the role off234, 1994
hypoxic and/or ischemic injury as a secondary, rather 9. YanowitzinT, Yao A, Pettigrew KD,infants.
et al: Postnatal hemodynamic
J Appl Physiol 87:370-
than primary, contributing factor to NEC.2 Bacterial changes very-low birthweight
toxins could initiate endothelial disruption in infants
,380, 1999
immature vasculature, resulting in vascular compro-
mise.8 A recent study examining postnatal hemody- -

SHORT BOWEL SYNDROME

namic blood flow in very low birth weight infants con-
cluded that early feedings do not significantly influence~ Background
postnatal splanchnic blood flow in the first week off Short bowel syndrome (SBS) has been defined as the
life.9 One infant in the study experienced NEC, but hisi anatomic or functional absence of more than 50% of the
blood flow velocity did not differ from the other 19) normal small intestine.~ This is a good working defini-

111SA
112SA

tion because SBS cannot strictly be defined by anat- t)ination of factors including carbohydrate malabsorp-
omy. Accurate measurement of remaining bowel is dif- tion with increased delivery of nutrients to the colon,
ficult, and absorption of nutrients may not correlate 1iigh carbohydrate intake, colonic flora of the type that
with bowel length if the remaining bowel is damaged. I)roduce D-lactic acid, decreased colonic motility, and
There is typically an attempt at the time of intestinal i mpaired D-lactate metabolism.23
resection to save as much bowel as possible; however, The optimal formula for feeding infants and children
some of the salvaged bowel may not function nor- Nvith SBS is not known. Elemental amino acid based

mally.2 In an animal model, intestinal surgery and formulas are suggested by some clinicians and have
anastomosis without resection has a significant affect t)een shown to be well tolerated. 24,25
3
on gut growth, maturation, and disaccharidase activity.3 There is no agreement on the amount of stool
Intestinal loss and injury can result from necro- ()output that should be accepted. Usually, limits

tizing enterocolitis, mid-gut volvulus, abdominal E;hould be imposed on feeding once the stool output
wall defects, intestinal atresias, vascular infarct, E,xceeds 45 ml/kg. per day. However, a higher volume of
cloacal extrophy, long-segment Hirschsprungs dis- E,tool output may be acceptable.26 Careful fluid and elec-

ease, or trauma. 1,4 The injury may not only be t;rolyte management is essential as dehydration can occur
reflected in abnormal absorption, but also in altered iapidly.
motility. Premature infants who undergo bowel Long-term survival of infants and children with SBS
resection may have more potential than term (lepends on the ability of the intestine to adapt and
infants for intestinal growth. The mean length of t;he remaining intestine to increase its absorptive
small bowel is 142 22 cm in infants 19 to 27 weeks (~apacity.27 Many agents have been promoted as sup-

gestational age, 217 24 cm in infants between 27 Iporting gut adaptation; hopefully, clinical trials in
and 35 weeks gestational age, and 304 44 cm in i nfants and children will be forthcoming.
infants 35 weeks gestational age and older.55
Infants and children with SBS have less surface area
lwidence
for absorption of nutrients and decreased transit time.
Malabsorption of nutrients results in excessive fluid PN is used to manage SBS until bowel adaptation
and electrolyte losses from stool output. The nutrients iand gut growth is sufficient to permit normal growth
malabsorbed will depend on the area of the bowel iwith EN or oral nutrition.~8 Because of the life-saving
resected or damaged. Reviews suggest that infants inecessity to administer PN acutely in patients with
without an ileocecal valve are dependent on PN longer I3BS, most of the studies on nutrition management
those with an intact valve.6-9 ;3trategies for SBS involve retrospective chart review
PN is used for the initial management of SBS. This iarticles or cohort analyses. Most pediatric centers do
use of replacement fluids may be necessary as well if ]lot have sufficient numbers of these patients to per-
fluid and electrolyte losses are high. Urine electrolytes Iform clinical trials. Cross-over designs for intestinal
are more helpful in determining total body sodiumiadaptation may encounter difficulties because of the
status than serum electrolytes. Urine electrolytes will Ilingering effect of one treatment on another. It is dif-
reflect total body status if renal function is normal. jIficult to match patients exactly, as gestational age and
Urinary changes in sodium excretion will occur before Ilength of time from initial resection may affect adap-
any change is noted in serum sodium concentration. 1tation. Multicenter trials appear to be the best way to
Sodium-depleted infants do not grow normally.10-13 I~onduct nutrition research for infants and children
Sodium can be added to PN or EN formulations and with SBS.28 The use of a coordinated interdisciplinary
1

urine electrolytes monitored to titrate the amount of 1team for the management of SBS has been shown to be
supplementation needed. Zinc losses from ileostomy 1useful in maintaining growth and decreasing depen-
fluid may be 12 mg/L and 17 mg/L from diarrhea.&dquo;,5 Idence on PN.28
These losses should be considered when developing the Optimal timing of the initiation of EN has not been
nutrition care plan. < established. A controlled trial of 11 infants with intes-

Hypersecretion can be seen in infants and children 1tinal disease showed improved absorption of nutrients
after a major intestinal resection and the start of i(fat, nitrogen, calcium, zinc, and copper) as well as
enteral feedings. 16 An H2 blocker can be added to PN to :improved weight gain with the use of continuous ver-
treat the associated gastric acid hypersecretion.17,18 sus intermittent administration of EN.29 Hydrolyzed
Bacterial overgrowth may occur as a result of poor :formulas may also be better tolerated by some
motility and dilated bowel. Stasis of intestinal contents patients.24 There is no agreement on the type of for-
leads to bacterial overgrowth, which can alter absorp- mula or breast milk to be used to treat SBS in neonates
tion and cause increased stooling.lg The ~3C-xylose ; and infants. There has been a prospective, randomized,
breath test has been used to diagnose overgrowth. 20 < cross-over design study of two protein hydrolysate for-
For infants prone to overgrowth, routine scheduled mulas given by continuous infusion. Energy absorption
antibiotic treatment may be useful. D-Lactic acidosis was the same with both formulas, but differences in
has been reported in children with bacterial over- the amount of malabsorbed carbohydrate existed. The
growth, causing metabolic acidosis, drowsiness, and authors suggested use of a hydrolysate formula with a
confusion. 21,22 This diagnosis should be considered in a lower percentage of carbohydrate and a higher percent-
child with SBS who presents with metabolic acidosis, age of fat.3o
high serum anion gap, normal lactate level, and Many nutrients and factors have been discussed as
without urinary ketones.23 It may result from a com- possible pro-adaptation agents. Until clinical trials on
 113SA

pediatric patients occur, recommendations cannot be 18. Redel CA, Schulman RJ: Gastrointestinal disorders. IN Pediat-
made concerning their use. ric Enteral Nutrition. Baker RD Jr, Baker SS, Davis AM (eds).
Chapman & Hall, New York, 1997, p 315
19. Kaufman SS, Loseke CA, Lupo JV, et al: Influence of bacterial
Practice Guidelines
.

overgrowth and intestinal inflammation on duration of paren-

o :i ~ teral nutrition in children with short bowel syndrome. J Pediatr
i ,

131:356, 1997
20. Dellert SF, Nowicki MJ, Farrell MK, et al: The 13C-xylose breath
1. Children with SBS are at nutrition risk and test for the diagnosis of small bowel bacterial overgrowth in
children. J Pediatr Gastroenterol 25:153, 1997
should undergo nutrition screening to identify 21. Perlmutter DH, Boyle JT, Campos JM, et al: D-lactic acidosis in
those who require formal nutrition assessment children: An unusual metabolic complication of small bowel
with development of a nutrition care plan. (B) resection. J Pediatr 102:234, 1983
2. PN should be initiated as soon as possible postop- 22. Gurevitch J, Sela B, Jonas A, et al: D-lactic acidosis: A treatable
encephalopathy in pediatric patients. Acta Paediatrica 82:11,
eratively in patients with SBS. (B) 1993
3. Continuous gastric feedings should be used ini- 23. Uribarri J, Oh MS, Carroll HJ: D-Lactic acidosis. A review of
tially in children with SBS receiving EN. (B) clinical presentation, biochemical features, and pathophysiolog-
ical mechanisms. Medicine. 77:73-82, 1998
4. Patients must be monitored for macronutrient
24. Bines J, Francis D, Hill D: Reducing parenteral requirement in
and micronutrient deficiencies. (C) children with short bowel syndrome: Impact of an amino acid
5. A coordinated interdisciplinary team approach based complete infant formula. J Pediatr Gastroenterol Nutr
should be involved with the management of SBS 26:123-128, 1998
25. Vanderhoof JA, Matya SM: Enteral and parenteral nutrition in
patients. (B) patients with short bowel syndrome. Eur J Surg 9:214-219,
1999
26. Alkalay AL, Fleisher DR, Pomerance JJ, et al: Management of
REFERENCES premature infants with extensive bowel resection with high vol-
ume enteral infusates. Israel J Med Sci 31:298, 1995
1. Ziegler MM: Short bowel syndrome in infancy: Etiology and 27. Piena-Spoel M, Shaman-Koendjibharie M, Yamanouchi T, et al:
management. Clin Perinatol 13:167 ,1986
2. Taylor SF, Sokol RJ: Infants with short bowel syndrome. IN "Gut-feeling" or evidence based approaches in the evaluation and
treatment of human short bowel syndrome. Pediatr Surg Int
Neonatal Nutrition and Metabolism. Hay WW (ed). Mosby, St
16:155-164, 2000
Louis, 1991, p 437 28. Koehler AN, Yaworski JA, Gardner M, et al: Coordinated inter-
3. Stringel G, Uuay R, Guertin L: The effect of intestinal anasto- disciplinary management of pediatric intestinal failure: A 2 year
mosis on gut growth and maturation. J Pediatr Surg 24:1086, review. J Pediatr Surg 35:380-385, 2000
1989 29. Parker P, Stroop S, Greene H: A controlled comparison of con-
4. Georgeson KE, Breaux CW Jr: Outcome and intestinal adapta- tinuous versus intermittent feeding in the treatment of infants
tion in neonatal short bowel syndrome. J Pediatr Surg 27:344- with intestinal disease. J Pediatr 1981, 99:360-364, 1981
348, 1992 30. Galeano NF, Lepage G, Leroy C, et al: Comparison of two special
5. Touloukian RJ, Smith GJ: Normal intestinal length in preterm infant formulas designed for the treatment of protracted diar-
infants. J Pediatr Surg 18:720, 1983 rhea. J Pediatr Gastroenterol Nutr 7:76-83, 1998
6. Georgeson KE, Breaux CW Jr: Outcome and intestinal adapta-
tion in neonatal short-bowel syndrome. J Pediatr Surg 27:344, LIVER DISEASE
1992
7. Goulet OJ, Revillon Y, Jan D, et al: Neonatal short bowel syn- Background
drome. J Pediatr 119:18, 1991
8. Ladd AP, Rescoria FR, West KW, et al: Long term follow-up after Nutrition management of the infant and child with
bowel resection for necrotizing enterocolitis: Factors affecting liver disease depends on the type of liver disease.
outcome. J Pediatr Surg 33:967, 1998 Nutrition disturbances are uncommon in acute liver
9. Chaet MS, Farrell MK, Ziegler MM, et al: Intensive nutrition
disease, but common and often severe in chronic liver
support an remedial surgical intervention for extreme short disease. The nutritional abnormalities that accompany
bowel syndrome. J Pediatr Gastroenterol Nutr 19:295, 1994
10. Mews CF: Topics in neonatal nutrition. Early ileostomy closure liver disease in children, and in the management have
to prevent chronic salt and water losses in infants. J Perinatol been reviewed in detail by several authors.l-3
12:297, 1992 In acute liver disease, weight loss may occur because
11. Sacher P, Hirsign T, Gressler J, et al: The importance of oral of vomiting and anorexia, but malnutrition is uncom-
sodium replacement in ileostomy patients. Prog Pediatr Surg
mon. In chronic liver diseases of childhood, there
24:226, 1989
12. Bower TR, Pringle KC, Soper RT, et al: Sodium deficit causing are multiple causes of malnutrition, including (1)
decreased weight gain and metabolic acidosis in infants with decreased intake secondary to nausea, vomiting,
ileostomy. J Pediatr Surg 23:567, 1988 anorexia, ascites, and depression; (2) impaired nutri-
13. Schwarz KB, Tennberg JL, Bell MJ, et al: Sodium needs of
infants and children with ileostomy. J Pediatr 102:509, 1983
ent digestion and absorption secondary to bile salt
14. Shulman RJ: Zinc and copper balance studies in infants receiv- deficiency and pancreatic insufficiency that accompa-
ing TPN. Am J Clin Nutr 49:879, 1989 nies some liver diseases; and (3) increased energy
15. Solomons NW, Ruz M: Essential and beneficial trace elements in
requirements secondary to hypermetabolism and infec-
pediatric parenteral nutrition. IN Pediatric Enteral Nutrition. tion.4 Adults with chronic liver disease exhibit acceler-
Baker RD Jr, Baker SS, Davis AM (eds). Chapman & Hall, New
York, 1997, p 181 ated protein breakdown and inefficient protein synthe-
16. Hyman PE, Everett SL, Harada T: Gastric acid hypersecretion SiS5; whether or not these phenomena occur in children
in short bowel syndrome in infants: Association with extent of with chronic liver disease is unknown.
resection and enteral feeding. J Pediatr Gastroenterol Nutr Nutrition assessment in infants and children with
5:191-197, 1986 chronic liver disease is important but problematic.
17. Hyman PE, Garvey TQ III, Harada T: Effect of ranitidine on
gastric acid hypersecretion in an infant with short bowel syn- Useful parameters include height, upper extremity
drome. J Pediatr Gastroenterol Nutr 4:316-319, 1985 anthropometrics, subjective assessment, and 24-hour
114SA

dietary recall. A decrease in height-for-age percentile atorrhea. 16 It should be noted that medium-chain tri-
has been shown to be a useful indicator of the duration glycerides do not contain essential fatty acids, and thus
of malnutrition in children with chronic liver disease. 6 long-chain fatty acids must also be administered. Poor
Body weight can be misleading because of the contri- absorption of fat soluble vitamins is common, and vita-
bution of hepatosplenomegaly, ascites, and edema, min supplementation is an important part of the man-
which can mask underlying weight IOSS.7 Lower agement of these children.
extremity anthropometrics can be erroneous because of Although vitamin A is malabsorbed in the presence
edema. of cholestasis, plasma retinol concentrations may be
Because the plasma proteins conventionally used in misleading. Mourey et al 17 have suggested that the
nutrition assessment (eg, albumin, prealbumin, trans- molar ratio of retinol to retinol-binding protein may be
ferrin) are synthesized by the liver, their concentration better than plasma retinol in assessing the vitamin A
can be depressed by liver failure and/or malnutrition. status of children with liver disease. According to
In fact, in adults it has been shown that the plasma Heubi et al,l8 25-OH vitamin D3 is better absorbed by
concentration of these proteins correlates more with cholestatic children than vitamin D2, and thus is the
the severity of liver injury rather than with the degree supplement of choice for such children. Sokol et all9
of malnutrition as assessed by anthropometric meth- have demonstrated that vitamin E-deficiency induced
ods.8 Nitrogen balance studies done in adults with neuropathy is common in children with chronic cho-
chronic liver disease are difficult to interpret because lestasis and is preventable by administration of D-a-
decreased hepatic urea synthesis leads to underesti- tocopherol polyethylene glycol-1000 succinate, the
mation of urinary nitrogen losses9; presumably, such form of vitamin E that is best absorbed by children
studies would also be problematic in children, as would with chronic cholestasis. Vitamin K deficiency is a pre-
the use of immune parameters as an index of nutrition ventable cause of coagulopathy in infants with chronic
status cholestasis2; oral supplements may suffice, although
Although plasma concentrations of vitamins are parenteral vitamin K may be necessary. The specific
often used to nutrition status, there are several
assess amounts of fat-soluble vitamin supplementation recom-
drugs given to children with chronic liver disease that mended for oral and parenteral administration as well as
affect the blood concentrations of some vitamins. For the method of monitoring have been detailed in a recent
example, bile-acid binding resins such as colestipol and review article.21
cholestyramine may interfere with the absorption of Although decreased intake and malabsorption sec-
the fat-soluble vitamins A, D, E, and K. Diphenylhy- ondary to enteropathy may predispose children with
dantoin and phenobarbital increase hepatic metabo- chronic liver disease to deficiencies of the water-soluble
lism of vitamin D, thereby lowering the plasma con- vitamins, there are no data to support this postulate.
centration of 25-hydroxy-cholecalciferol. Adults with chronic liver disease are prone to develop
deficiency of zinc and/or selenium, but similar data in
children are not available. In theory, children with
Evidence
liver disease are at risk for iron deficiency because of
Protein metabolism is impaired in children with bil- recurrent variceal hemorrhage and for calcium defi-
iary atresia, the most common indication for liver ciency because of vitamin D deficiency. However, cal-
transplantation in the pediatric age group. Typically, cium absorption in these children is normal.22
in healthy infants, about 4% to 9% of overall energy
expenditure is due to protein oxidation.ll In contrast, Special Considerations
in children with biliary atresia, 17% of overall energy
expenditure is due to protein oxidation, and nitrogen In the setting of acute liver failure, despite the risk of
balance is near zero.4 In patients with chronic liver hyperammonemia, it is important not to overrestrict
disease, plasma concentrations of the aromatic amino protein, because endogenous ammoniagenesis can
acids are elevated, and those of the branched-chain result from catabolism of body proteins. Infants should
amino acids depressed.&dquo; Pierro et a14 have shown that be given 1.0 to 1.5 g protein/kg per day and children
resting energy expenditure was about 29% higher than and teenagers 0.5 to 1.0 g protein/kg per day dry
expected in infants with biliary atresia and that only weight. Glucose infusions should provide 6 to 8 mg/kg
35% of the metabolizable energy intake was retained per minute of glucose to prevent hypoglycemia. There
for growth in these children. As measured by the respi- is some evidence that hepatic encephalopathy in adults
ratory quotient, infants with biliary atresia probably can be improved by administration of oral or intrave-
metabolize carbohydrate predominantly, as opposed to nous branched-chain amino acid supplements23; simi-
adults with chronic liver disease, in whom carbohy- lar studies in children are lacking. Because hypokale-
drate metabolism is decreased.l3 mia can exacerbate renal ammoniagenesis, attention
Infants with biliary atresia exhibit deficiencies of should be given to providing sufficient potassium to
long-chain polyunsaturated fatty acids, 14 which are avoid this problem.
improved but not entirely reversed 1 year after liver Moukarzel et al24 have shown that pretransplant
transplantation. 15 Dietary interventions to prevent/ nutrition status in children with end-stage liver dis-
treat these deficiencies have yet to be developed. How- ease correlates significantly with the outcome of ortho-
ever, administration of medium-chain triglyceride sup- topic liver transplantation. Children with a pathologic
plements to infants and children with biliary atresia height z score had a higher incidence of posttransplan-
has been shown to improve growth and decrease ste- tation infections and surgical complications, and a
 115SA

