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Invited Review

Hypocaloric Considerations in
Patients With Potentially
Hypometabolic Disease States

Nutrition in Clinical Practice


Volume 26 Number 3
June 2011 253-260
2011 American Society for
Parenteral and Enteral Nutrition
10.1177/0884533611405673
http://ncp.sagepub.com
hosted at
http://online.sagepub.com

Barbara Magnuson, PharmD, BCNSP; Amy Peppard MHA,


RD, LD, CNSC; and Deborah Auer Flomenhoft, MD
Financial disclosure: none declared.

CP pose a particular challenge in nutrition assessment. Several


studies demonstrate that patients with CP have significantly
lower caloric requirements than anticipated using predictive
equations; thus, patients with CP benefit from indirect calorimetry. Provision of nutrition for obese patients is briefly addressed,
as this is an increasingly important consideration for nutrition
support in both the critical care and long-term care settings.
When indirect calorimetry is not available, clinicians should
remember that most patients will have low resting energy
expenditure regardless of functional status and require frequent
evaluation during institution of nutrition recommendations to
guard against overfeeding and obesity. (Nutr Clin Pract.
2011;26:253-260)

The provision of nutrition has traditionally been driven by the


desire to provide adequate calories. However, over the past decade it has become evident that provision of excess calories can
be detrimental to patients outcomes in both critical care and
long-term care settings. This review examines patient populations for whom hypocaloric nutrition can be both appropriate
and beneficial. In specific situations, critically ill patients, such
as those with obesity, stroke, and spinal cord injury, may have
decreased energy requirements. In patients with spinal cord
injury, the level of injury significantly correlates with the extent
of reduced caloric energy expenditure. Ventilator-dependent
patients with amyotrophic lateral sclerosis (ALS) have decreased
energy needs; energy expenditure for ALS patients is lower than
the predictive equation value. Aging patients will have decreased
energy needs relative to a reduction in lean body mass. Patients
with cerebral palsy (CP) have significantly lower caloric requirements than anticipated using predictive equations. Patients with

Keywords: energy expenditure, nutrition therapy, nutrition


assessment, stroke, spinal cord injury, cerebral palsy,
amyotrophic lateral sclerosis

previous baseline because of their injury, rehabilitation,


or their chronic disease state. Not all patients require
additional calories and protein in the acute disease
state. In specific situations, caloric requirements are not
increased during the critical care phase as once thought.
This article addresses acute and chronic clinical situations in which patients can experience a decrease in
caloric requirements.
Energy expenditure comprises the basal metabolic
rate (BMR), thermic effect of food and digestion, and
physical activity.1 The BMR accounts for about 65% of
the total energy expenditure (TEE). Specific calculations,
such as the Harris Benedict equation (HBE) and number
of calories per kg of body weight, are used to assess the
caloric needs of patients and are referenced throughout
this article; however, indirect calorimetry remains the
gold standard for determining the caloric needs of an
individual. Calculations used to estimate the total daily
energy requirements often factor weight, and will factor
height, and age into the equation. Changes in lean body
mass composition can change the BMR and ultimately
the total daily energy requirements. A neurological impairment with an altered sympathetic nervous system can also

ollowing injury or the acute onset of a disease


state, many patients are hypermetabolic and
hypercatabolic, requiring additional calories and
protein. Energy requirements can be increased for several reasons. Catecholamine response to severe stress
and severity of injury can be magnified by preexisting
acute and chronic disease. The hypermetabolic/hypercatabolic state can last for weeks or months depending
on the severity of the injury, chronic or acute disease
states, and the type of and extent of rehabilitation.
Clinicians must avoid both acute and chronic malnutrition or face treating the consequences once they develop.
At some point during the rehabilitation phase, most
patients will revert from the hypermetabolic phase to
their previous baseline, providing that activity level and
preexisting disease are comparable. However, some
patients caloric requirements will decrease from their

From the University of Kentucky HeathCare, Lexington, Kentucky.