higher mortality rate. Chin et al25 have shown that 5. McCullough AJ, Tavill AS: Disordered energy and protein
metabolism in liver disease. Semin Liver Dis 11;265, 1991
administration of branched-chain amino acid-rich 6. Goulet OJ, deGoyet DV, Otte JB, et al: Preoperative nutritional
nutritional supplements to children with chronic liver evaluation and support for liver transplantation in children.
disease awaiting liver transplantation increases Transplant Proc 4:3249, 1987
7. Sokol RJ, Stall C: Anthropometric evaluation of children with
weight, height, total body potassium, mid-upper arm chronic liver disease. Am J Clin Nutr 52:203, 1990
circumference, and subscapular skin-fold thickness 8. Merli M, Romiti A, Riggio O, et al: Optimal nutritional indexes in
and reduces the need for albumin infusions. In an un- chronic liver disease. JPEN 11:130S, 1987
controlled trial, Guimber et a126 demonstrated that 9. Dolz C, Raurich JM, Ibanez J, et al: Ascites increases the resting
children with end-stage liver disease who fail EN energy expenditure in liver cirrhosis. Gastroenterology 100:738,
1991
can increase weight when given PN. In the presence 10. OKeefe SJ, Carraher TE, El-Zayadi AR, et al: Malnutrition and
of hyperaldosteronism, which so often accompanies immuno-incompetence in patients with liver disease. Lancet
end-stage liver disease, dietary sodium restriction may 2:615, 1980
be necessary as may potassium supplementation. 11. Pierro A, Carnielli V, Riller RM, et al: Metabolism of intravenous
fat emulsion in the surgical newborn. J Pediatr Surg 24; 95,
1
Although there are no randomized, controlled trials 1989
that demonstrate efficacy, PN in the immediate post- 12. Rosen HM, Yoshimura N, Hodgman BA, et al: Plasma amino
operative period may facilitate ventilator weaning, acid patterns in hepatic encephalopathy of differing etiology.
reduce risk of infection, and improve wound repair.27 A Gastroenterology 72:483-87, 1977
13. Schneeweiss B, Graninger W, Ferenci P, et al: Energy metabo-
cholesterol-lowering drug may be necessary to treat lism in patients with acute and chronic liver disease. Hepatology
the chronic hyperlipidemic effects of cyclosporine. 11:387, 1990
There are a number of rare inborn errors of metab- 14. Gourley GR, Farrell PM, Odell BG: Essential fatty acid defi-
olism that cause liver disease, each of which may ciency after hepatic portoenterostomy for biliary atresia. Am J
Clin Nutr 36:1194-1199, 1982
require specific dietary supplementation. One of the 15. Lapillonne A, Hakme C, Mamoux V, et al: Effects of liver trans-
more common of these disorders is galactosemia, in
plantation on long-chain polyunsaturated fatty acid status in
which dietary management consists of removing milk infants with biliary atresia. JPGN 30:528-532, 2000
and milk products from the diet. Hereditary fructose 16. Cohen MI, Gartner LM: The use of medium chain triglycerides in
intolerance is treated by strict elimination of fructose the management of biliary atresia. J Pediatr 79(3):379, 1971
17. Mourey MS, Siegenthaler G, Amadee-Manesme O: Regulation of
from the diet. In Wilsons disease, the mainstay of
metabolism of retinol-binding protein by vitamin A status in
treatment is administration of copper-chelating agents children with biliary atresia. Am J Clin Nutr 51:638, 1990
such as penicillamine; restriction of high-copper foods 18. Heubi JE, Hollis BW, Specker B, et al: Bone disease in chronic
such as shellfish, liver, nuts, seeds, and chocolate also childhood cholestasis. I. Vitamin D absorption and metabolism.
is important. Dietary management of hereditary tyrosin- Hepatology 9:252-264, 1989
19. Sokol RJ, Guggenheim MA, Iannaccone ST, et al: Improved
emia is focused on restriction of phenylalanine, tyrosine,
neurologic function following long-term correction of vitamin E
and methionine. deficiency in children with chronic cholestasis. N Engl J Med
313:1580, 1985
Practice Guidelines 20. Yanofsky RA, Jackson VG, Lilly JR, et al: The multiple coagu-

Liver j ,, , ,
lopathies of biliary atresia. Am J Hematol 16:171, 1984
21. Ramaccioni V, Soriano HE, Arumugam R, et al: Nutritional
aspects of chronic liver disease and liver transplantation in
1. Children with liver disease are at nutrition risk children. JPGN 30:361-367, 2000
22. Bucuvalas JC, Heubi JE, Specker BL, et al: Calcium absorption
and should undergo nutrition screening to iden- in bone disease associated with chronic cholestasis during child-
tify those who require formal nutrition assess- hood. Hepatology 12:1200, 1990
ment with development of a nutrition care plan. (B) 23. Cerra RB, Cheung NK, Fisher JE, et al: Disease-specific amino
2. In patients with chronic cholestatic liver dis- acid infusion (F080) in hepatic encephalopathy: A prospective,
randomized, double-blind, controlled trial. JPEN 9:288, 1985
ease, intake of vitamins A, D, E, and K should be 24. Mourkarzel AA, Najm I, Vargas J, et al: Effects of nutritional
supplemented. (B) status on the outcome of orthotopic liver transplantation in
3. Medium-chain triglycerides should be given to pediatric patients. Transplant Proc 22,4:1560-63, 1990
children with chronic liver disease to promote 25. Chin SE, Shepherd RW, Thomas BJ, et al: Nutritional support in
children with end-stage liver disease: a randomized crossover
growth. (B) trial of a branched-chain amino acid supplement. Am J Clin
4. Preoperative and postoperative SNS may be ben- Nutr 56:158-163, 1992
eficial for malnourished children with end-stage 26. Guimber D, Michaud L, Ategbo S, et al: Experience of parenteral
chronic liver disease undergoing liver transplan- nutrition for nutritional rescue in children with severe liver
tation. (B) disease following failure of enteral nutrition. Pediatr Transplan-
tation 3:139-145, 1999
27. ESPEN guidelines for nutrition in liver disease and transplan-
REFERENCES tation: Consensus guidelines. Clin Nutr 16:43, 1997

1. Novy MA,Schwarz KB: Nutritional considerations and manage-

ment of the child with liver disease. Nutrition 13:177-184, 1997
INFLAMMATORY BOWEL DISEASE
2. Protheroe SM: Feeding the child with chronic liver disease.
Nutrition 14:796-800, 1998
Background
3. Kaufman SE, Murray ND, Wood RP, et al: Nutritional support Inflammatory bowel disease is actually a continuum
for the infant with extrahepatic biliary atresia. J Pediatr 110(5): of diseases characterized by contiguous inflammation
679, 1987 of the rectum and colon (ulcerative colitis) on one end of
4. Pierro A, Koletzko B, Carnielli V, et al: Resting energy expendi-
ture is increased in infants and children with extrahepatic bili- the spectrum and by patchy inflammation, which can
ary atresia. J Pediatr Surg 24;534, 1989 occur anywhere in the gastrointestinal tract (Crohns
116SA

disease) onthe other end of the spectrum. The etiology Several studies in adults have shown no role for SNS
is not clearly defined. Both EN and PN have been used in inducing or maintaining remission in patients with
to treat malnutrition and to replace specific nutrient ulcerative colitis. No studies are available in children.
deficiencies patients with either ulcerative colitis or Clearly, SNS is appropriate in patients unable to main-
Crohns disease. tain normal nutrition status with oral intake alone.
Crohns disease most commonly starts in the distal
ileum. Growth failure is often present and may be the
Special Considerations
sole manifestation. The most common cause of growth
failure in Crohns disease is energy deficiency second- Several nutrient deficiencies may occur in patients
with inflammatory bowel disease. In a study of 162
ary to poor oral intake. 2,3 This decline in intake may be
a learned response because of associated abdominal children with inflammatory bowel disease, bone min-
pain and diarrhea often caused by food. Proinflamma- eral density was significantly lower than in controls9;
tory cytokines may also induce anorexia.4 Other con- no effective treatments are known at this time. Bone
tributing factors may include malabsorption, increased density was lowest in pubertal or prepubertal girls
with Crohns disease. The degree of bone density loss
energy expenditure, and losses in the stool. Hypoalbu-
minemia and micronutrient deficiencies are also com- was correlated with corticosteroid dose. Zinc deficiency

mon.33 The hypoalbuminemia is due primarily to has also been described in patients with inflammatory
inflammation and an associated protein-losing enter- bowel disease.2 This deficiency is secondary to malab-
opathy.3 In severe Crohns disease, prednisone is gen- sorption, and is predominately seen in patients who
are already malnourished.
erally prescribed. However, it is difficult to regulate the
steroid dose to both minimize disease activity while
optimizing growth. Importantly, although steroids Practice Guidelines
,

have a role in the decrease of linear growth rate, the Inflammatory Bowel I ,

overall level of disease activity has a greater impact.5

Excessive doses of prednisone may compromise linear 1. Children with inflammatory bowel disease are at
growth by modulating growth hormone (GH)/insulin- nutrition risk and should undergo nutrition
like growth factor-I (IGF-1) axis. Glucocorticoids screening to identify those who require formal
inhibit GH release, interfere with GH-binding, and nutrition assessment with development of a
suppress IGF-1 activity.6 nutrition care plan. (B)
Evidence 2. EN should be given to children with IBD and
growth retardation to help induce a growth spurt.
EN support can improve weight gain and linear (A)
growth, particularly in adolescents with compromised 3. EN should be used as an adjunct to medical ther-
growth .2,7-9 Adjunctive night-time feedings given one apy in patients with IBD who are unable to main-
out of every fourth month resulted in prolonged disease tain their nutrition status with oral intake. (B)
remission in eight patients.2 A larger study showed 4. PN should be used in children with IBD who are
that long-term supplementation with enteral feedings unable to maintain normal growth and develop-
each night prolonged remission when used in conjunc- ment on EN or a standard diet. (B)
tion with an otherwise unrestricted diet.8 Others have
shown that peptide-based supplemental feedings also REFERENCES
improve disease activity and the sense of well-being. A 1. Kanof ME, Lake AM, Bayless TM: Decreased height velocity in
more recent study has shown that in children with
children and adolescents before the diagnosis of Crohns Disease.
Crohns disease and growth failure, the use of night-
Gastroenterology 95:1523-1527, 1988
time feeds was associated with catch-up growth.9 2. Belli DC, Seidman E, Bouthillier L, et al: Chronic intermittent
These effects are postulated to be derived from normal- elemental diet improves growth in children with Crohns disease.
ization of nutrition status and repletion of lean tissue Gastroenterology 94:603-610, 1988
3. Seidman EG, LeLeiko N, Ament M, et al: Nutritional issues in
mass.l Although primary EN therapy contributes to pediatric inflammatory bowel disease. Symposium report.
the maintenance of remission,8,11 some studies have J Pediatr Gastroenterol Nutr 12:424-438, 1991
suggested that EN alone induces remission, in the 4. Ruemmele FM, Roy CC, Leby E, et al: Nutrition as primary
absence of other medical treatments.l2-14 However, therapy in pediatric Crohns disease: Fact or fantasy. J Pediatr
136:285-291, 2000
meta-analyses, which include studies of pediatric 5. Motil KJ, Grand RJ, Davis-Kraft L, et al: Growth failure in
patients, performed by two , different groups, showed children with inflammatory bowel disease: A prospective study.
that steroids are more effective than EN in achieving Gastroenterology 105:681-691, 1993
remission. 15,16 Much of this work has been criticized in 6. Allen DB: Growth and growth disorders. Endocrinol Metabol
that many of the studies assessed efficacy based on Clin 25:699-717, 1996
7. Morin CL, Roulet M, Roy CC, et al: Continuous elemental
subjective parameters; because steroids induce a feel- enteral alimentation children with Crohns disease and growth
ing of well-being, this may influence the perceived effi- failure. Gastroenterology 79:1205-1210, 1980
cacy of steroid therapy over EN.17 More recent studies 8. Kirschner BS, Klich JR, Kalman SS, et al: Reversal of growth
also suggest that newly diagnosed patients respond to retardation in Crohns disease with therapy emphasizing oral
EN better than patients who have recurrent disease.8 nutritional restitution. Gastroenterology 80:10-15, 1981
9. Wilchanski M, Sherman P, Pencharz P, et al: Supplementary
EN may provide essential small intestinal nutrients(ie, enteral nutrition maintains remission in pediatric Crohns dis-
glutamine) and/or may modify the production of ease. Gut 38:543-554, 1996
inflammatory mediators.4 10. Khoshoo V, Reifen R, Neuman MG, et al: Effect of low-and
 117SA

high-fat, peptide-based diets on body composition and disease tomy small bowel stoma. Symptoms may be im-
or
activity in adolescents with active Crohns disease. JPEN proved using a decompressing stoma when the dysmo-
20:401-405, 1996
11. Polk DB, Hattner JA, Kerner JA: Improved growth and disease tile segment is distal to the stoma.3 Jejunal tube feed-
activity after intermittent administration of a defined formula ings, in children who were unable to tolerate gastros-
diet in children with Crohns disease. JPEN 16:499-504, 1992
12. Sanderson IR, Udeen S, Davies PS, et al: Remission induced by
tomy tube feedings were tolerated and successful in
an elemental diet in small bowel Crohns disease. Arch Dis Child maintaining nutrition status in 11 of 18 children.4 The
62:123-127, 1987 best predictor of jejunal tube feeding tolerance was
13. Ruuska T, Savilahti E, Maki M, et al: Exclusive whole protein preservation of a migrating motor complex in either
enteral diet versus prednisolone in the treatment of acute the duodenum or the jejunum.4 Appropriate treatment
Crohns disease in children. J Pediatr Gastroenterol Nutr
19:175-180, 1994 of bacterial overgrowth may protect the liver. Short-
14. Fujimura Y, Honda K, Sato I, et al: Remarkable improvement of ened intestinal length and urinary tract involvement
3
growth and developmental retardation in Crohns disease by were poor prognostic factors.3
parenteral and enteral nutrition therapy. Intern Med 31:39-43,
1992
15. Griffiths AM, Ohlsson A, Sherman PM, et al: Meta-analysis of Practice Guidelines
,

enteral nutrition as a primary treatment of active Crohns dis- Gastrointestinal Psuedo-Obstruction

ease. Gastroenterology 108:1056-1067, 1995
16. Fernandez-Banares F, Cabre E, Esteve-Comas M, et al: How
effective is enteral nutrition in inducing clinical remission in 1. Children with intestinal pseudo-obstruction are
active Crohns disease? A meta-analysis of the randomized clin- at nutrition risk and should undergo nutrition
ical trials. JPEN 19:356-364, 1995
17. Perman JA, Beattie RM, Bentsen BS, et al: Concepts in pediatric screening to identify those who require formal
gastroenterology and nutrition, Part IV: Childhood Crohns dis- nutrition assessment with development of a
ease and the efficacy of enteral diets. Nutrition 14:345-350, 1998 nutrition care plan. (B)
18. Seidman E: Nutritional therapy for Crohns disease: Lessons 2. Continuous EN in combination with a stoma
from the Ste-Justine hospital experience. Inflamm Bowel Dis
49-53, 1997 placed above an isolated dysmotile segment
19. Gokhale R, Favis MJ, Karrison T, et al: Bone mineral density should be considered in patients with pseudo-ob-
assessment in children with inflammatory bowel disease. Gas- struction unable to tolerate oral feedings. (B)
troenterology 114(5):902-911, 1998 3. Jejunal-tube feeding should be attempted in
20. Valberg LS, Flanagan PR, Kertesz A, et al: Zinc absorption in
inflammatory bowel disease. Dig Dis Sci 31(7):724-731, 1986 children with gastrointestinal pseudo-obstruc-
tion who have an intact intestinal migrating
motor complex in either the duodenum or the
GASTROINTESTINAL
PSEUDO-OBSTRUCTION jejunum. (B)
Background REFERENCES
Pseudo-obstruction is a term that describes a func-
tional obstruction of the intestinal tract in the absence
1. Vargas JH, Sachs P, Ament ME: Chronic intestinal pseudo-ob-
struction syndrome in pediatrics. Results of a national survey by
of mechanical obstruction. Pseudo-obstruction is char- members of the North American Society of Pediatric Gastroenter-
acterized by dysmotility, which results in abdominal ology and Nutrition. J Pediatr Gastroenterol Nutr 7:323-332,
distention, nausea, vomiting, and variable degrees of 1988
malabsorption.~ Primary pseudo-obstruction is caused 2. Rudolph CD, Hyman PE, Altshculer SM, et al: Diagnosis and
treatment of chronic intestinal pseudo-obstruction in children:
by an abnormality of either the gastrointestinal vis-
Report of consensus workshop. J Pediatr Gastroenterol Nutr
ceral smooth muscle or its innervation.22 Diseases
24:108-112, 1997
include familial and sporadic visceromyopathies and 3. Heneyke S, Smith VV, Spitz L, et al: Chronic intestinal pseudo-
visceral neuropathies. Secondary causes include endo- obstruction: Treatment and long-term follow-up of 44 patients.
crine diseases (diabetes, hypothyroidism, hypopara- Arch Dis Child 81:21-27, 1999
4. DiLorenzo C, Flores AF, Buie T, et al: Intestinal motility and
thyroidism), drugs, radiation, and connective tissue
diseases. Intestinal pseudo-obstructive disorders are jejunal feeding in children with chronic intestinal pseudo-obstruc-
tion. Gastroenterology 108:1379-1385, 1995
diagnosed manometrically.3 The potential use of EN
depends which segment(s) of the gastrointestinal
on
tract affected. Prolonged obstructive episodes can
are INTRACTABLE DIARRHEA OF INFANCY
result in acute or chronic calorie deficits. Prokinetic
agents are useful in some patients.4
Background
The term &dquo;intractable diarrhea of infancy&dquo; refers to
infants less than 3 months of age who develop diarrhea
Evidence
that lasts for more than 2 weeks. Their underlying
There is a recent long-term follow-up of 44 pa- diagnoses may include cystic fibrosis, Hirschsprungs
tients with intestinal pseudo-obstruction.33 In this disease, protein intolerance, and disaccharidase defi-
study, 20 (45%) were surviving on enteral feedings ciency. 1,2 However, frequently the etiology is unclear.
alone. However, 14 (32%) had died and another 10 These infants will most likely require SNS to maintain
(23%) were PN-dependent because of recurrent epi- appropriate weight gain and growth. Data in this area
sodes of obstruction. Sixty-four percent of the infants are limited. Some of the data offered below were
who died had PN-related complications.3 Treatment obtained from infants beyond this age group and is also
may include placement of a decompressing gastros- extrapolated from studies in acute care settings.
118SA

Evidence 2. Lo CW, Walker WA: Chronic protracted diarrhea of infancy: A

nutritional disease. Pediatrics 72:786-800, 1983
Continuous enteral feedings may improve nutrient 3. Orenstein SR: Enteral versus parenteral therapy for intractable
tolerance and nutrient balance compared to bolus feed- diarrhea of infancy: A prospective, randomized trial. J Pediatr
109:277-286, 1986
ings of the same composition.4 However, exclusive EN 4. Parker P, Stroop S, Greene H: A controlled comparison of con-
may be impossible because of malaborption of fats or tinuous versus intermittent feeding in the treatment of infants
carbohydrates. Infants who have signs of carbohy- with intestinal disease. J Peds 99:360-364, 1981
drate malabsorption on elemental or semi-elemental 5. Clark JH, Bullock L, Fitzgerald JF: Dietary fructose in the
formulas may be unable to digest long-chain carbohy- management of intractable diarrhea of infancy. J Pediatr Gas-
troenterol Nutr 5:81-86, 1986
drates. Diet may be advanced more effectively by 6. Galeano NF, Lepage G, Leroy C, et al: Comparison of two special
gradually adding fructose to a carbohydrate-free for- infant formulas designed for the treatment of protracted diar-
mula.5 There are a few small, controlled studies that rhea. J Pediatr Gastroenterol Nutr 7:76-83, 1988
assess the efficacy of different formulas. Casein and 7. Paerregaard A, Hjelt K, Christiansen L, et al: Postenteritis

whey hydrolysates were shown to be equally effective enteropathy in infancy. A prospective study of 10 patients, with
in one study.6 In another prospective study of 10 special relevance to growth pattern, long-term outcome, and
incidence. Acta Pediatr Scand 79:1045-1051, 1990
patients, an elemental formula improved malnutrition 8. Margolis PA. Litteer T, Hare N, et al: Effects of unrestricted diet
and supported catch-up growth over 3 years.~ A high on mild infantile diarrhea. A practice-based study. Am J Dis
Child 144(2): 162-164, 1990
proportion of MCTs in the diet may improve tolerance. 9. Anonymous: Evaluation of an algorithm for the treatment of
More recent studies have critically examined the issues
persistent diarrhoea: A multicentre study. International Work-
of other constituents in the hopes of decreasing the ing Group on Persistent Diarrhoea. Bull WHO 74(5): 479-489,
duration of diarrhea and stool volumes. Importantly, 1996
most investigators feel that normal dietary feeding 10. Wan C, Phillips MR, Dibley MJ, et al: Randomised trial of
different rates of feeding in acute diarrhoea. Arch Dis Child
through an acute diarrheal episode is acceptable.&dquo; The 81(6): 487-491, 1999
World Health Organization (WHO) found that many 11. Chew F, Penna FJ, Peret Filho LA, et al: Is dilution of cows milk
infants will improve with normal feedings (65%). How- formula necessary for dietary management of acute diarrhoea in
ever, a significant number need to be transitioned to a infants aged less than 6 months? Lancet 341(8839):194-197,
1993
specialized diet.9 Additionally, although breast feeding 12. Fayad IM, Hashem M, Hussein A, et al: Comparison of soy-based
is the preferred method of feeding, full-strength cows formulas with lactose and with sucrose in the treatment of acute
milk appears to be quite adequate in the setting of diarrhea in infants. Arch Pediatr Adoles Med 153(7):675-680,
acute diarrhea.lo11 Children who fail cows milk will 1999
need to be transitioned to a specialized diet. Use of a 13. Santosham M, Brown KH: Oral rehydration therapy and dietary

lactose-free, soy-based product appears to be benifi- therapy for acute childhood diarrhea. Pediatr Rev 8:273-278,
1987
cial.12,13 Supplementation of the diet with fiber may 14. Brown KH, Perez F, Peerson JM, et al: Effect of dietary fiber (soy
reduce the duration of liquid stool excretion. 14 polysaccharide) on the severity, duration, and nutritional out-
Because EN alone may be insufficient to overcome come of acute, watery diarrhea in children. Pediatrics 92(2):241-

malabsorption, PN may be used as an additional 247, 1993

energy source along with EN. However, in one study,
PN in the absence of EN delayed recovery and pro- PULMONARY: BRONCHOPULMONARY
longed hospitalization in 8 of 13 patients who had DYSPLASIA
3
severe chronic diarrhea.3
Background
.

Practice Guidelines Bronchopulmonary dysplasia (BPD) is a chronic lung

Intractable Diarrhea I i disease defined by the abnormal development of the
lungs and air passages exacerbated by the effects of
mechanical ventilation. It occurs predominantly in pre-
1. Infants with intractable diarrhea are at nutrition
mature infants. Criteria for diagnosis of this disease
risk and should undergo nutrition screening to
vary, but it is generally agreed that the need for sup-
identify those who require formal nutrition plemental oxygen beyond day 28 of life and signs of
assessment with development of a nutrition care
chronic chest x-ray changes defines BPD. Symptom
plan. (B) management, growth, nutrition, and psychosocial
2. Continuous EN should be given to children with
intractable diarrhea unable to maintain normal development are all vital areas of infant care in
nutrition status with oral intake. (B) patients with BPD.
3. PN should be given to children with intractable
diarrhea unable to maintain normal nutrition sta- Evidence
tus with oral intake and EN. (B) Growth standards for premature infants are based
4. A high-fat, high-MCT containing EN formulation on in utero growth curves. To approximate these
should be given to children with intractable diar- growth patterns, energy needs have been estimated to
rhea who are carbohydrate intolerant. (C) be 120 to 130 kcal/kg in this population. Growth fail-
ure in BPD patients results from increased metabolic
REFERENCES expenditure, inadequate caloric intake, or a combina-
Nutritional
tion of both.2 The increased metabolic demand may
1. Kleinman RE, Galeano NF, Ghishan F,et al: man-

agement of chronic diarrhea and/or malabsorption. J Pediatr necessitate provision of even greater amounts of
Gastroenterol Nutr 9:407-415, 1989 energy (130 to 160 kcal/kg per day) as infants with
 119SA

BPD go from the neonatal phase to a convalescence 5. Johnson DB, Cheney C, Monsen ER: Nutrition and feeding in

phase.3 Infants fed a protein- and mineral-enriched infants with bronchopulmonary dysplasia after initial hospital
formula versus a standard isocaloric formula experi- discharge: Risk factors for growth failure. J Am Diet Assoc
98:649-656, 1998
enced catch-up growth in the first month of corrected 6. Laron Z, Pertzolan A: The comparative effect of 6-fluoropred-
gestational age.4 However, complete catch up growth nisolone, 6-methylprednisolone, and hydrocortisone on linear
was not attained even at 3 months corrected age and
growth of children with congenital adrenal virilism and Addi-
sons disease. J Pediatr 73:774-783, 1968
multiple factors, including dexamethasone treatment, 7. Weiler HA, Paes B, Shah JK, et al: Longitudinal assessment of
may play a growth inhibitory role. Socioeconomic sta- growth and bone mineral accretion in prematurely born infants
tus and illness after hospital discharge are also asso- treated for chronic lung disease with dexamethasone. J Early
Hum Dev 47:271-286, 1997
ciated with growth failure in BPD patients .5 Compre- 8. Skinner AM, Battin M, Solimano A, et al: Growth and growth
hensive nutrition counseling, ensuring adequate factors in premature infants receiving dexamethasone for
intake and parental support and education after hos- bronchopulmonary dysplasia. Am J Perinatol 14:539-546,
1997
pital discharge may benefit these patients. 9. Kennedy KA, Stoll BJ, Ehrenkranz RA, et al: Vitamin A to
Short- and long-term steroid use in children may prevent bronchopulmonary dysplasia in very-low-birth-weight
impair growth.6 Preterm infants treated with dexa- infants: Has the dose been too low? Early Hum Dev 49:19-31,
methasone show delayed linear growth up to 6 months 1997
10. Atkinson SA, Abrams SA: Symposium: Pediatric pulmonary
corrected age.7 Lower levels of serum growth factors, insufficiency: Nutritional strategies for prevention and treat-
including insulin growth factor 1 and its binding pro- ment-special nutritional needs of infants for prevention of and
tein, are also associated with steroid administration recovery from bronchopulmonary dysplasia. J Nutr 131:9335-
and impaired physical growth in this population.88 9345, 2001
11. Darlow BA, Graham PJ: Vitamin A supplementation for pre-
Vitamin A deficiency has been associated with BPD. venting morbidity and mortality in very low birthweight infants.
In a pilot study to determine appropriate supplemental Cochrane Database Syst Rev 2000 [computer file] (2) ICD00501,
doses to achieve a normal, full term-infant serum vita- 2001
min A level, preterm infants were given various
enteral and intramuscular vitamin A supplements. PULMONARY: EXTRACORPOREAL
Intramuscular vitamin A supplementation of 5000 IU MEMBRANE OXYGENATION
three times per week was needed before serum levels
were normalized. 10,11 A meta-analysis of five studies in Background
which neonates were either randomized or quasiran- Extracorporeal membrane oxygenation (ECMO)
domized to vitamin A versus placebo did not demon- involves the use of a modified heart-lung machine with
strate any effect on mortality. However, there was a a membrane oxygenator. This technology has been
trend toward more rapid weaning from oxygen depen- used successfully in the neonates to treat respiratory
dence in neonates receiving vitamin A. The use of failure. Persistent pulmonary hypertension (PPHN),
vitamin A must be weighed with potential risks of congenital diaphragmatic hernia, congenital heart dis-
repeated intramuscular injections. For some patients, eases, and meconium aspiration are some of the dis-
oral supplementation may be appropriate. ease states treated with this short-term therapy.
ECMO is also used to treat pediatric and adult respi-
Practice Guidelines ratory failure.
Bronchopulmonary Dysplasia ,

Evidence
1. Children with BPD are at nutrition risk and PN is commonly begun as soon as possible in the
should undergo nutrition screening to identify neonatal patient. The newborn infant has limited body
those who require formal nutrition assessment
reserves; therefore, prolonged starvation is dangerous.
with development of a nutrition care plan. (B) The ECMO circuit may be used to administer PN.~2
2. Infants with BPD should be provided as much as Fluid management in these patients is often challeng-
130 kcal/kg per day to promote growth. (B)
ing because of the underlying lung disease. The PN is
often concentrated to maximize caloric delivery and
REFERENCES minimize infusion volume.
Recent work, using stable isotope methodology,
1. Oh W: Nutritional management of infants with bronchopulmo-
looked at energy expenditure in nine parenterally fed
nary dysplasia. IN Bronchopulmonary Dysplasia and Related
Chronic Respiratory Disorders. Farrell PM, Taussig LM (eds). neonates on ECMO, and post-ECMO therapy.3 Energy
Ross Laboratories, Columbus, OH, 1986, pp 96-104 expenditure was similar while on ECMO and post-
2. Kurzner SI, Garg M, Bautista DB, et al: Growth failure in ECMO treatment (88.6 kcallkg per day versus 84.3
infants with bronchopulmonary dysplasia: Nutrition and ele-
vated resting metabolic expenditure. Pediatrics 81:379-84, 1988 kcal/kg per day) and ECMO did not provide a &dquo;meta-
3. Cox JH: Bronchopulmonary dysplasia. IN Nutritional Care for bolic rest.&dquo;
High-Risk Newborns. Groh-Wargo S, Thompson M, Cox J (eds). Nitrogen balance and protein metabolism has also
Precept Press, Chicago, 1994 been studied in this population. Earlier work examin-
4. Brunton JA, Saigal S, Atkinson SA: Growth and body composi-
tion in infants with bronchopulmonary dysplasia up to 3 months
ing various intravenous nitrogen and calorie feeding
corrected age: A randomized trial of a high-energy nutrient- regimens in 11 newborns on ECMO determined that
enriched formula fed after hospital discharge. J Pediatr 133: nonprotein calories greater than 60 kcalikg per day
340-345, 1998 and protein intake greater than 1.5 g/kg per day were
120SA

necessary to achieve positive nitrogen balance.4 Pro- CHRONIC RENAL FAILURE

tein intake greater than 2.5 g/kg per day promoted Background
maximum positive balance. Recently, nitrogen balance
in 12 neonates on ECMO was studied using isotope Nutrition plays a critical role in the treatment of
children with chronic renal failure. Nutrition manage-
methodology.5 Increasing total caloric delivery from 60 ment depends upon the type and stage of the kidney
to 113 kcal/kg per day did not change protein catabo-
lism, but C02 production was increased. disease, whether the child is on dialysis, and the
EN in the neonatal ECMO patient is rarely per-
method of dialysis. Nutrition status has an important
effect on growth velocity, brain growth, and overall
formed because of concerns of risk of necrotizing
enterocolitis and hypoxia. There is little evidence to development. This is particularly true in early child-
hood. Growth impairment occurs more often and is
support this statement. Enteral feedings have been more severe in children with congenital renal anoma-
performed in two limited studies. EN was introduced to lies or with onset of renal failure before age 2 years.
1
seven patients on ECMO, six with meconium aspira-
Chronic metabolic acidosis, azotemia, chronic malnu-
tion syndrome and one with PPHN.6 Using the sugar
trition, and anorexia contribute to compromised
absorption test, which measures urinary excretion of growth and nutritional deficits.
2 Protein-calorie mal-
inert markers, intestinal permeability and absorption nutrition (PCM) is a major risk factor for morbidity and
of neutral molecules did not differ between groups fed 3Causes of PCM include (1)
mortality in these patients.
parenterally or enterally. These authors note that inadequate dietary intake, (2) dialytic losses of protein,
intestinal integrity is compromised in ECMO neonates amino acids, vitamins, and other essential nutrients,
but feeding them enterally did not exacerbate that (3) inadequate dialysis, (4) hormonal and metabolic
condition. Successful EN in thirteen pediatric-aged disturbances, and (5) catabolic diseases associated
patients7 has been documented in a retrospective with uremia, especially infections.
2 Elevated uremic
review.7 toxins that cause inflammation and ulceration of the
gastrointestinal mucosa may cause gastritis, esophagi-
Practice Guidelines tis, nausea, vomiting, diarrhea, and anorexia.
4 Factors
that contribute to growth retardation include acidosis,
Extracorporeal Membrane Oxygenation #

Vitamin D deficiency, bone disease, and possible dis-

turbances in growth hormone and insulin-like growth
1. Children on ECMO are at nutrition risk and
factor- 1.
5
should undergo nutrition screening to identify Renal osteodystrophy is a major concern for infants
those who require formal nutrition assessment and children with chronic renal failure because of their
with development of a nutrition care plan. (B) altered calcium and phosphate homeostasis. Plasma
2. PN, using the ECMO circuit for access, should be concentrations of 1,25 dihydroxy Vitamin D3 have been
initiated as soon as hemodynamic stability is found to be significantly reduced when the glomerular
attained. (B) filtration rate (GFR) is below 50% of normal.
6 Chronic
3. PN should be administered to ECMO patients to acidosis alters the normal accretion of hydroxyapatite
deliver 60 to 90 kcal/kg per day and a maximum of into bone matrix, resulting in the loss of bone mineral
2.5 g/kg per day protein. (B) and an increase in urinary calcium excretion. These
factors contribute to the development of renal
7
osteodystrophy.
Nutrition assessment in children with renal failure
should include growth parameters such as mid-arm
circumference, triceps skinfold thickness, head circum-
1. Cilley RE, Wesley JR, Zwischenberger JB, et al: Gas exchange ference (in 3 year olds or less), weight or estimated dry
measurements in neonates treated with extracorporeal mem- weight, and standard deviation score for height (SDS
brane oxygenation. J Pediatr Surg 23(4):306-311, 1988 or Z 8
score).
2. Brown RL, Wessel J, Warner BW: Nutrition considerations in the
neonatal extracorporeal life support patient. Nutr Clin Pract Evidence
9:22-27, 1994
3. Keshen TH, Miller RG, Jahoor F, et al: Stable isotopic quantita- Because of the lack of controlled studies in the pedi-
tion of protein metabolism and energy expenditure in neonates atric population, recommendations are frequently
on- and post-extracorporeal life support. J Pediatr Surg 32(7):
958-963, 1997 extrapolated from adult scientific trials.9 Research has
4. Weber TR, Shah M, Stephens C, et al: Nitrogen balance in focused on the use of enteral supplements and tube
patients treated with extracorporeal membrane oxygenation. feedings to improve energy and protein intake when
J Pediatr Surg 28(7):906-908, 1993
5. Shew SB, Keshen TH, Jahoor F, et al: The determinants of protein
growth failure occurs or is threatened. It is well docu-
mented that energy intake in this population is subop-
catabolism in neonates on extracorporeal membrane oxygenation.
J Pediatr Surg 34(7):1086-1090, 1999 timal. Numerous studies have shown that growth fail-
6. Piena M, Albers MJIJ, VanHaard PMM, et al: Introduction of ure occurs in infants with renal failure who have
enteral feeding in neonates on extracorporeal membrane oxygen- caloric intakes less than 70% of the RDA.
10
ation after evaluation of intestinal permeability changes. J Pedi- such
atr Surg 33(1):30-34, 1998
Feeding disorders, as gastroesophageal reflux,
7. Pettignano R, Heard M, Davis R, et al: Total enteral nutrition may be present in more than 70% of infants with
versus total parenteral nutrition during pediatric extracorporeal chronic renal failure; suggesting that organic factors
membrane oxygenation. Crit Care Med 26(2):358-363, 1998 may contribute significantly to inadequate nutrient
 121SA

intake. 11 Provision of tube feedings within the first few showed improvement in serum albumin, weight gain,
months of life in children with congenital renal failure and anthropometric measurements. The cost of pre-
can allow them to achieve normal growth rates and venting and/or treating malnutrition with supple-
meet energy requirements. The benefits of tube feed- ments appears significantly less than the cost of hos-
ings must be weighed against their potential adverse pitalization for patients with end-stage renal disease
consequences. Severe eating difficulties such as the (ESRD) and superimposed malnutrition.19
inability to chew and swallow, and food refusal are Children with polyuric renal disease who were pre-
found in children when chronic nasogastric feedings scribed a high-volume, low-concentration formula with
are started before 1 year of ague. 12 Catch-up growth can sodium supplementation were able to maintain normal
be achieved when caloric supplementation greater growth velocity without the use of growth hormone and
than the recommended dietary allowance (RDA) for to postpone initiation of dialysis despite a creatinine
age is initiated with glucose polymers. Weight gain in clearance <10 mL/min. This specific nutrition therapy
these children includes proportional increases in both may be advantageous when dialysis is not easily avail-
body fat and lean body mass. able and growth hormone cannot be used because of
Chronic intravascular depletion caused by severe Cost. 13
polyuria and polydipsia has been hypothesized to con- Data on vitamin status in ESRD patients are contro-
tribute to growth failure in children with obstructive versial. Water-soluble vitamin deficiencies have been
uropathy or renal dysplasia. A very high intake of studied in chronic dialysis patients. Causes include
dilute formula (at 180 to 240 mL/kg per 24 hours) inadequate dietary intake, losses during dialysis, and
with sodium supplementation (2 to 4 mEq/100 mL altered vitamin metabolism.3 Dietary vitamin intake
of formula) promotes intravascular volume repletion, provided by infant formula plus a daily water-soluble
catch-up growth, and maintenance of growth veloc- vitamin supplement was associated with normal or
ity.13 In contrast, children with oliguria often require greater than normal vitamin levels in infants on
fluid restriction and calorically dense formulas to chronic peritoneal dialysis. Vitamin A levels were ele-
simultaneously maintain fluid balance and meet calo- vated despite the absence of vitamin A in the oral
rie needs. An increased mortality rate has been shown vitamin supplement .20 Vitamin A and its potential tox-
in newborns receiving formula densities of greater icity in chronic renal failure patients receiving PN
than 50 kcal/30 mL.9 remains controversial. Infants and young children may
Protein restriction to limit excessive filtration and have low stores and need vitamin A for appropriate
subsequent deterioration of renal function has been development.9 Levels of vitamin A must be monitored
suggested in children. However, the benefits are in patients with chronic renal failure, and if they
unproven, and restriction may not be compatible with become elevated, supplementation should be stopped.
normal growth.l4 Children requiring peritoneal dialy- Homocysteine, carnitine, and glutamine are three
sis suffer from significant protein losses through the nutrients currently under study. Elevated blood homo-
dialysate effluent, which can contribute to PCM.15 cysteine levels may be used in the future to detect
Aggressive nutrition support via nasogastric or gas- &dquo;subclinical&dquo; vitamin B deficiency and suggest subse-
trostomy feedings may be required. Children less than quent treatment.21 There are insufficient data to sup-
6 years old on continuously cycled peritoneal dialysis port the routine use of L-carnitine in chronic dialysis
(CCPD) were found to have greater peritoneal protein patients; however, it may help treat erythropoeitin-
losses than older children.6 The trend toward obesity resistant anemia.8 Patients with chronic renal failure
in aggressively fed infants and young children may be are at risk for metabolic bone disease. There are no
a consequence of tube feeding. Excessive calorie intake, published guidelines. In general, treatment of meta-
plus dialysate glucose resorption in infants with bolic bone disease is indicated when the intact PTH
enhanced peritoneal membrane permeability may be levels are above 240 pg/mL. If phosphate restriction or
partially responsible. 15,16 binders do not lower the iPTH <220 pg/mL, then Vita-
Nutrition support in acute renal failure requiring min D replacement therapy is recommended. Dosage is
continuous renal replacement therapies (CRRT) such dependent on serum calcium, serum phosphorus, alka-
as continuous veno-venous hemofiltration (CVVH) or line phosphatase, and PTH. Hypercalcemia should be
continuous veno-venous hemodiafiltration (CVVHD) avoided.
often requires SNS to meet the demands of the cata- A recent study on children undergoing peritoneal
bolic state. 17 Indirect calorimetry may be helpful to dialysis noted the following age-appropriate diet guide-
measuring energy expenditure; overfeeding is contra- lines22: 102 kcal/kg and 2 to 2.5 g protein/kg for ages 1
indicated in this patient population.l8 Negative nitro- to 3 years; 90 kcal/kg and 2 to 2.5 g protein/kg for ages
gen balance occurs in patients despite the delivery of 4 to 6 years; 70 kcal/kg and 2 to 2.5 g protein/kg for
standard PN containing 1.5 g/kg per day of protein and ages 7 to 10 years; and 40 to 55 kcal/kg and 1.5 g
calorie intake of 20% to 30% above resting energy protein/kg for ages 11 to 18 years.
expenditures. 17 No significant differences in amino acid Nonurea nitrogen excretion in children receiving
losses were measured between CVVH and CVVHD mo- PD was significantly greater than previous
dalities.17 reported, and it varied with age and with growth
hormone therapy. Children with residual renal
Special Considerations function excreted more nitrogen, which may have
A 3-month trial of oral nutrition supplementation in reflected a higher protein intake. Although urea
both hemodialysis and peritoneal dialysis patients nitrogen excretion in dialysate and urine can be
122SA