Address correspondence to: Barbara Magnuson, PharmD,
BCNSP, UK Hospital - H110, 800 Rose Street, Lexington, KY
40536; e-mail: blmagn0@email.uky.edu.

253

254 Nutrition in Clinical Practice / Vol. 26, No. 3, June 2011

account for significant changes in BMR. Several studies


and reviews have postulated why BMR decreases. The
thermic effect of food is fairly consistent. Physical activity, which varies based on the patients capacity to ambulate and exercise, should be factored into the total daily
caloric requirements.
Inappropriate nutrition in the acute and long-term
care settings directly and indirectly increases costs and
contributes to patient debilitation. Just as undernutrition
can become detrimental, chronic overnutrition can have
deleterious results as well. Weight gain and eventual
obesity occur with prolonged positive caloric intake. In
turn, obesity with or without decreased BMR can result
in detrimental conditions, such as hyperglycemia, cardiac
disease, and respiratory compromise.

Critical Care Settings


Typically, the critically ill patient experiences hypermetabolism due to his or her injuries or the exacerbation of
a disease state. However, in specific situations, critically
ill patients, such as those with obesity, stroke, and spinal
cord injury, can have decreased energy requirements. The
nutrition support assessment and therapy should account
for the changes in metabolic demand, as they can have
clinical implications. Acute overfeeding can produce deleterious effects in this patient population. Hyperglycemia
has been correlated with increased infection in the critically ill population as well as worsening the neurological
outcome.2,3 Acute overfeeding can result in a refeedinglike syndrome with drastic potassium and phosphorus
serum depletions. Ventilator weaning can become compromised with hypercarbia.
In the past, it has been suggested that hospitalized
patients have increased caloric needs because of illness.
However, Miles4 reviewed 19 studies and concluded that
the mean resting energy expenditure (REE), as determined
by indirect calorimetry, for hospitalized patients, excluding
patients with head injuries, burns, or fevers, is on average
only 113% of the basal energy expenditure (BEE) calculated using the HBE. This indicates that the only modification needing to be applied to the HBE is a 1.13 stress
factor. Miles reviewed studies using patients with cancer,
pulmonary disease, cardiovascular disease, and sepsis, in
addition to trauma and surgery patients. The highest measurements were made in patients while they were being fed.
This is inconsistent with earlier studies of extremely high
estimated caloric requirements.
Ligget and Renfro5 found similar results in their
study of 73 nonsurgical, mechanically ventilated patients.
These researchers compared the results of measured
energy expenditure (MEE) with estimated nutrition needs
using the HBE. No statistical differences were reported
between the measured and HBE-predicted values for