used to predict dialysate and protein needs in pedi- 16. Schaefer F, Klaus G, Mehls O, et al: Peritoneal transport prop-
atric patients, it is clinically erties and dialysis dose affect growth and nutritional status in
impractical. children on chronic peritoneal dialysis. J Am Soc Nephrol
10:1786-1792, 1999
Practice Guidelines 17. Maxvold N, Smoyer W, Custer J, et al: Amino acid loss and
I Renal i ,
nitrogen balance in critically-ill children with acute renal fail-
ure: A prospective comparison between classic hemofiltration vs
hemofiltration with dialysis. Crit Care Med 28:1161-1165, 2000
1. Children with chronic renal failure are at nutri- 18. Monson P, Mehta R: Nutritional considerations in continuous
tion risk and should undergo nutrition screening renal replacement therapies. Semin Dialysis 9:152-160, 1996
to identify those who require formal nutrition 19. Fedje L, Moore L: A role for oral nutrition supplements in the
malnutrition of renal disease. J Renal Nutr 6:198-202, 1996
assessment with development of a nutrition care 20. Warady B, Kriley M, Alon U, et al: Vitamin status of infants
plan. (B) receiving long-term peritoneal dialysis. Pediatr Nephrol 8:354-
2. Oral supplements or SNS should be given to 356, 1994
infants and children with renal failure who are 21. Makoff R, Dwyer J, Rocco M: Folic acid, pyridoxine, cobalamin,
and homocysteine and their relationship to cardiovascular dis-
not growing normally. (B) ease in end-stage renal disease. J Renal Nutr 6:2-11, 1996
3. Supplemental fluid and sodium should be given to 22. Mendley SR, Majkowski NL: Urea and nitrogen excretion in
children with polyuric, salt wasting renal dis- pediatric peritoneal dialysis patients. Kidney Int 58:2564-2570,
ease. (B) 2000
4. Energy intakes for children with chronic renal
failure and for those treated with maintenance CENTRAL NERVOUS SYSTEM DISORDERS
hemodialysis, or peritoneal dialysis, should be at Background
the RDA level for chronological age, and modified
depending upon the childs response. (C) According to a position statement of the American
5. Vitamin A levels should be monitored closely in Dietetic Association, &dquo;all children with special health
children with renal failure. (C) needs should have access to nutrition services pro-
6. SNS should be given to patients with acute renal vided within a system of interdisciplinary services
failure receiving continuous renal replacement that is preventive, family centered, community based,
and culturally competent.&dquo;- Neurologically impaired
therapies to promote positive nitrogen balance describes those children with special needs, chronic
and meet energy needs. (B)
conditions, and developmental delay that affect growth
and development. A large percentage of this popula-
REFERENCES
tion has at least one nutrition-based problem that can
1. Reed E, Roy L, Gaskin K, et al: Nutrition intervention and complicate their overall condition.2-4
growth in children with chronic renal failure. J Renal Nutr Growth failure is a common problem in neurologi-
8:122-126, 1998
2. Massie M, Niimi K, Yang W, et al: Nutrition assessment of cally impaired children. Measurement of mid-upper
children with chronic renal insufficiency. J Renal Nutr 2:2-12, arm circumference and triceps skinfold thickness may
1992 be useful in assessing adiposity and identifying
3. Pereira A, Hamani N, Nogueira, et al: Oral vitamin intake of reduced muscle mass.2 Children with severe disabili-
children receiving long-term dialysis. J Renal Nutr 10:24-29,
ties often fall below the 10th and 25th percentile on the
2000
4. Lancaster L: Renal failure: Pathophysiology, assessment and NCHS growth chart. Children who exhibit growth two
intervention. Part II. Nephrol Nurse 30-38, 1983 standard deviations or more below the norm should be
5. Kurtin P, Shapiro A: Effect of defined caloric supplementation on monitored carefully.5 Weight for height above the 50th
growth of children with renal disease. J Renal Nutr 2:13-17, percentile may represent excess adipose tissue. In
1992
some neurologically impaired children, muscle mass
6. Weiss R: Management of chronic renal failure. Pediatr Ann
17:584-589, 1988 may be low so they may be obese even though weight
7. Sedman A, Friedman A, Boineau F, et al: Nutritional manage- plots are within the norm for age or height. Children
ment of the child with mild to moderate chronic renal failure. with histories of malnutrition and poor ,growth should
J Pediatr 129:S13-S18, 1996
be monitored every 6 months after weight goals have
8. NKF-DOQI Clinical Practice Guidelines for Nutrition in Chronic
Renal Failure. Am J Kidney Dis 35:S105-S108, S112-S121, 2000 been achieved.6
9. Spinozzi N, Nelson P: Nutrition support in the newborn inten- Damage to the developing central nervous system
sive care unit. J Renal Nutr 6:188-197, 1996 may result in significant dysfunction in the gastroin-
10. Yiu V, Harmon W, Spinozzi N, et al: High calorie nutrition for testinal tract and may be reflected in impaired oral-
infants with chronic renal disease. J Renal Nutr 6:203-206, 1996
11. Ruley E, Bock G, Kerzner B, et al: Feeding disorders and gas-
motor function, rumination, gastroesophageal reflux,
troesophageal reflux in infants with chronic renal failure. Pedi- delayed gastric emptying, and constipation. Addition-
atr Nephrol 3:424-442, 1989 ally, a variety of drugs may lead to nutrition defi-
12. Strologo L, Principato F, Sinibaldi D, et al: Feeding dysfunction cits.3,7,8 All of these factors can contribute to feeding
in infants with severe chronic renal failure after long-term naso-
difficulties. When oral intake does not keep up with
gastric tubefeeding. Pediatr Nephrol 11:84-86, 1997
13. Sedman AS, Parekh RS, DeVee JL, et al: Cost effective manage- growth demands, EN may be indicated.49 Selectively,
ment of children with polyuric renal failure [abstract A0763]. a fundoplication may need to be performed along with
J Am Soc Nephrol 7:1398, 1996 the gastrostomy to prevent GER.lO,l1 Oral feeding
14. Raymond N, Dwyer J, Nevins P, et al: An approach to protein skills should be maintained if at all possible during the
restriction in children with renal insufficiency. Pediatr Nephrol
4:145-151, 1990 period of EN.1 PN may be indicated in cases of malab-
15. Quan A, Baum M: Protein losses in children on continuous cycler sorption, aspiration, or chronic intractable vomiting
peritoneal dialysis. Pediatr Nephrol 10:728-731, 1996 when small-bowel feedings are not possible.l Feeding
 123SA

and swallowing difficulties can result in decreased gain in those older than 12 years.2,4,6 Although a vari-
nutrient intake. Intervention strategies include assis- ety of complications may occur with tube feedings, in
tance with swallowing, texture modification, increased one extensive review, there was no mortality associ-
energy density nutrition supplements, and alternative ated with surgical placement of the tube. i6 It has been
routes of feeding.35-7,10 shown that endoscopic gastrostomy is a safe procedure
for children. 13 Enteral feeding results in a trend
Evidence toward normalized weight/height ratio for children
with CP younger than 4 years and significant weight
Children with developmental disabilities may expe-
rience deficiencies of calcium, iron, thiamin, vitamin C,
gain in those older than 12 years.~7 There is a statis-
folic acid, vitamin A, riboflavin, and thiamine. 3,4,7
tically significant difference in mortality rates between
tube-fed and non-tube-fed children. EN of neurologi-
Dietary reference intakes (DRI) based on ideal weight cally impaired children who have a tracheostomy
for height or other reference charts should be used to
estimate nutrition needs.2 Equations have been pro-
reduces mortality.ll
Fractures related to osteoporosis are a problem in
posed that calculate energy needs based on activity
levels and muscle tone. 3,5 Motor dysfunction and stat- severely disabled children. Activity and nutrition fac-
ure can also be used to refine estimates of energy
tors are the major determinants of bone-mineral den-
needs. For children 5 to 11 years old, energy needs may sity. Risk factors for low bone-mineral density include
be estimated at 13.9 kcal/cm with mild to moderate lack of ambulation, use of anticonvulsant medications,
motor dysfunction or 11.1 kcal/cm for severe dysfunc- low calcium intake (<500 mg/d), low calorie and nutri-
ent intake, low body-mass index, and reduced skinfold
tion. Athetotic forms of cerebral palsy (CP) require
additional caloric intake, perhaps up to as much as thickness. 18,19
6000 kcal/d.3 It is suggested that nomograms be used There is an increase in postoperative complications
to determine energy needs of disabled children;6 appro- in patients with CP who have a serum albumin level
below 3.5 g/dL or a total lymphocyte count less than
priate growth charts are available for those with Tri- 1500 celIS/MM3 .o Although not proven, it is suggested
somy 21, Turners, Prader-Willi, and Williams Syn-
dromes, and spastic quadriplegia. 2,5,6 Many severely by these authors that aggressive measures should be
used to improve the nutrition status before surgery.2l
impaired children remain below the 5th percentile for It has been shown that whey-based formulas can
height and weight. Upper arm length may be less com- decrease gastric emptying time compared with a case-
promised than lower leg length and can be used to in-based formulas in children with spastic quadriple-
follow linear growth.4 Triceps skinfold using cutoff val-
ues less than the 10th percentile for age, and gender gia, developmental delay, scoliosis, and profound men-
has been shown to identify malnourished children and tal retardation. Whey-based formulas may improve
screen for depleted fat stores in children with CP.12
nutrition status and decrease the risk of aspiration
Children with spastic quadriplegia cerebral palsy pneumonia.21 Soy polysaccharide fiber has been shown
to improve bowel function in nonambulatory, pro-
(SQCP) with low fat stores measured by triceps skin-
fold have a lower resting energy expenditure (REE) foundly disabled youths.22
Pulse oximetry has been used to monitor hemoglobin
adjusted for fat-free mass than children with adequate saturation during oral feeding in children with multi-
fat stores. Total energy expenditure (TEE) and the
ratio of TEE to resting energy expenditure (REE) is ple disabilities and should be considered for all chil-
lower for the SQCP group than a control group. Well dren with severe dysphagia and multiple disabilities.
nourished SQCP children have a lower TEE:REE ratio The finding of hypoxemia can help support the decision
than poorly nourished SQCP children. Improved linear to use gastrostomy tube feedings.o Respiratory induc-
tance plethysmograph and nasal airflow measurement
growth and weight gain is seen in children who have
the shortest duration of time between onset of the by thermistors are also accurate, noninvasive methods
of monitoring cardiopulmonary adaptation during oral
neurologic disorder and institution of nutrition ther-
apy.2 It appears that nutrition-related growth failure feedings. Positioning patients in the left lateral decu-
and abnormal REE in these neurologically impaired bitus position may provide temporar3 relief in
children is related to inadequate energy intake.l3-i5 impaired children who have recurrent gastric disten-
Infants who are small for gestational age and do not tion and vomiting. Complete resolution of the disten-
exhibit catch-up growth in head circumferecne are at sion and/or vomiting does not occur, however, until
2 after adequate weight gain. 21
particular risk for developmental delay.2
Studies have shown improved weight gain and TSF
thickness with EN. 15 Undernutrition causes growth Practice ,.
failure in patients with disabilities. 1-5 Tube feeding of Central Nervous Disorders
the special needs population has been shown to have a
positive influence on the lives of the children and fam- 1. Children with neurologic impairment children are
ilies including weight gain, ease of feeding after tube at nutrition risk and should undergo nutrition
placement, decrease of feeding time, decrease in aspi- screening to identify those who require formal
ration, and resolution of reflux with concomitant fun- nutrition assessment with development of a
doplication procedure. There is a trend toward nutrition care plan. (B)
improved weight/height ratio in children less than 4 2. Protein and energy needs should be targeted
years of age with gastrostomy placement and a weight according to the neurologically impaired childs
124SA

estimated energy needs modified by their level of ing time and episodes of regurgitation in children with spastic
disability and current nutritional deficits. (B) quadriplegia fed a whey-based formula. J Pediatr 120:569-572,
1992
3. SNS should be initiated in children with neuro-
22. Liebl BH, Fisher MH, VanCakar SC, et al: Dietary fiber and
logic impairment in cases of failure to thrive as long-term large bowel response in enterally nourished nonam-
determined by growth charts and disease-specific bulatory profoundly retarded youth. JPEN 14:371-375, 1990
nomograms. (B)
CANCER AND BONE MARROW
REFERENCES
TRANSPLANTATION
1. Position of The American Dietetic Association: Nutrition services
for children with special health needs. J Am Diet Assoc 95:809- Background
812, 1995 Treatment for childhood cancer is typically inten-
2. Bonnema S: Neurological Compromise. IN Nutrition Manual for
At-Risk Infants and Toddlers. Cox J (ed). Precept Press, Chicago, sive, nearly always involving surgery and/or combina-
1997, pp 113-133 tion chemotherapy to eradicate the malignancy. Radi-
3. Tilton ACH, Miller MD: Nutritional support of the developmen- ation therapy may also be required. Side effects of
tally disabled child. IN Textbook of Pediatric Nutrition. Suskind these treatments include anorexia, altered taste acu-
RM, Lewinger-Suskind L (ed). Raven Press, New York, 1993, pp
485-491 ity, catabolism, immunosuppression, and gastrointes-
4. Motil K: Enteral nutrition in the neurologically impaired child. tinal problems such as nausea, mucositis, gastric sta-
IN Pediatric Enteral Nutrition. Baker S, Baker R, Davis A (eds).
Chapman & Hall, New York, 1994, pp 217-237 sis, malabsorption, and diarrhea.1-3 The incidence of
5. Krick J, Murphy P, Savidge S: Physical handicap/nutritional malnutrition among newly ill pediatric patients
management of cerebral palsy. IN Encyclopedia of Human Nutri- appears to be the same whether the diagnosis is malig-
tion. Sandler M, Strain JJ, Cabalero B, et al (eds). Academic nant or benign illness4,5 ; however, poor nutrition sta-
Press, London, 1998, pp 1531-1539 tus at diagnosis of malignancy has been found to cor-
6. Amundson J, et al: Early identification and treatment necessary
to prevent malnutrition in children and adolescents with severe relate with decreased survival.4 Further, when a child
disabilities. J Am Diet Assoc 94:880-883, 1994 begins treatment for malignancy, food intake often
7. Bandini L, Ekvall SW, Patterson, et al: Neurological disorders.
decreases and the risk for protein-calorie malnutrition
IN Pediatric Nutrition in Chronic Diseases and Developmental
Disabilities. Ekvall S (ed). Oxford University Press, New York, (PCM) increases. 5,6 Malnourished children experience
1993, pp 89-161 more treatment delays and have a higher infection
8. Cloud H: Developmental disabilities: IN Handbook of Pediatric rate, which may adversely affect outcome.7 SNS has
Nutrition, 2nd ed. Samour PQ, Helm KK, Lang CE (eds). Aspen been shown to improve quality of life in some situa-
Publications, Gaithersburg MD, 1999, pp 293-314
9. Young C: Nutrition. IN Pediatric Swallowing and Feeding, tions by increasing the childs sense of well-being and
Arvedson JC, Brodsky L (eds). Singular Publishing Group, San ability to play.8
Diego, 1993, pp 157-208 Nutrition assessment of children with cancer should
10. Rogers BT, et al: Hypoxemia during oral feeding of children with be done at the start of treatment and periodically
severe cerebral palsy. Dev Med Child Neurol 35:3-10, 1993
11. Strauss D, Kastner T, Ashwal S, et al: Tube feeding and mortal- thereafter. This should include a standard pediatric
ity in children with severe disabilities and mental retardation. age appropriate assessment including a diet history, a
Pediatrics 99:358-362, 1997
12. Samson-Fang LJ, Stevenson RD: Identification of malnutri-
weight history, a physical examination, and attention
tion in children with cerebral palsy: poor performance of to psychosocial factors such as interest in food, irrita-
weight-for-height centiles. Dev Med Child Neurol 42:162-8, bility, and energy level.9 A comprehensive nutrition
2000 care plan should be developed, including goals for pre-
13. Stallings VA, Cronk C, Zemel B, et al: Body composition in vention or reversal of PCM and support for the childs
children with spastic quadriplegic cerebral palsy. J Pediatr 126:
normal growth. 1,5 Nutrition counseling should aim to
833-839, 1995
14. Stallings VA, Cronk C, Davies J, et al: Energy expenditure of enable parents/caregivers to cope with appetite
children and adolescents with severe disabilities: a cerebral changes, early satiety, and other problems that can
palsy model. Am J Clin Nutr 64: 627-634, 1996 arise after treatment is begun.5 Appetite stimulants
15. Isaacs JS, Georgeson K, Cloud H, et al: Weight gain and triceps such as megestrol acetate may be considered, although
skinfold fat mass after gastrostomy placement in children with
their use in children with cancer has not been ade-
developmental disabilities. J Am Diet Assoc 94:849-854, 1994
16. Smith S, Camfield C, Camfield P: Living with cerebral palsy and quately studied. Criteria for the initiation of nutrition
tube feeding: A population-based follow-up study. J Pediatr 135: intervention were recommended by the American
307-310, 1999 Academy of Pediatrics task force on the special nutri-
17. Brant CQ, Stanich P, Ferrari AP: Improvement of childrens
tion needs of children with malignancies. These recom-
nutritional status after enteral feeding by PEG: An interim
report. Gastrointest Endosc 50:183-188, 1999 mendations should be followed by all clinicians who
18. Henderson R, Lin P, Greene W: Bone-mineral density in children care for pediatric oncology patients. During cancer
and adolescents who have spastic cerebral palsy. J Bone Joint treatment, ongoing nutrition assessment can be accom-
Surg Am 77-A:1671-1681, 1995 plished effectively using weight changes and weight-
19. Baer M, Kozlowski B, Blyler E, et al: Vitamin D, calcium, and
bone status in children with development delay in relation to for-height-measurements, and standardized subjective
anticonvulsant use and ambulatory status. Am J Clin Nutr assessment of oral intake.9-11
65:1042-1051, 1997
20. Jevsevar D, Karlin L: The relationship between preoperative
nutrition status and complications after an operation for scolio- Evidence
sis in patients who have cerebral palsy. J Bone Joint Surg Am
75-A:880-884, 1993 Nutrition assessment is an important element of the
21. Fried M, Khoshoo V, Secker D, et al: Decrease in gastric empty- care of children with cancer. It has been shown that
 125SA

poor oral intake is the best predictor of the need for SNS should be used only if it will improve the patients
SNS.12 quality of life
The intent of SNS should be the prevention or rever-
sal of PCiVL 13 Decisions regarding the use of EN or PN Practice Guidelines
will depend on the clinical setting. PN via a central Cancer and
, Bone Marrow
Transplantation

venous catheter appears more effective in reversing

pre-existing PCM during intensive cancer therapy 1. Children with cancer are at nutrition risk and
than peripheral parenteral nutrition (PPN) or oral should undergo nutrition screening to identify
therapy.&dquo; The use of PN must be tempered with the those who require formal nutrition assessment
potential for complications. A meta-analysis of pub- with development of a nutrition care plan. (B)
lished controlled studies concluded that the use of PN 2. SNS and dietary interventions should be under-
is associated with an increased infection rate in chil- taken to promote normal growth and development
dren who have a central venous catheter in place for and to provide for energy requirements in those
cancer patients who cannot meet their needs
cancer therapy. 15
EN has been shown to be successful at reversing orally. (B)
PCM during intensive chemotherapy, especially when 3. Palliative administration of SNS in terminally ill
administered via a feeding protoco1.16,1 children with cancer is rarely indicated. (B)
Gastrostomy tube (GT) placement is becoming more REFERENCES
common to provide EN. GT feeding has been shown to
1. Mauer AM, Burgess JB, Donaldson SS, et al: Special nutritional
be effective at reversing PCM, with relatively minor
needs of children with malignancies: A review. JPEN 14:315-
complications. 18-20 There is some evidence that the 324, 1990
appetite stimulant megestrol acetate may be effective 2. Pencharz PB: Aggressive oral, enteral or parenteral nutrition:
in the treatment of chemotherapy-induced anorexia; Prescriptive decisions in children with cancer. Int J Cancer
however, adrenal insufficiency is a potential side Suppl 11:73-75, 1998
3. Andrassy RJ, Chwals WJ: Nutritional support of the pediatric
effect .2 EN, whether via nasogastric tube or GT, is less oncology patient. Nutrition 14:124-129, 1998
expensive than PN. 18,22 4. Donaldson SS, Wesley MN, DeWys WD, et al: A study of the
Home EN may be less stressful for the patient and nutritional status of pediatric cancer patients. Am J Dis Child
family than home PN.23 Using the gut whenever 135:1107-1112, 1981
5. Carter P, Carr D, Van Eys J, et al: Energy and nutrient intake of
possible during and after treatment may enhance children with cancer. J Am Diet Assoc 82:610-615, 1983
patients ability to consume adequate amounts of 6. Skolin I, Axelsson K, Ghannad P, et al: Nutrient intakes and
food. The use of PN after discharge after bone mar- weight development in children during chemotherapy for malig-
row transplantation delays return to normal oral nant disease. Oral Oncol 33:364-368, 1997
7. Rickard KA, Detamore CM, Coates TD, et al: Effect of nutrition
intake.24 staging on treatment delays and outcome in stage IV neuroblas-
toma. Cancer 52:587-598, 1983
8. VanEys J: Benefits of nutritional intervention on nutritional
Special Considerations status, quality of life and survival. Int J Cancer Suppl 11:66-68,
1998
Pediatric patients undergoing bone marrow
9. Hammill PV, Drizd TA, Johnson CL, et al: Physical growth:
transplantation are very likely to require SNS for at National Center for Health Statistics percentiles. Am J Clin
least part of the transplant hospitalization. Nutr 32:607-6629, 1979
Although PN has been the standard nutrition sup- 10. Motil KJ: Sensitive measures of nutritional status in children in
port therapy, EN may be appropriate under certain hospital and in the field. Int J Cancer Suppl 11:2-9, 1998
11. Attard-Montaldo SP, Hadley J, Kingston JE, et al: Ongoing
circumstances.25 assessment of nutritional status in children with malignant
Trials of nutritional pharmacology (high doses of disease. Pediatr Hematol Oncol 15:393-403, 1998
specialized nutrients) have yielded conflicting results. 12. Tyc VL, Vallelunga L, Mahoney S, et al: Nutritional and treat-
Recent studies using the amino acid glutamine during ment-related characteristics of pediatric oncology patients
bone referred or not referred for nutritional support. Med Pediatr
marrow transplantation have not shown statisti-
Oncol 25:379-388, 1995
cally significant benefit, although trends suggest fur- 13. Klein S, Koretz R: Nutrition support in patients with cancer:
ther research is warranted.26,27 A recent controlled what do the data really show? Nutr Clin Pract 9:91-100, 1994
study has shown that low-dose glutamine can reduce 14. Rickard KA, Godshall BJ, Loghmani ES, et al: Integration of
the incidence of painful stomatitis .2 The use of phar- nutrition support into oncologic treatment protocols for high and
low nutritional risk children with Wilms tumor. A prospective
macologic doses of nutrients should be limited to con- randomized study. Cancer 64:491-509, 1989
trolled trials until the data clearly indicate presence or 15. Christensen ML, Hancock ML, Gattuso J, et al: Parenteral nutri-
absence of benefit. tion associated with increased infection in children with cancer.
Alternative or complementary nutrition treatments Cancer 72:2732-2738, 1993
are of unproven efficacy.29 When the caregiver of a
16. Den Broeder E, Lippens RJ, vant Hof MA, et al: Effects of
child with cancer intends to give alternative nutri- naso-gastric tube feeding on the nutritional status of children
with cancer. Eur J Clin Nutr 52:494-500, 1998
tional therapy products to the child, the product(s) 17. Pietsch JB, Ford C, Whitlock JA: Nasogastric tube feedings in
should be evaluated for their potential to harm and the children with high-risk cancer: a pilot study. J Pediatr Hematol
Oncol 21:111-114, 1999
findings communicated to the family. When children 18. Aquino VM, Smyrl CB, Hagg R, et al: Enteral nutritional sup-
are terminally ill from their disease, nutrition cannot
port by gastrostomy tube in children with cancer. J Pediatr
change the outcome. The burden of using SNS must be 127:58-62, 1995
weighed against the benefits. In terminally ill children, 19. Mathew P, Bowman L, Williams R, et al: Complications and
126SA

effectiveness of gastrostomy feeding in pediatric cancer patients. account for these alterations in energy metabolism,
J Pediatr Hematol Oncol 18:81-85, 1996 measured energy expenditure values or basal energy
20. Barron MA, Duncan DS, Green GJ, et al: Efficacy and safety of
radiologically placed gastrostomy tubes in paediatric requirements should be provided. The significance of
haematology/oncology patients. Med Pediatr Oncol 34:177-182, this therapeutic strategy is to avoid the provision of
2000 calories and/or nutritional substrates in excess of the
21. Aconza C, Castro L, Crespo D, et al: Megestrol acetate therapy
energy required to maintain the metabolic homeostasis
for anorexia and weight loss in children with malignant solid
tumours. Aliment Pharmacol Ther 10:577-586, 1996
of the injury response. Overfeeding has deleterious
22. Lipman TO: Grains or veins: Is enteral nutrition really better consequences.1 It increases ventilatory work by
than parenteral nutrition? A look at the evidence. JPEN 22:167- increasing C02 production.4 This can prolong the need
182, 1998 for mechanical ventilation. 3,4 Overfeeding may also
23. Padilla GV, Grant MM: Psychosocial aspects of artificial feeding.
Cancer 55(Suppl 1):301-304, 1985
impair liver function by inducing steatosis and cho-
24. Charuhas PM, Fosberg KL, Bruemmer B, et al: A double-blind lestasis, ,and increase the risk of infection secondary to
randomized trial comparing outpatient parenteral nutrition hyperglycemia.
with hydration: effect on resumption of oral intake after marrow Nutrition assessment of critically ill pediatric
transplantation. JPEN 21:157-161, 1997 patients can be quantitatively accomplished by mea-
25. Szeluga DJ, Stuart RK, Brookmeyer R, et al: Nutritional support
of bone marrow transplant recipients: a prospective, randomized suring (1) the visceral (or constitutive) protein pool; (2)
the acute-phase protein (3) nitrogen balance; and
clinical trial comparing total parenteral nutrition to an enteral
feeding program. Cancer Res 47:3309-3316, 1987
~ool;
(4) energy expenditure. Prealbumin is readily mea-
26. Dickson TM, Wong RM, Negrin RS, et al: Effect of oral glutamine sured in most hospitals and is a good marker for the
supplementation during bone marrow transplantation. JPEN visceral protein pool.5 Albumin, which has a large pool
24:61-66, 2000 and much longer half-life, should not be used because it
27. Schloerb PR, Skikne BS: Oral and parenteral glutamine in bone
marrow transplantation: A randomized study. JPEN 23:117- is not indicative of the immediate nutrition status and
122, 1999 may be skewed by changes in fluid status. Within 12 to
28. Anderson PM,. Ramsay NK, Shu XO, et al: Effect of low-dose oral 24 hours of initiation of stress, serum acute-phase pro-
glutamine on painful stomatitis during bone marrow transplan- tein levels rise because of hepatic reprioritization of
tation. Bone Marrow Transplantation. 22(4): 339-344, 1998
29. Weitzman S: Alternative nutritional cancer therapies. Int J Can- protein synthesis in response to injury.5 The rise is
cer Suppl 11:69-72, 1998 proportional to the severity of injury. Some hospitals
30. Torelli GF, Campos AD, Meguid MM: Use of TPN in terminally are capable of measuring C-reactive protein (CRP) as
ill cancer patients. Nutrition 15:665-667, 1999
an index of the acute-phase response. When measured

serially (once a day during the acute response period),

CRITICAL CARE-PEDIATRICS serum prealbumin and CRP are inversely related (ie,
serum prealbumin levels decrease and CRP levels
Background increase with the magnitude proportional to injury
Alterations in the energy requirements of pediatric severity and then return to normal as the acute injury
patients due to the response to an acute metabolic response resolves). Decreases in serum CRP values to
stress can be quite dramatic, even in contrast to the less than 2 mg/dL have been associated with the return
stressed, hypermetabolic adult. Growth velocity during of anabolic metabolism6 and are followed by increases
early infancy is higher than at any other time during in serum prealbumin levels. Energy expenditure can
childhood and is exceeded only by intrauterine growth be measured at bedside using indirect calorimetry.11
rates. These additional growth requirements must be Although a variety of predictive equations have been
met in critically ill pediatric patient. proposed,7 clinical and patient variability (especially in
Acute injury markedly alters energy needs. First, the infant population) makes these estimates problem-
acute injury induces a catabolic response that is pro- atic.8~ Direct measurement of energy use in individual
portional to the magnitude, nature, and duration of the patients achieves greater accuracy and can help avoid
injury. Increased serum counter-regulatory hormone overfeeding. In addition, actual serial measurements
concentrations induce insulin and growth hormone show changes in respiratory quotient, which help to
resistance,2 resulting in the catabolism of endogenous identify resumption of anabolic metabolism after
stores of protein, carbohydrate, and fat to provide injury
essential substrate intermediates and energy neces-
sary to support the ongoing metabolic stress response. Evidence
During this catabolic response, somatic growth can not
occur, and, therefore, the caloric allotment for growth, To avoid overfeeding children during acute metabolic
which is substantial in infancy, should not be admin- stress, energy expenditure should be measured.
istered. Second, children treated in the intensive care Energy delivery should not exceed measured values.
setting are frequently sedated, and their activity level When the respiratory quotient decreases to 1.0 in
is markedly reduced; this may reduce energy needs. infants up to 1 year of age, calorie intake may be
Third, the intensive care environment is temperature- advanced slowly to meet predicted energy require-
controlled and insensible energy losses are substan- ments for age and weight. In the absence of indirect
tially reduced. This is especially true for children who calorimetry, published basal energy requirements
are mechanically ventilated because, in addition to based on age, weight, and gender offer reasonable
reduced energy needs for the work of breathing, these guidelines for basal energy requirements.10 During
patients are ventilated with heated, humidified air. metabolic stress, for infants up to 2 years of age, micro-
This can reduce insensible losses by one third. To nutrient substrates should be provided as follows: pro-
 127SA

tein (2.5 to 3.0 g/kg per day), carbohydrate (8.5 to 10 g/kg 3. If indirect calorimetry is not feasible, energy
per day), and fat (lgm/kg per day). From 2 to 11 years of should be provided to critically ill children based
age, protein should be decreased to 2.0 g/kg per day and on published formulas or nomograms to avoid

carbohydrate to 5 g/kg per day. Above 12 years of age, overfeeding. (B)

protein should be reduced to 1.5 to 2.0 g/kg per day and 4. When SNS is indicated in critically ill children,
fat to 0.5 g/kg per day. A study of critically ill children less EN is preferable to PN whenever feasible. (B)
than 2 years of age in a pediatric intensive care setting
showed that actual measured energy expenditure values REFERENCES
average about 50% of what the predicted energy require-
ment would be for those children if they were healthy and 1. Chwals WJ: Pediatric enteral and parenteral surgical nutrition.
3 IN Grenvik, Ayres, Holbrook, et al (eds.), Textbook of Critical
normally active.3 Care, 4th ed. WB Saunders, Philadelphia, 2000
Decrease of serum CRP values to less than 2 mg/dL 2. Rowe MI, Chwals WJ: The neonate as a patient. IN ONeill JA,
and rising prealbumin values may be used as guide- Rowe MI, Fonkalsrud EW, et al (eds.), Pediatric Surgery, 5th ed.
lines for advancing SNS to normal predicted levels Mosby-Year Book, St Louis, MO, 1997
based on age and weight. 1,6 Decrease in total urinary 3. Chwals WJ, Lally KP, Woolley MM, et al: Measured energy
expenditure in critically ill infants and young children. J Surg
nitrogen may also be used as an indicator of the Res 1988, 44:467
resumption of normal (versus stressed) metabolism. 4. Letton RW, Chwals WJ, Jamie A, et al: Neonatal lipid utilization
Increasing serum prealbumin concentrations are asso- increases with injury severity: Recombinant human growth hor-
ciated with increased energy intake after the acute mone versus placebo. J Pediatr Surg 31:1068-1072, 1996
5. Dickson PW, Bannister D, Schreiber G: Minor burns lead to
metabolic stress has resolved,&dquo; and can be useful to
major changes in synthesis rates of plasma proteins in the liver.
assess the adequacy of energy delivery during the post- J Trauma 27:283-286, 1987
stress recovery period. EN is preferred to PN whenever 6. Letton RW, Chwals WJ, Jamie A, et al: Early postoperative
possible. The visceral protein response is significantly alterations in infant energy utilization increases the risk of over-
greater and occurs earlier with EN versus PN after feeding. J Pediatr Surg 30(7):988-992, 1995
7. White MS, Shepherd RW, McEniery JA: Energy expenditure in
severe injury.l2 In severely injured infants and chil-
100 ventilated, critically ill children: Improving the accuracy of
dren, a soft, transpyloric feeding tube can provide safe predictive equations. Crit Care Med 28:2307-2312, 2000
enteral access for early postinjury support (particu- 8. McClave SA, Lowen CC, Kleber MJ, et al: Are patients fed
larly in premature infants with delayed gastric empty- appropriately according to their caloric requirements? JPEN
22(6):375-381, 1998
ing).13 A number of studies have demonstrated a sig- 9. Mayes T, Gottschlich MM, Khoury J, et al: Evaluation of pre-
nificant benefit of EN over PN in appropriately dicted and measured energy requirements in burned children.
matched, critically ill adults.l4-16 Few data, however, J Am Diet Assoc 96(1):24-29, 1996
are available in the pediatric age group. 10. Talbot FB: Basal metabolism standards for children. Am J Dis
Child 55:455-459, 1938
11. Chwals WJ, Fernandez ME, Charles BJ, et al: Serum visceral
Special Considerations protein levels reflect protein-calorie repletion in neonates recov-
The supplemental use of growth hormone in severely ering from major surgery. J Pediatr Surg 27(3):317-321, 1992
12. Kudsk KA, Minard G, Wojtysiak SL, et al: Visceral protein
burned pediatric patients has been shown to offer sig- response to enteral versus parenteral nutrition and sepsis in
nificant benefit by accelerating wound healing and patients with trauma. Surgery 116(3):516-523, 1994
13. Lucas A, Bloom SR, Aynsley-Green A: Gut hormones and mini-
reducing hospital stay17,18 and has been associated mal enteral feeding. Acta Paediatr Scand 75:719-723, 1986
with significantly greater and earlier increases in the
14. Moore FA, Feliciano DV, Andrassy RJ, et al: Early enteral feed-
visceral protein pool response.19 ing, compared with parenteral, reduces postoperative septic
Monitoring the acute metabolic response to injury may complications. The results of a meta-analysis. Ann Surg 216(2):
be advantageous. Stratification of injury severity can be 172-183, 1992
15. Kudsk KA, Croce MA, Fabian TC, et al: Enteral versus paren-
accomplished by monitoring either acute-phase pro- teral feeding. Effects on septic morbidity after blunt and pene-
tein pool changes or energy expenditure .20 The devel-
trating abdominal trauma. Ann Surg 215(5):503-511; discussion
opment of postinjury sepsis can be detected by serial 511-513, 1992
monitoring of acute-phase protein pool changes.21 EN 16. Kudsk KA, Minard G, Croce MA, et al: A randomized trial of
intolerance can also be useful for this purpose in isonitrogenous enteral diets after severe trauma. An immune-
severely burned children.22 Both acute-phase and vis- enhancing diet reduces septic complications. Ann Surg 224(4):
ceral protein pool injury-induced changes have been 531-5340; discussion 540-543, 1996
17. Herndon DN, Barrow RE, Kunkel KR, et al: Effects of recombi-
shown to predict mortality in critically ill infants.23 nant human growth hormone on donor-site healing in severely
burned children. Ann Surg 212(4):424-429; discussion 430-431,
Practice Guidelines
. 1990
18. Gilpin DA, Barrow RE, Rutan RL, et al: Recombinant human
Critical Care-Pediatrics growth hormone accelerates wound healing in children with
large cutaneous burns. Ann Surg 220(1):19-24, 1994
19. Jeschke MG, Barrow RE, Herndon DN: Recombinant human
1. Children with critical illnesses are at nutrition
risk and should undergo nutrition screening to growth hormone treatment in pediatric burn patients and its
role during the hepatic acute phase response. Crit Care Med
identify those who require formal nutrition 28:1578-1584, 2000
assessment with development of a nutrition care 20. Chwals WJ, Letton RW, Jamie A, et al: Stratification of injury
plan. (B) severity using energy expenditure response in surgical infants.
J Pediatr Surg 30:1161, 1995
2. Energy expenditure should be measured serially 21. Chwals WJ, Fernandez ME, Jamie AC, et al: Detection of post-
to determine the energy needs of critically ill chil- operative sepsis in infants using metabolic stress monitoring.
dren. (B) Arch Surg 129:437-442, 1994
128SA

22. Wolf SE, Jeschke MG, Rose JK, et al: An indicator of sepsis- oral supplementation, EN, PN, and behavioral modifi-
associated mortality in burned children. Arch Surg 132:1310- cation. The CF Foundation Clinical Practice Guide-
1314, 1997 lines suggest that nutrition management be guided by
23. Chwals WJ, Fernandez MD, Jamie AC, et al: Relationship of
metabolic indices to postoperative mortality in surgical infants. &dquo;a graded response that is appropriate for the needs of
J Pediatr Surg 28:819-822, 1993 each patient.&dquo;4
These guidelines describe a tiered
approach. All CF patients should receive nutrition
CYSTIC FIBROSIS instruction, dietary counseling, pancreatic enzyme
replacement, and vitamin supplementation. For those
Background patients at risk of developing energy imbalance (eg,
Cystic Fibrosis (CF) is an autosomal recessive frequent pulmonary infections or periods of rapid
genetic syndrome characterized by viscid exocrine growth), further education and monitoring are impor-
gland secretions that may obstruct the bronchi, pan- tant. Additionally, these patients may need calorically
creatic and bile ducts, and the intestines. CF currently dense feedings and behavioral assessment and coun-
affects approximately 30,000 children and adults in the seling. For those patients with a weight to height index
United States. One in 31 Americans is a carrier of the of 85% to 90% of ideal weight, oral supplements should
abnormal gene. The major cause of death in patients be given. For those patients with a weight-to-height
with CF is pulmonary insufficiency leading to respira- index consistently less than 85% of ideal body weight,
tory failure. Nutrition status has been found to EN should be initiated. There is no compelling evi-
strongly correlate with pulmonary status and to affect dence to support the use of any specialized formula,
recovery from illness.2 Median survival is 32.3 years although supplements should be nutritionally bal-
based on data from the Cystic Fibrosis Foundation anced with respect to micronutrients.4 Finally, for
Patient Registry 1998.33 those children with a weight-to-height index of less
The relationship between nutrition status and long than 75% of ideal weight, continuous EN or PN should
term survival in patients with CF is well documented. be initiated. With continuous drip tube feedings, pan-
Factors that affect nutrition status include pancreatic creatic enzyme supplements are required for diges-
insufficiency, maldigestion/malabsorption of fat and tion. It is generally recommended that patients take
fat-soluble vitamins, and loss of bile salts and bile acids enzymes at the start of bedtime tube feedings,
associated with steatorrhea, and bulky stools. In addi- although this can be altered to allow for individual
tion, patients who have undergone intestinal resection tolerances. PN is usually indicated for short-term ther-
secondary to bowel obstruction resulting from meco- apy with specific problems such as short-gut syndrome,
nium ileus may have reduced absorptive capabilities.4 pancreatitis, severe gastroenteritis, and postoperative
Chronic pulmonary infections and deteriorating pul- management in patients who have had major surgical
monary function are associated with anorexia and procedures.4 PN may be required for lung transplant
increased energy requirements that can lead to malnu- candidates and individuals who refuse EN. 4
trition. Two additional factors that contribute to poor
nutrition status in CF patients are cystic fibrosis-
Special Considerations
related diabetes (CFRD) and cholestatic liver disease.
Nutrition assessment in CF patients is accomplished Growth rates and energy requirements are highest
by first determining energy requirements, taking into during the first 2 years of life.4 Pancreatic enzyme
account the effects of dietary intake, activity, pulmo- replacement therapy should be initiated with each
nary status, extent of malabsorption (pancreatic suffi- feeding in the presence of maldigestion/malabsorp-
cient or insufficient), and hypermetabolism. Labora- tion.7 Enzymes should be given with all types of milk
tory measurements suggested at time of diagnosis and products including human breast milk and predigested
yearly include electrolyte and acid-base parameters, formulas. Predigested formulas are used for CF infants
7
complete blood count, serum albumin, and plasma or who have short gut syndrome or cholestasis.~ CF
serum retinal and alpha tocopherol levels.4 Careful, infants fed human breast milk can sustain normal
consistent monitoring of growth parameters (height, growth while on pancreatic enzyme replacement. Spe-
weight, weight-for-height, and head circumference) is cial attention should be given to their caloric needs and
also essential. potential metabolic complications such as hypopro-
teinemia and hyponatremic alkalosis.4,7,8 Nutrition
and electrolyte status and growth velocity should be
Evidence
monitored at 1- to 3-month intervals.4 Because of the
Children with CF have augmented energy needs low sodium content of breast milk, supplemental
during periods of growth, such as infancy and adoles- sodium chloride, especially during summer months,
cence. Energy requirements remain high in advanced may be indicated. An appropriate/safe dosage is 2 to 4
lung disease. To offset these energy needs, 120 to 150% mEq/kg per day.4
of Recommended Daily Allowance (RDA) for energy is The increasing life expectancy of patients with CF
encouraged.3 However, recent studies have shown that allows the development of additional medical compli-
CF children often do not achieve this level of energy cations such as CFRD and osteoporosis. Up to 75% of
intake. Energy intake should also increase during CF adults have some form of glucose intolerance, and
pregnancy and CFRD.6
6
15% have frank CFRD.66
A meta-analysis of nutrition intervention and man- CFRD has features of both Type 1 and Type II dia-
agement addressed four types of medical interventions: betes, but is a separate, unique condition. Causes of
 129SA

CFRD include pancreatic scarring due to thickened REFERENCES

excretions, insulin resistance due to chronic infections, 1. Facts about Cystic Fibrosis. Cystic Fibrosis Foundation, Revised
and elevated cortisol levels. CFRD can be intermittent; January 24, 2000, http: //www.cff.org/facts.htm
in such cases, insulin is needed during infections and 2. Jelalian E, Stark LJ, Reynolds L, Seifer R: Nutrition interven-
tion for weight gain in cystic fibrosis: A meta analysis. J Pediatr
with steroid treatment. In chronic CFRD, insulin is
486-492, 1998
required at all times. The goal of CFRD therapy is to 3. Cystic Fibrosis Foundation, Patient Registry: Annual Data
maintain blood glucose in a range as close to normal as Report. Cystic Fibrosis Foundation, September 1999, pp 1 and
possible.6 With CFRD, patients are instructed to con- 19, 1998
4. Clinical Practice Guidelines for Cystic Fibrosis: Cystic Fibrosis
tinue a high-calorie, high-protein, high-fat, high-salt
Foundation 1997, Appendix IV, Volume I, Section V
diet to maintain body weight. Individuals with CF
5. Luder E: Achieving Optimal Nutrition for People with Cystic
should understand the effect of carbohydrates on blood Fibrosis Home Line. June 1997 Edition. http://www.cff/org/
glucose levels as well as how to balance food, insulin, homeline199706.htm
and physical activity to maintain near normal blood 6. Hardin D, Brunzell C, Schissel K, et al: Managing Cystic Fibro-
sis Related Diabetes (CFRD) An Instruction Guide for Patients
glucose levels. and Families. Cystic Fibrosis Foundation, 1999
Osteoporosis and fractures are a recognized problem 7. Ramsey B, Farrell P, Pencharz P, and the Consensus Committee.
in both children and adults with CF.9 Several studies Nutritional Assessment and Management in Cystic Fibrosis: A
have documented diminished bone mineralization in Consensus Report. Am J Clin Nutr 55:108-116, 1992
adults with CF. There is also concern over skele- 8. Durie PR, Pencharz PB: Nutrition. Br Med Bull 48(4):823-847,
1992
tal growth and development in children with CF.-o
9. Donovan Jr DS, Papadopoulas A, Staron RB, et al: Bone mass
Possible risk factors for low bone density include small and vitamin D deficiency in adults with advanced cystic fibrosis
body size, low weight-for-height, decreased physical lung disease. Am J Respir Crit Care Med 157:1892-1899, 1998
activity, use of corticosteroids, delayed skeletal or sex- 10. Henderson RC, Madsen CD: Bone mineral content and body
ual maturation, gonadal dysfunction, and severity of composition in children and young adults with cystic fibrosis.
illness.11 Current treatment options include increased Pediatr Pulmonol 27:80-84, 1999
11. Bhudhikanok GS, Wang M-C, Marcus R, et al: Bone acquisition
calcium and vitamin D intake, weight-bearing physical and loss in children and adults with cystic fibrosis: A longitudi-
activity, and use of bisphosphonates, calcitonin, and/or nal study. J Pediatr 133:18-27, 1998
estrogens. 12 Further studies must be conducted to 12. Zemel B: Clinical Assessment of Bone Health in Children and
identify the etiology of osteoporosis in CF patients Young Adults. The Childrens Hospital of Philadelphia. Thir-
teenth Annual North American Cystic Fibrosis Conference, 1999
and to determine the best prevention and treatment 13. Lambert JP: Osteoporosis: A new challenge in cystic fibrosis.
methods. 13 Pharmacotherapy 20:34-51, 2000
Because of malabsorption, the fat soluble vitamins
A, D, E, and K may become depleted in patients with
CF. Fat soluble vitamin serum levels should be moni- INBORN ERRORS OF METABOLISM
tored annually. CF patients with pancreatic insuffi- Background
ciency should receive a water miscible vitamin therapy is often the primary, or even
Nutritional
designed specifically for CF. only, treatment for children with inborn errors or
metabolism and requires an in-depth understanding of
Practice Guidelines the metabolic processes involved. Depending on the
Cystic Fibrosis particular inborn error, inadequate or inappropriate
nutrition can result in mental retardation, growth fail-
1. Patients with CF are at nutrition risk and should ure, and metabolic/neurologic crises. Goals of nutri-
undergo nutrition screening to identify those who tion support in children with inborn errors of metabo-
require formal nutrition assessment with devel- lism include optimizing growth and development and
opment of a nutrition care plan. (B) minimizing any metabolic complications. Examples of
2. CF patients with exocrine pancreatic insufficiency nutritional therapy for these disorders include the fol-
require enzyme replacement therapy and a water lowing :
1. Restricting substrates in patients with blocked
miscible multivitamin specifically designed for
metabolic pathways to prevent accumulation of
CF. (C)
toxic precursors such as phenylalanine (phenyl-
3. Vitamins A, D, E and K serum levels should be
monitored annually in CF patinets. (B) ketonuria), galactose (galatosomia), and leucine
4. A weight-height index greater than 90% of ideal (maple syrup urine disease);
2. Facilitating alternative metabolic pathways to
should be maintained during periods of rapid decrease accumulated toxic precursors in blocked
growth (infancy and adolescence), pulmonary reaction sequences (eg, glycine therapy in
insufficiency, or infection in CF patients. (C) patients with isovaleric acidemia);
5. CF children with a weight-for-height index less 3. Supplying products of blocked primary pathways
than 85% should have dietary intake monitored [eg, arginine in patients with urea cycle disorders,
and undergo behavioral assessment and counsel- tyrosine in phenylketonuria (PKU), and glucose
ing. (B) in glycogen storage disease type I];
6. SNS should be initiated in children with CF with 4. Supplementing conditionally essential nutrients
a weight-for-height index less than 90%. (A) (eg, carnitine in patients with organic acidemias);
130SA

5. Stabilizing altered enzyme proteins (eg, thiamine disease type I), a deficiency of energy production (eg,
to increase enzyme activity in patients with disorders of fatty acid oxidation), or a breakdown of
maple syrup urine disease); protein or fat leading to accumulation of toxic metab-
6. Replacing deficient cofactors (eg, vitamin B-12 olites.l Disorders of fatty acid oxidation and transport
therapy in patients with methylmalonic aciduria result in an inability to mobilize fatty acids for energy
and vitamin B-6 in homocystinuria); metabolism.11,12 Symptoms occur when the carbohy-
7. Inducing enzyme production (eg, glucose to affect drate stores of glycogen in liver are exhausted and the
gene transcription in patients with type I tyro- body begins to depend on fat for energy. When trans-
sinemia) ; portor-oxidation of fatty acids cannot go to completion,
8. Supplementing nutrients that are inadequately hypoglycemia results. If untreated, death may occur.
absorbed or not released from their apoenzyme In some disorders, myopathy and cardiomyopathy
(eg, biotin in patients with biotinidase deficiency). develop. Fever, anorexia, nausea and vomiting, which
9. Avoidance of fasting in disorders in which catab-
olism results in toxicity from metabolic break- accompany typical intercurrent illnesses in infants and
down products or in lack of energy supply because small children, or major metabolic stresses such as
of inability to utilize the energy of fatty acid oxi- trauma or surgery, worsen the catabolic state and the
dation [eg, medium chain acylCoA dehydrogenase rapidity of decompensation. Toxic concentrations of
substrate also decrease appetite and result in nausea
deficiency (MCAD)] .
and vomiting. In many of these disorders, acute nutri-
tion intervention, including the provision of adequate
Evidence
glucose and/or fat calories to prevent catabolism, may
The use of SNS in children with inborn errors of be essential to prevent neurologic injury or death. The
metabolism, including the use of specialized formula- provision of protein is far more complex6,13 and usually
tions, must be individualized for the specific patient not necessary for short-term treatment, although
and for the specific inborn error of metabolism. 1,2 PN can be safely used by experienced metabolic
Chemically defined formulations have been developed specialists. 14
for many of the inborn errors of metabolism, including
phenylketonuria, homocystinuria, maple syrup urine Practice Guidelines
. ,

disease, propionic acidemia, methylmalonic acidemia, ~i D i ~ . ~i

histidinemia, hyperlysinemia, tyrosinemia, and the
urea cycle disorders. Protocols have been developed for 1. Children with inborn errors of metabolism are at
each of these inborn errors of metabolism to optimize
nutrition support.2 With most of the inborn errors of nutrition risk and should undergo nutrition
metabolism, short-term studies clearly demonstrate screening to identify those who require formal
improvement with nutrition intervention (eg, in nutrition assessment with development of a
patients with methylmalonic and propionic acidemia, nutrition care plan. (B)
type I glycogen storage disease, maple syrup urine 2. Adequate nutritional intake in infants and chil-
disease, and phenylketonuria). 1-6 However, because of dren with inborn errors of metabolism should be
the small number of children diagnosed with each of assured to support normal growth and minimize
these conditions, data from prospective long-term neurologic impairment. (B)
studies demonstrating the effect of nutrition support 3. Many children with inborn errors of metabo-
are not conclusive, except in the case of phenyl- lism should eat only small amounts of normal
ketonuria. 7-9 Studies in the United States showed that foods and often need to rely upon special for-
IQ in children with PKU, diagnosed by newborn mulations (medical foods) for most of their
screening programs and treated within the first 4 needs for calories, protein, trace minerals, and
weeks of life with a phenylalanine-restricted diet, was vitamins. (B)
within 5 to 10 points of their unaffected siblings. This 4. Infants and children with inborn error; of metab-
compared with un IQ of about 40 to 50 in untreated olism require frequent monitoring of their condi-
children. In the United Kingdom, the Medical
Research Council showed that outcome in PKU was
tion, with appropriate changes in diet to achieve
closely related to degree of dietary compliance through- adequate growth and minimize metabolic compli-
cations. (B)
out childhood. The international collaborative project
5. SNS is required in children with inborn errors of
on maternal PKU demonstrated that the severe mental
metabolism to maintain growth development and
retardation, microcephaly, and congenital heart dis- metabolic homeostasis; special attention should
ease that occurred in more than 90% of infants born to
mothers with PKU untreated by diet during pregnancy be focused on the particular metabolic pathway
could be nearly completely prevented by good dietary that is abnormal to assure appropriate, disease
control established before pregnancy. specific formula modification. (B)
In most of these conditions, abnormal concentrations 6. Aggressive nutritional intervention should be
of metabolites can severely affect neurologic function. used in children with inborn errors of metabolism
Fasting even for a brief period may lead to potentially at times of catabolic stress to prevent, metabolic
life-threatening metabolic decompensation due to an decompensation, severe neurologic complications
inability to mobilize substrate (eg, glycogen storage and death. (B)
 131SA

REFERENCES short period of time after transplant until bowel func-

1. Seashore M, Wappner R: Genetics in Primary Care and Clinical tion is reestablished, or if complications develop.
Medicine. Appleton Lange, Englewood Cliffs, NJ, 1996, Chapters Aggressive nutrition support in the immediate postop-
13-15 erative period improves immune function parameters,
2. Acosta PB, Ryan AS: Functions of dietitians providing nutrition
support to patients with inherited metabolic disorders. J Am
promotes wound healing, promotes positive nitrogen
Diet Assoc 97:783-786; quiz 787-788, 824 (IV), 1997 balance, facilitates weaning from ventilatory support,
3. Winter S, Buist N: Clinical treatment guide to inborn errors of and shortens intensive care unit length of stay. PN
metabolism 1998. J Rare Dis 4:19-46 (IV), 1998 can be weaned as the postoperative ileus resolves and
4. Cockburn F, Clark BJ: Recommendations for protein and amino oral feedings are instituted. Supplemental EN may be
acid intake in phenylketonuric patients. Eur J Pediatr 155:
S125-S129 (IV), 1996 necessary for some infants and young children to com-
5. van der Meer SB, Poggi F, Spada M, et al: Clinical outcome and plement oral intake and to provide adequate calories
long-term management of 17 patients with propionic acidaemia. and protein for repletion. Nocturnal feedings, the pre-
Eur J Pediatr 155:205-210 (III), 1996 ferred method of supplementation, allow ambulation
6. Parsons HG, Carter RJ, Unrath M, et al: Evaluation of branched-
chain amino acid intake in children with maple syrup urine
and development of appetite during daytime hours.
disease and methylmalonic aciduria. J Inherit Metab Dis Nocturnal supplementation also helps to normalize
13:125-136 (III), 1990 eating behaviors with family and peers.56
7. Smith I, Beasley M: Intelligence and behaviour in children with Poor nutrition status, catch-up growth require-
early treated phenylketonuria. A report from the MRC/DHSS ments, postoperative medications, and surgical or med-
phenylketonuria register. Eur J Clin Nutr 43:1-5. (IIA), 1989 ical complications must all be taken into account dur-
8. Koch R, Azen C, Friedman EG, et al: Paired comparisons
between early treated PKU children and their matched sibling ing the posttransplant phase in an effort to achieve
controls on intelligence and school achievement test results at nutrition goals. For infants and young children, energy
eight years of age. J Inherit Metab Dis 7:86-90 (IIA), 1984 requirements are generally estimated at 100 to 130
9. Koch R, Levy HL, Matalon R, et al: The international collabora-
tive study of maternal phenylketonuria: status report 1994. Acta kcal/kg per day with 2.5 to 3.0 g/kg per day of protein.
Paediatr Suppl 407:111-119 (IIA), 1994 Older children generally require 70 to 90 kcal/kg per
10. Morris AA, Leonard JV: Early recognition of metabolic decom- day with 2.0 to 2.5 g/kg per day of protein. Needs must
pensation. Arch Dis Child 76:555-556 (III), 1997 be adjusted frequently based on clinical status and
11. Brivet M, Boutron A, Slama A, et al: Defects in activation and
transport of fatty acids. J Inherit Metab Dis 22:428-441 (III),
graft function. 2,4
1999 Evidence
12. Cederbaum SD: SIDS and disorders of fatty acid oxidation:
Although growth retardation is reported in pediatric
where do we go from here? J Pediatr 132:913-914 (IV), 1998
13. Acosta PB, Yannicelli S: Protein intake affects phenylalanine
patients both before and after transplantation, some
requirements and growth of infants with phenylketonuria. Acta
improvements have been seen with changes in immu-
Paediatr Suppl 1994, 407:66-67. (IIA)
nosuppressive protocols, early weaning of corticoste-
14. Koga Y, Iwanaga T, Yoshida I, et al: Maple syrup urine disease:
roids, and careful monitoring of nutrition support.
Nutritional management by intravenous hyperalimentation and
A study of 119 children after liver transplant
uneventful course after surgical repair of dislocation of the hip.
J Inherit Metab Dis 21:177-178 (III), 1998
reported linear growth improvement in most patients,
with the onset of catch-up growth between 6 and 24
SOLID ORGAN TRANSPLANTATION months after transplantation. Further, a study exam-
Background ining the outcomes of children with or without malnu-
trition showed significantly improved 1-year survival
Malnutrition and growth failure from end-stage rates in those
patients who were identified as being
organ diseases predisposes pretransplant pediatric well nourished. This was true whether the child had
patients to increased morbidity and mortality. Organ undergone a liver transplant or remained on a waiting
transplantation is an effective and often necessary list.
treatment for children with end-stage liver, kidney, or Impaired growth has been reported in 79% of prepu-
cardiac diseases. Liver and kidney are the most com- bertal cardiac transplant recipients who received daily
mon pediatric solid organ transplants performed. 1,2 prednisone for 1 or more years, yet normal range
End-stage organ disease often precludes the ability to weight and height is achieved by 5 years in 88% of
consume, metabolize, and adequately utilize nutrients children receiving heart transplants in infancy.1
to maintain adipose tissue and lean body mass. The North American Pediatric Renal Transplant
Nutrient requirements for these infants and pediat- Cooperative Study concluded that 75% of pediatric
ric patients are much higher then normal because of patients postrenal transplant have persistent growth
increased energy expenditure, need for repletion, and retardation. Of various factors that could predict
(in some instances) malabsorption. growth posttransplant, only age at transplant and the
The primary goal of nutrition care for pediatric original height deficit are significant. Children with
patient posttransplantation is to provide appropriate preexisting growth retardation who are over the age of
nutrition support to reestablish normal growth and 6 years at transplant are unlikely to exhibit catch-up
development. The ultimate objectives are complete growth after kidney transplant. 1,7 Although improve-
rehabilitation and improved quality of life.33 ments in linear growth have been seen after pediatric
During the acute posttransplant period, patients are liver and heart transplants, growth retardation
catabolic. There are increased nitrogen losses second- remains problematic after renal transplantation.
ary to preexisting malnutrition, surgical stresses and Children with congenital chronic renal failure (CRF)
the use of corticosteroids.4 PN may be required for a are at highest risk for growth retardation. During
 32SA

infancy and early childhood, malnutrition and electro- tion, the primary treatment for acute rejection. This
lyte imbalances are the main contributors to reduced increase in steroids can also lead to exacerbation of
growth. During puberty, hormonal disturbances are nutrition drug-nutrient interaction. Dietary modifi-
responsible for growth impairment. In infancy, loss of cations to treat the side effects caused by immunosup-
growth potential can be prevented by adequate nutri- pressive medications may be required, such as sodium
tion. However, later in life, catch-up growth can not be restriction for hypertension or ascites, carbohydrate
induced by nutrition intervention or dialysis. Renal restriction for hyperglycemia, and vitamin and mineral
transplantation allows for catch-up growth in a small supplementation. 1,2
percentage of patients. Administration of corticoste- Excessive weight gain may occur after solid organ
roids on an alternate day schedule can improve growth transplantation secondary to increased appetite from
in some but not all patients. Treatment with recombi- corticosteroids and the freedom of an unrestricted diet.
nant human growth hormone (rhGH) has been shown Hyperlipidemia, seen more commonly in renal trans-
to improve growth velocity and growth in all stages of plantation, hypertension, hyperglycemia, and osteopo-
renal disease and after transplantation. rhGH is able rosis can also occur from the use of steroids and other
to antagonize several of the side effects of long-term immunosuppressive drugs. 2,6
glucocorticoid administration posttransplant, such as Bone disease is common risk in transplant
a

growth failure, protein wasting, and osteoporosis, patients. Pretransplant bone demineralization in con-
without significant side effects. The improvement of junction with high-dose steroids causes calcium deple-
growth is most marked in the prepubertal patients and tion through decreased intestinal absorption and
during the first year of rhGH treatment. increased bone reabsorption. Detailed diet histories
An optimal quality of life with restoration of normal can provide insight into the actual calcium intakes of
growth and development is a primary goal of pediatric these patients. Many of these children have poor
transplant. Linear growth is of critical importance to intakes of dairy products because of previous diet
the emotional well-being and reintegration of trans- restrictions or intolerance. Calcium supplementation
plant recipients into normal childhood activities. Body may be helpful in some cases of mild disease. Careful
image may be affected by changes in appearance monitoring of serum electrolytes and mineral levels
caused by medications, poor growth, and surgical along with periodic bone density studies during the
scars. Adolescents are at highest psychosocial risk. follow-up period can provide information needed to
These issues can lead to risk taking behavior, which consider drug therapy to treat bone disease.2
may evolve into medication noncompliance, poor med- Management of immunosuppression depends on
ical follow-up, and drug or alcohol abuse. Noncompli- nutrition status. In a study of pediatric patients after
ance is a major cause of late rejection episodes in ado- renal transplantation, those who were malnourished
lescents. Once suspected, intervention to resolve before their transplant had lower cyclosporine levels
noncompliance should be initiated to meet the psycho- compared with those with normal nutrition.9
social needs of the adolescent.1
Practice Guidelines
,

Solid
,
Organ / / / /
Special Considerations
Posttransplant complications that most significantly 1. Children awaiting solid organ transplants or who
affect nutrition management include organ rejection, have received solid organ transplants are at
infection, fever, wound complications, and renal insuf- nutrition risk and should undergo nutrition
ficiency. screening to identify those who require formal
Chronic illness and anorexia can alter a childs eat- nutrition assessment with development of a
ing habits. Because some children have been exclu- nutrition care plan. (B)
sively fed formula, they may have difficulty accepting 2. Nutrition support in patients awaiting solid organ
different solid foods because of taste and texture sen-
sitivities. Taste aversions can occur because of the oral
transplantation should be used to maximize nutri-
tion status before surgery. (C)
administration of multiple medications and changes in 3. After transplantation, patients should receive
formula types.4 Another factor specific to pediatric
regular nutrition monitoring and counseling. (C)
transplantation that can negatively influence feeding
habits and nutrition status is oral aversion secondary REFERENCES
to intubations and preoperative enteral feedings. Sub- 1. Kosmach B, Webber S, Reyes J: Care of the pediatric solid organ
sequently, some chronically ill children 2may experience transplant recipient. Pediatr Clin N Am 45:1395-1418, 1998
developmental and feeding difficulties.2 2. Parkman-Williams C: Nutritional management following kidney
Growth retardation is reported in children both or liver transplant. Pediatric Manual of Clinical Dietetics. Amer-
ican Dietetic Association, 299-308, 1998
before and after transplantation. More recently, trends 3. Becht MB, Pedersen S, Ryckman F, Balistreri W: Growth and
in growth have improved because of careful monitoring nutritional management of pediatric patients following ortho-
of nutritional status, aggressive uses of SNS, and early topic liver transplant. Gastroenterol Clin N Am 22:367-380,
reduction of corticosteroid dose. Compromises in graft 1993
function and multiple operative interventions because 4. Kelly DA: Nutritional factors affecting growth before and after
liver transplantation. Pediatr Transplant 1:80-84, 1997
of postoperative complications can also contribute to 5. Shepard RW: Pre and postoperative nutritional care in liver
poor linear growth. Graft rejection negatively affects transplantation in children. J Gastroenterol Hepatol 11:S7-S10,
growth because of pulsed corticosteroid administra- 1996
 133SA

6. Hasse JM: Solid organ transplantation. IN Matarese L, its duration.16 Children with severe undernutrition
Gottschlich M (eds). Contemporary Nutrition Support Prac-
tice&mdash;A Clinical Guide. WB Saunders, Philadelphia, 40:547-560,
(less than 70% of median body weight for height)
present a life threatening acute problem; nutrition
1998
7. Tejani A, Sullivan K: Long-term follow-up of growth in children support takes precedence in the treatment priorities.
post-transplantation. Kidney Int Suppl 43:S56-S58, 1993 The risk for serious complications of malnutrition is
8. Mehls O, Blum WF, Schaefer F, Tonschoff B, Scharer K: Growth increased with decreasing age.17 A nasogastric tube
Failure in Renal Disease. Baillieres Clin Endocrinol Metab
affords the best short-term access for EN.18 Nasogas-
6:665-685, 1992 tric tubes can be safely used for a few months, if nec-
9. Lares-Asseff I, Zaltzman S, Perez Guille MG, et al: Pharmaco-
kinetics of cyclosporine as a function of energy-protein deficiency essary.19 Placement of a nasogastric tube can exacer-
in children with chronic renal failure. J Clin Pharm 37:179-185, bate a feeding problem caused by
1997 psychological,
behavioral, or environmental issues. 1 Immediate
nutrition rehabilitation may give the child more energy
EATING DISORDERS for feeding. In addition, this treatment reduces the
Background parents anxiety about the child starving. Potential
refeeding complications should be monitored if tube
Nutrition support is an important component of the feedings are initiated. Rarely, long-term nutrition sup-
treatment of infants and children with eating port by tube feeding may be needed for children with
disorders.l-3 Children presenting with serious eating eating disorders. In this case, a gastrostomy tube
problems may be affected by both physical illnesses should be placed. Many children further decrease their
and environmental stresses. Common physical ill- oral intake after tube feedings have been started, and
nesses associated with eating disorders include gastro- this option should be considered only when other
esophageal reflux,4-7 cancer,~ and prolonged periods options have failed and undernutrition becomes health
without eating due to endotracheal intubation99 or or life threatening. These children should receive
other medical treatment. Also at risk are infants with behavioral therapy with the goal of eventual weaning
congenital cardiac disease, a history of prematurity, from gastrostomy tube feeding.2 A nutritionally com-
and with physical disabilities, developmental delay, plete formula should be used to nourish the child. As
and chronic illness. Oromotor dysfunction may cause the child increases oral intake, the gastrostomy tube
disordered eating. These children usually have hypo- feeding should be decreased accordingly. There is
tonia and drooling or tongue protrusion. Children with rarely a role for PN in children with eating disorders. A
spastic cerebral palsy may also have oromotor prob- common complication of tube feeding in children with
lems. 10 eating disorders is conditioned retching, gagging, or
Infants and children may develop anorexia in situa- vomiting at the time of tube feeding. A calm reaction by
tions of chaos and stress, including periods of anxiety the parents and pleasant feeding routine are helpful.
or depression or a disordered parent-child relation- Children with mild-to-moderate undernutrition
ship. 111-14 Additionally, emotional disturbances can (more than 70% of median body weight for height) can
present as feeding problems in infancy. 15 Rarely, an usually be nutritionally rehabilitated using high calo-
infant eating disorder can develop in conjunction with rie foods without tube feeding. The use of high calorie
Munchausen syndrome by proxy or factitious food formulas and the addition of high fat foods to the
allergies. Some infants and children develop condi- childs diet may be adequate for increasing the childs
tioned aversions to some or all foods. An aversion could caloric intake.2i An organized schedule of meals for
be to a taste, a texture, or a combination of tastes and school age children is effective.22,23 Limitation of non-
textures. These children may have gagging, wretching, nutritious foods, drinks, and continuous snacking
or vomiting as part of their symptom complex. In the (grazing) is also helpful. Many children with eating
most severe cases the thought of food, or eating, or an disorders do not have normal hunger-satiety experi-
activity associated with eating (such as sitting in the ences. Therefore, the use of hunger as a motivator for
high chair) can stimulate vomiting. eating may not be helpful.24,25
One of the most common mistakes made in the eval- Behavioral therapy is an important component to
uation of infants and children with feeding disorders is the treatment of children with mild-to-moderate
emphasis on nutrition to the exclusion of eating behav- undernutrition. In some cases, children with eating
ior and mechanics. It is important to separately eval- disorders require partial or complete care away from
uate the childs nutrition status, the childs physical their families, such as in therapeutic day care or foster
ability to eat, and the childs psychological state related placement. Inpatient treatment programs are avail-
to eating. Therefore, the assessment should include a able for refractory eating.
nutrition evaluation, a medical evaluation, and a feed- EN should provide 1.5 to 2.0 times maintenance calo-
ing evaluation with particular emphasis on the neuro- ries for children with moderate-to-severe malnutrition.26
logical exam. The feeding evaluation should include When the child reaches an acceptable weight-for-height,
assessment of mechanical functions of eating and the the amount of EN should be decreased to maintenance
psychological conditions associated with eating. Older calories (including the childs oral intake). Children with
children may be evaluated as outpatients. Breast- or mild malnutrition, who require tube feeding, should be
bottle fed babies are often more easily evaluated in a started on maintenance calories.
clinical setting. Circadian rhythms should be considered when plan-
Nutrition treatment options for children with eating ning tube feedings for children who may regain their
disorders depend on their degree of malnutrition and ability to eat orally. The desire to eat is linked to
134SA

REFERENCES
physiologic cues stemming from the bodys normal
diurnal experience of the timing of eating.27-29 Chil- 1. Linscheid TR: Eating problems in children. IN Handbook of
dren who are maintained on night time drip-feedings Clinical Child Psychology, 2nd ed. Walter CE, Roberts MC (eds).
will often experience the desire for feeding because John Wiley & Sons, New York, 1992, pp 451-473
2. Linscheid TR, Budd KS, Rasnake LK: Pediatric feeding disor-
they are going to bed. This creates an inconvenient ders. IN Handbook of Pediatric Psychology, 2nd ed. Roberts MC
conflict for families trying to optimize oral feeding. The (ed). Guildford Press, New York, 1995, pp 501-515
choice of formula for children with eating disorders is 3. Christophersen ER, Hall CL: Eating patterns and associated
based on caloric density, cost, and availability. 30,3 For- problems encountered in normal children. Issues Compr Pediatr
mulas with fiber may be helpful to avoid constipation Nurs 3:1-16, 1978
4. Hart JJ: Pediatric gastroesophageal reflux. Am Fam Physician
for children than 1 year of age.
more
54:2463-2472, 1996
Monitoring of height, weight, and head circumfer- 5. Hillemeier AC: Gastroesophageal reflux: Diagnostic and thera-
ence should be done monthly when children are started peutic approaches. Pediatr Clin N Am 43:197-212, 1996
on tube feedings. 6. Hyman, PE: Gastroesophageal reflux: One reason why baby
wont eat. J Pediatr 125:S103-S109, 1994
7. Orenstein SR: Gastroesophageal reflux. Pediatr Rev 13:174-182,
Evidence 1992
8. Morris CS, Lough LR, Weinberger E: Infant with lethargy, fail-
There has been little research clinical decision-
on ure thrive, and abnormal blood smear. Invest Radiol 25:1054-
to
making concerning nutrition support in children with 1057, 1990
9. Berkowitz CD: Cardiopulmonary problems and disorders of the
eating disorders. There is a need for well-designed head and neck. IN Failure to Thrive and Pediatric Undernutri-
studies to compare the outcomes of patients treated
tion, A Transdisciplinary Approach. Kessler DB, Dawson P (eds).
with SNS and oral therapy compared with patients Brookes, Baltimore, MD, 1999, pp 227-238
treated with behaviorally only. It is important that 10. Rudolph CD: Feeding disorders in infants and children. J Pedi-
atr 125:S116-S124, 1994
comparison groups have similar degrees of malnutri- 11. Birch LL: Childrens preferences for high-fat foods. Nutr Rev
tion and of behavioral dysfunction.7 There is also very
50:249-255, 1992
little research on the outcomes of behavioral treatment 12. Birch LL, Johnson SL: Appetite control in children. IN Appetite
for children with eating disorders. and Body Weight Regulation. Fernstrom JD, Miller GD (eds).
CRC Press, Boca Raton, FL, 1994, pp 5-15
13. Black M, Hutcheson J, Dubowitz H, Berenson-Howard J, Starr
Practice Guidelines RH: The roots of competence: Mother-infant interaction among
Eatingy f I low-income. African-American families. Appl Dev Psychol
17:367-391, 1996
14. Chatoor I: Feeding disorders of infants and toddlers. IN Hand-
1. Children with eating disorders are at nutrition book of Child and Adolescent Psychiatry: Volume I. Infants and
risk and should undergo nutrition screening to Preschoolers: Development and Syndromes. Greenspan S,
Wieder S, Osofsky J (eds). John Wiley & Sons, New York, 1997,
identify those who require formal nutrition pp 367-386
assessment with development of a nutrition care 15. Rutter M: Psychosocial resilience and protective mechanisms.
plan. (B) Am J Orthopsychiatry 57:316-331, 1987
2. Infants and children with eating disorders should 16. Foy T, Czyzewski D, Phillips S, Ligon B, Baldwin J, Klish W:
Treatment of severe feeding refusal in infants and toddlers.
receive an oromotor assessment by an occupa- Infants Young Children 9(3):26-35, 1997
tional therapist, speech therapist, nurse, or phy- 17. Krebs NF: Gastroiontestinal Problems and Disorders, IN Failure
sician with training in pediatric oromotor dys- to Thrive and Undernutrition, A Transdisciplinary Approach.
function. (B) Kessler DB, Dawson P (eds). Brookes, Baltimore, MD, 1999, p
224
3. Infants and children with eating disorders should 18. Foy T, Czyzewski D, Phillips S, Ligon B, Baldwin J, Klish W:
receive a behavioral feeding assessment by an Treatment of severe feeding refusal in infants and toddlers.
infant mental health specialist, psychologist, Infants Young Children 9(3): 26-35, 1997
social worker, nurse, or physician with training 19. Moore MC, Greene HL: Tube feeding of infants and children.
Pediatr Clin N Am 32:401-417, 1985
in the behavioral aspects of infant and child feed-
20. Luiselli JK, Luiselli TE: A behavioral analysis approach toward
ing. (B) chronic food refusal in children with gastrostomy-tube depen-
4. Infants and children with eating disorders and dency. Topics Early Childhood Special Ed 15(1):1-18, 1995
severe malnutrition (less than 70% ideal weight 21. Cunningham KF, McLaughlin M: Nutrition. IN Failure to
for height) should receive high-calorie supplemen- Thrive and Pediatric Undernutrition: A Transdisciplinary
tal nutrition, using SNS if necessary. (B) Approach. Kessler DB, Dawson P (eds). Paul H. Brookes Pub-
lishing Co, Baltimore, MD, 1998, pp 99-119
5. Infants and children requiring nasogastric tube 22. Satter E: How To Get Your Kid To Eat ... But Not Too Much.
feedings for more than 2 months should be eval- Bull Publishing, Palo Alto, CA, 1987
uated for gastrostomy tube placement. (B) 23. Macht J: Poor Eaters: Helping Children Who Refuse To Eat.
6. Infants and children requiring tube feedings for Plenum, New York, 1990
24. Toomey KA: [Caloric intake of toddlers fed structured meals and
eating disorders should receive the minimum sup- snacks vs. on demand]. Unpublished raw data, 1994
plemental support necessary to maintain growth 25. Frank D: Failure to thrive. IN Behavioral and Developmental
and development. (B) Pediatrics: A Handbook for Primary Care. Parker S, Zuckerman,
7. A therapeutic plan for rehabilitation of oral feed- BS (eds). Mosby Year Book, St Louis, 1994, pp 134-140
26. Ashworth A, Millward DJ: Catch-up growth in children. Nutr
ing should be developed for children with feeding Rev 44:157-163, 1986
disorders who require feeding via nasogastric or 27. Thomas K: Biorhythms in infants and role of the care environ-
gastrostomy feeding tubes. (C) ment. J Perinat Neonatal Nurs 9:61-75, 1995
 135SA

28. Hellbrugge T, Lange JE, Rutenfranz J, Stehr K: Circadian peri- Special Considerations
odicity of physiological functions in different stages of infancy
and childhood. Ann NY Acad Sci 117:361-373, 1964 The etiology of diabetes in children is still uncertain.
29. Birch LL, Fisher JA: Appetite and eating behavior in children.
Pediatr Clin N Am 42:931-953, 1995
Recently, a close association between obesity and an
30. Cunningham KF, McLaughlin M: Nutrition. IN Failure to increased incidence of non-insulin dependent diabetes
Thrive and Pediatric Undernutrition: A Transdisciplinary mellitus has been found. 12,13 This finding strongly sup-
Approach. Kessler DB, Dawson P (eds). Paul H. Brookes Pub- ports the control of childhood obesity to reverse this
lishing Co, Baltimore, MD, 1998, pp 99-119 trend. The optimal glucose levels for hospitalized chil-
31. American Academy of Pediatrics. Committee on Nutrition: Com-
mentary on breast feeding and infant formulas, including pro- dren with diabetes mellitus have not been established.
posed standards for formulas. Pediatrics 58:276, 1976 However, it seems reasonable to maintain blood glu-
cose concentrations between 100 and 200 mg/dL. These
DIABETES values avoid the extremes of hypo- and hyperglycemia.
Background The former is particularly important, since identifying
the neuroglyopenic and adrenergic symptoms of low
Most children with diabetes have type 1 diabetes blood glucose concentrations may be difficult in
mellitus, which involves an absolute lack of insulin severely ill patients who are sedated and/or on
secretion. However, the incidence of type 2 diabetes mechanical ventilation.
mellitus in childhood appears to be increasing, partic-
The nutrition assessment, indications for nutrition
ularly in the black and hispanic populations.2 In this support, and estimation of nutrition needs for critically
latter group of patients, the diabetes is usually related
to obesity and is due to a relative lack of insulin secre- ill diabetic patients are similar to those of the nondia-
betic patient. Diabetic gastroparesis, which can be seen
tion, along with insulin resistance.
The normal mechanisms that maintain euglycemia in adults with type 1 diabetes mellitus, 14 is rarely
in the postabsorptive state and prevent hyperglycemia observed in children.
in the postprandial state are impaired, presumably There are no established protocols existing for the
because of excessive hepatic glucose release and optimal control of blood glucose concentrations in dia-
3
impaired glucose uptake.3 betic children. However, children with type 1 diabetes
Children who are stressed can have elevated blood mellitus are particularly prone to develop ketoacidosis;
glucose concentrations without a prior history of dia- therefore, prolonged elevation of plasma glucose con-
betes. In adults, severe stress is associated with eleva- centrations should be avoided. Usually, if patients are
tions in the counterregulatory hormones (specifically, receiving all of their feedings intravenously, a dose of
glucagon, epinephrine, cortisol, and growth hor- 0.1 units of regular human insulin is added for each
mone).1,5 These hormones counteract the effects of gram of dextrose in the infusate. i4 Such dosing is
insulin and lead to increased hepatic glucose release rarely associated with hypoglycemia; frequently,
and decreased peripheral uptake of glucose. In pediat- increased doses of regular insulin may be needed to
ric patients with diabetes, stress can cause even keep blood glucose concentrations within the goal
greater derangement in glucose metabolism, because range. If enteral feedings are being given, short-acting
children are unable to produce additional insulin in insulin is usually given as intermittent boluses until it
response to the elevations in counterregulatory hor- is clear the patient is tolerating feedings. Then, the
mones. patient can be switched to intermediate acting insulin.
No data exist concerning the optimal formula to utilize
Evidence in this situation. i4 Enteral formulas that are lower in
There are no prospective, randomized studies that carbohydrate and higher in fat have not been shown to
define optimal glucose management in hospitalized lead to an attenuated glycemic response. Despite lack
children with diabetes. Most strategies are extrapo- of controlled trials, the American Diabetes Association
lated from adult studies. has established guidelines for pediatric and adolescent
There is a growing body of evidence in adults that insulin dependent diabetes mellitus patients.15 These
include the provision of 50% to 65% of total calories as
hyperglycemia increases the incidence of nosocomial
infections in stressed, hospitalized patients .6-10 The complex carbohydrates and with high fiber content.
rate of central catheter infection was about five times Protein should contribute 12% to 20% and fat less than
30% of caloric intake, with less than 10% saturated fat
higher in diabetic patients receiving PN compared with and less than 300 mg/d from cholesterol. Similarly,
nondiabetic patients. In addition, elevated blood glu-
cose concentrations have been reported to be the most
recommendations for the fiber content of the formula
are the same as for the nondiabetic hospitalized child.
common risk factor for candida infection. However, all
of these reports have been in adults.
The explanation for these findings appears to be a Practice Guidelines
direct effect of hyperglycemia on leukocyte function. In I . ~, ,
vitro studies have shown that high blood glucose con-
centrations are associated with abnormalities in gran- 1. Children with diabetes mellitus are at nutrition
ulocyte adhesion, chemotaxis, phagocytosis, and intra- risk and should undergo nutrition screening to
cellular killing. 8 Respiratory burst function and identify those who require formal nutrition
superoxide anion production, as well as complement assessment with development of a nutrition care
function, also seem to be adversely affected. 11 plan. (B)
136SA

2. Blood glucose should be maintained between 100 The etiology of childhood obesity appears to be
and 200 mg/dL in hospitalized children with dia- multifactorial. 3-7 At least 20 genes, loci, or chromo-
]

betes. (B) Isomal regions have been identified that may be impor-
3. If PN is being given, intravenous insulin should 1tant in creating the human obesity phenotype. Recent
administered starting with 0.1 units of regular 4iata in children have demonstrated high serum leptin
human insulin for each gram of dextrose in the < concentrations in obese children, similar to what has
infusate. (B) 1been reported in obese adults.
4. If EN is being given, subcutaneous insulin should Many studies have suggested that obese and normal
be used to maintain the blood glucose level weight children have similar caloric intake, implicat-
between 100 and 200 mg/dL. (C) :ing differences in metabolic rate as being important in
the etiology of this condition. However, no consistent
REFERENCES differences in resting energy expenditure have been
1. Anonymous: Report of the expert committee on the diagnosis and found between obese and normal weight children.
classification of diabetes mellitus. Diabetes Care 20:1183-1197, Some data exist that overweight children may have a
1997 decreased food-induced thermogenesis. Previous theo-
2. Dabelea D, Pettitt DJ, Jones KL, et al: Type 2 diabetes mellitus
in minority children and adolescents: An emerging problem.
ries blaming abnormalities in adipocyte number have
Endocrinol Metab Clin N Am 28:709-729, 1999 not been substantiated. There are some recent studies
3. Dinneen SF: The postprandial state: Mechanism of glucose intol- suggesting that while obese children have similar
erance. Diabetes Med 14(Suppl 3):S19-S24, 1997 caloric intake to normal weight children, the composi-
4. Shamoon M, Hendler R, Sherwin R: Synergistic interactions tion of their diets may be different, with obese children
among anti-insulin hormones in the pathogenesis of stress
hyperglycemia in humans. J Clin Endocrinol Metab 52:1235- eating more fat and less fiber. There are also a num-
1241, 1981 ber of studies showing an association between child-
5. Schade DS, Eaton RP: The temporal relationship between endo- hood obesity and decreased energy expenditure during
genously secreted stress hormones and metabolic decompensa- exercise.
tion in diabetic man. J Clin Endocrinol Metab 50:131-136, 1980
6. Hostetter M: Perspectives in diabetes: Handicaps to host
Evidence
defense: Effects of hyperglycemia on C3 and candida albicans.
Diabetes 39:271-275, 1990 One recent study shows long-term benefit from
7. MacRury SM, Genmell CG, Paterson KR, et al: Changes in
phagocytic function with glycemic control in diabetic patients. behavioral, family-based treatment of childhood obe-
J Clin Pathol 42:1143-1147, 1989 sity in children ages 6 to 12 years.8,9 Up to a 10-kg
8. McMahon M, Bistrain BR: Host defenses and susceptibility to improvement in weight was demonstrated 10 years
infection in patients with diabetes mellitus. Infect Dis Clin N Am later when compared with controls. No role for SNS in
1-9, 1995 the treatment of childhood obesity uncomplicated by
9. Pomposelli JJ, Baxter JK, Babineau TJ, et al: Early postopera-
tive glucose control predicts nosocomial infection rate in diabetic intercurrent illness has been established.
patients. JPEN 22:77-81, 1998 No prospective, randomized studies exist to help the
10. Wallace LK, Starr NJ, Leventhal MJ, et al: Hyperglycemia on practitioner decide the optimal support for hospital-
ICU admission after CABG is associated with increased risk of
mediastinitis or wound infection. Anesthesiology 85:1286, 1996
ized, obese children requiring SNS. Although mainte-
nance energy and protein may be adequate in critically
11. Ortmeyer J, Mohsenin V: Inhibition of phospholipase D and
superoxide generation by glucose in diabetic neutrophils. Life Sci ill, obese adults to prevent fat storage and allow for
59:255-262, 1996 preservation of lean body mass,l similar studies have
12. Pinhas-Hamiel O, Dolan LM, Daniels SR, et al: Increased inci- not been carried out in children.
dence of non-insulin-dependent diabetes mellitus among adoles-
cents [see comments]. J Pediatr 128:608, 1996
13. Scott CR, Smith JM, Cradock MM, et al: Characteristics of
Special Considerations
youth-onset noninsulin-dependent diabetes mellitus and insu- Because of concerns about energy restriction on
lin-dependent diabetes mellitus at diagnosis. Pediatrics 100:84, growth and central nervous system development, SNS
1997
14. McMahon M, Rizza RA: Nutitional support in hospitalized energy intake is not reduced in the obese hospitalized
patients with diabetes mellitus. Mayo Clin Proc 71:587-594, child requiring nutrition support.&dquo;
1996 In patients with developmental delay, standard
15. Brink SJ: Pediatric, adolescent, and young-adult nutrition issues
in IDDM. Diabetes Care 11:192, 1988
growth and energy requirements (eg, RDA) do not
apply. 2 If EN is needed in such a patient, care must be
taken to not overfeed the child (to avoid obesity). Typ-
OBESITY
ically, energy needs are two thirds of that of normally
Background active children.
Obesity may be the most refractory health problem
facing health practitioners who care for children. In the Practice Guidelines
United States, up to 1 in 4 children fit the criteria of Obesity
being obese; even worse, the prevalence of this diagno-
sis appears to be increasing. Newly released growth 1. Obese children are at nutrition risk and should
charts from the National Center for Health Statis- undergo nutrition screening to identify those who
tics (NCHS) have chosen to use data from earlier require formal nutrition assessment with devel-
National Health and Nutrition Examination Surveys opment of a nutrition care plan. (B)
(NHANESs) for older children because of the increase 2. Weight loss should not be a goal for the acutely ill,
in the average weight of children in the United States.2 hospitalized obese child. (C)
 137SA

3. SNS for the acutely ill, hospitalized child who is home care team should include: parents or caregivers,
obese should be based on actual weight and not pediatricians, case managers, nutrition case specialist,
energy restricted. (C) subspecialists, nurses, teachers, dietitians, pharma-
cists, and visiting nurses. Other individuals may
include speech and occupational therapists and social
REFERENCES workers. The team should develop a plan of care and
1. Barlow SE, Dietz WH: Obesity evaluation and treatment: Expert disseminate it to all health care providers with updates
committee recommendations. J Pediatr 102:e29, 1998 as needed. Education of caregivers should begin in the
2. CDC Growth Charts: United States. Advance Data 314, 28 pp
(PHS) 2000-1250
hospital and carry over into the home. Written check-
3. Klish WJ: Childhood obesity: Pathophysiology and treatment.
lists ensure caregivers receive complete education.
Acta Paediatr Jpn 37:1-6, 1995 Repeat demonstrations of enteral and parenteral tech-
4. Bouchard C: Genetics of obesity: An update on molecular mark- niques help facilitate education and adaptation to care.
ers. Int J Obesity. 19:S310-S313, 1995 Standards of care or guidelines have been established
5. Hassink SG, Sheslow DV, de Lancey E, Opentanova I, Considine to reduce inappropriate variations in practice and to
RV, Daro JG: Serum Leptin in children with obesity: Relation-
ship to gender and development. Pediatrics 98:201-203, 1996 promote the delivery of high quality care.2 The Joint
6. Gazzaniga JM, Burns TL: Relationship between diet composition Commission Accreditation of Healthcare Organiza-
and body fatness, with adjustment for resting energy expendi- tions (JCAHO) Standards for Home Care also assists
ture and physical activity, in pre-adolescent children. Am J Clin home care organizations to develop high-quality care
Nutr 58:21-528, 1993
7. Kimm SYS: The role of dietary fiber in the development and systems.33
treatment of childhood obesity. Pediatrics 96:1010-1014, 1995 Monitoring of growth, biochemical parameters,
8. Epstein LH, Valoski A, Eing RR, et al: Ten-year follow-up of energy intake, macronutrients and micronutrient sta-
behavioral, family-based treatment for obese children. JAMA tus, and gastrointestinal function should be under-
264:2519-2523, 1990 taken to prevent complications. Complications can be
9. Epstein LH, Valoski A, McCurley J: Effect of weight loss by obese
children on long-term growth. AJDC 147:1076-1080, 1993 categorized into four groups: mechanical, infectious,
10. Amato P, Keating KP, Quercia RA, et al: Formulaic methods of nutritional, and metabolic. Monitoring of SNS patients
estimating caloric requirements in mechanically ventilated at home varies from program to program; there are no
obese patients: a reappraisal. Nutr Clin Pract 10:229, 1995 established national standards or evidence-based rec-
11. Butte NF: Energy requirements. IN Nutritional Care During
ommendations. Caregivers should monitor weight,
Infancy. Tsang RC, Lucas A, Uauy R, et al (eds). CV Mosby Co,
St Louis, 1988, p 86 fluid status, intake, and output on a daily basis, with
12. Spender QW, Crok CE, Charney EB, et al: Assessment of linear temperature and urine glucose readings daily to
growth of children with cerebral palsy: Use of alternative mea- weekly. Physical exam, weight, height, and head cir-
sures to height or length. Dev Med Child Neurol. 31:2206-2214,
cumferences (if the child is less than 1 year of age)
1989
should be performed on a routine basis and plotted on
growth curves. Published schedules of biochemical
HOME SPECIALIZED NUTRITION SUPPORT monitoring recommend electrolytes, BUN/creatinine,
calcium, phosphorus, magnesium, acid-base status,
Background visceral proteins, liver function tests, glucose, triglyc-
Indications for home SNS mirror those for hospitalized erides and complete blood counts initially weekly to
patients with the exception that the patients clinical monthly with the frequency decreasing over time. 4,5
status has stabilized sufficiently to permit care in a the Iron studies, platelet, folate/vitamin B-12, and carni-
less acute home environment. With the transfer of tech- tine levels should be obtained as indicated. Trace ele-
nology into the home, patients are now being discharged ment studies every 2 to 6 months and fat-soluble vita-
who have more complex home care needs. Thus, before min assessment every 6 to 12 months are appropriate.
sending an infant, child or adolescent home, a critical
evaluation of not only the nutritional requirements but of
Evidence
all the health care needs must be undertaken.
Often, nutrition needs must be integrated with other Providing SNS in the home has been demonstrated to
services to promote growth and development. Meeting be cost-effective. Additionally, children can gain weight
all of the needs of children requiring high-tech support and stature with both PN and EN.6-11 In children receiv-
is often requires engagement of numerous health care ing PN long term, improvements have been seen in neu-
services. Coordination of care requires innovative rologic and intellectual development 6 months after hos-
approaches to keep all health care workers informed of pital discharge.9 For children who require frequent
the childs status. A discharge plan should be initiated rehospitalization, delays are seen in nonverbal perfor-
as soon as it is evident the child will recover and be mance, attention, and perceptual-motor abilities. These
sent home. Childien discharged on home SNS must be rehospitalizations may occur because of need for surgery
physiologically stable, have caregivers who are willing because of the childs primary medical problem or cathe-
and able to provide care, and have appropriate ter placement, cholestatic jaundice, catheter sepsis, and
resources available including a safe home environ- other significant infections.o Children who receive home
ment. EN and their caregivers have reported difficulties with
The establishment of interdisciplinary nutrition sup- sleep disturbances, mostly due to nocturia, vomiting and
port teams has proven to be beneficial to hospitalized infusion pump monitoring and malfunction.ll Although
patients. Many home care organizations have extrap- data are limited, numerous studies confirm that favor-
olated this concept into their practice. Members of the able outcomes may be achieved with long-term home PN
138SA

2. A.S.P.E.N Board of Directors: Standards for home nutrition sup-

as measured by maintenance of growth and weight
port. Nutr Clin Pract 14:151-162, 1999
gain.12 3. Joint Commission on Accreditation for Healthcare Organization
Board of Directors: 2000 Comprehensive Manual for Home Care.
Practice Guidelines
,

Oakbrook, IL, 1998, 1999

I .
I I n ~ I W I 4. Davis AM. Pediatrics: IN Contemporary nutrition support prac-
tice: A clinical guide. Matarese LE, Gottschlich MM (eds): WB
Saunders Company, Philadelphia, PA, 1998, pp 347-364
1. Children receiving home SNS are at nutrition risk 5. Ireton-Jones C, Orr M, Hennessy K: Clinical pathways in home
and should undergo nutrition screening to identify nutrition support. J Am Diet Assoc 97:1003-1007, 1997
those who require formal nutrition assessment with 6. Greene HL, Helinek GL, Folk CC, et al: Nasogastric tube feeding
development of a nutrition care plan. (B) at home: A method for adjunctive nutritional support of mal-
2. SNS should be initiated for the indications appro- nourished patients. Am J Clin Nutr 34:1131-1138, 1981
7. Bisset WM, Stapleford P, Long S, et al: Home parenteral nutri-
priate to the underlying disease. (C) tion in chronic intestinal failure. Arch Dis Child 67:109-114,
3. Discharge planning and follow-up care for home 1992
SNS patients should be interdisciplinary. (C) 8. Dahlstrom KA, Strandvik B, Kopple J, et al: Nutritional status
4. Education of caregivers for home SNS patients in children receiving home parenteral nutrition. J Pediatr 107:
should begin before discharge and continue in the 219-224, 1985
home care setting. (C) 9. Ralston CW, OConnor MJ, Ament M, et al: Somatic growth and
5. SNS, in a home environment, should only be given if developmental functioning in children receiving prolonged home
total parenteral nutrition. J Pediatr 105:842-846, 1984
patients have caregivers who are willing and able to 10. OConnor MJ, Ralston CW, Ament ME: Intellectual and percep-
provide care, and have appropriate community tual-motor performance of children receiving prolonged home
resources to assure a safe environment. (B) total parenteral nutrition. Pediatrics 81:231-236, 1988
6. Routine monitoring of home SNS should be per- 11. Holden CE, Puntis JWL, Charlton CPL, et al: Nasogastric feed-
formed to prevent complications. (C) ing at home: Acceptability and safety. Arch Dis Child 66:148-
151, 1991
REFERENCES 12. Leonberg BL, Chuang E, Eicher P, et al: Long term growth and
1. Nehme A: Nutritional support of the hospitalized patient. JAMA development in children after home parental nutrition. J Pediatr
243:1906-1908, 1980 132:461, 1998