patients with cardiogenic shock, cardiopulmonary edema,


acute respiratory distress syndrome, or pneumonia. Sepsis
was the only condition resulting in statistically significant
increases in metabolism. Ligget and Renfro concluded
that hypermetabolism is uncommon in nonsurgical, nonseptic, critically ill patients; therefore, the nutrition needs
of this population can be adequately predicted using the
HBE without any additional stress or activity factors.5
Pirat et al6 evaluated MEE using indirect calorimetry for
34 critically ill cancer patients and compared the patients
MEE with their estimated energy expenditure using the
HBE. The mean MEE (1623 384 kcal/d) was similar to
the mean HBE without an additional stress or activity
factor (1613 382 kcal/d, P = .87). This study concluded
that indirect calorimetry is the ideal method of determining the nutrition needs of this population. However, if
MEE is not feasible, the HBE without any stress or activity factors is ideal to avoid overfeeding.6
It is crucial to consider the effect that medications
have on the metabolic needs of the critically ill patient.
Swinamer et al7 reported that morphine infusions can
decrease MEE as measured by indirect calorimetry by an
average of 8% in the critically ill patient. Although this
alone may not be clinically significant, the neuromuscular blockade doses administered following trauma, and
especially traumatic brain injury, can produce significant
decreases in energy expenditure. McCall et al8 evaluated
18 severely head-injured adult patients receiving continuous infusions of the neuromuscular blocker pancuronium along with morphine and 14 severely traumatized
patients without severe head injury who received only
morphine. The MEE was determined by indirect calorimetry. The investigators reported an energy expenditure
decrease of 4.6 kcal/kg/d (20.3%, P = .002), which was
statistically and clinically significant. The decreased
expenditure was nearly 5% below the predicted energy
expenditure (PEE) from HBE using actual weight, which
nearly eliminates the typically severe hypermetabolism
resulting after traumatic brain injury.8 Barbiturateinduced coma to control refractory intracranial hypertension following traumatic brain injury also drastically
decreases energy expenditure. Dempsey and colleagues9
evaluated 10 patients with traumatic brain injury within
2 weeks of injury and compared the MEE by indirect
calorimetry with the HBE. The investigators demonstrated a change of nearly 40% when barbiturates were
administered. Dempsey et al9 reported that head-injured
patients averaged 26% above PEE using the HBE without barbiturates to a decrease of nearly 14% below the
PEE. These findings are consistent with results reported
from other studies. Fried and colleagues10 evaluated 7
severely head-injured patients within the first week of
injury. The investigators demonstrated a 42% decrease of
REE by indirect calorimetry during barbiturate therapy
(132% 28% without barbiturate vs 76% 23% with

Patients With Potentially Hypometabolic Disease States / Magnuson et al 255

barbiturate, P < .01), and nitrogen elimination decreased


by about 40%.10,11 Even though these therapies are not
intended for long-term use, the nutrition support assessment and therapy should adjust the calorie and protein
needs accordingly.
Bitzani and colleagues,12 in a study of 30 critically ill
patients with isolated head injuries, compared REE as
determined by indirect calorimetry with BMR as calculated by the HBE. Twenty patients were admitted with
brain death or progressed to brain death. The brain death
patients REE measured at 25% reduction compared with
their BMR. The investigators concluded that the decrease
in REE was attributable to the cessation of cerebral blood
flow and consequently cerebral metabolism and not to
hypothermia. These results proved clinically relevant for
a pregnant patient in the intensive care unit (ICU) at the
University of Kentucky Hospital who was determined to
be clinically brain dead. Calories were reduced for clinical condition with appropriate additional calories to
account for fetal growth and development. The reduced
calorie needs were verified by use of indirect calorimetry
on repeated occasions. An additional 300 kcal for fetal
growth was added to the measured energy needs. The
pregnant patient carried the fetus to near term without
any overfeeding-associated complications, which might
have led to extreme prematurity or fetal demise.
The Society of Critical Care Medicine and the
American Society for Parenteral and Enteral Nutrition
recently published guidelines addressing critically ill
obese patients and permissive underfeeding with enteral
nutrition (EN).13,14 For all classes of obesity where body
mass index (BMI) is >30, the goal of the EN regimen
should not exceed 60%-70% of target energy requirements, which equates to 11-14 kcal/kg of actual body
weight per day or 22-25 kcal/kg of ideal body weight per
day. Protein should be provided in a range 2.0 g/kg of
ideal body weight per day for class I and II patients
(BMI 30-40) and 2.5 g/kg of ideal body weight per day
for class III (BMI 40).13,14 These guidelines for critically ill obese patients and permissive underfeeding
with EN are based on class C evidence.13 In a retrospective review of 40 critically ill surgical patients, those
receiving hypocaloric EN had reduced ICU stays (18.6
vs 28.5 days, P < .03) and reduced duration of antibiotic therapy (16.6 days vs 27.4 days, P < .03).15
Hypocaloric feeds were suggested to promote glycemic
control and to improve body compositioning thereby
theoretically improve attendant comorbidities. However,
it may be that hypocaloric feeds more accurately meet
the obese patients nutrition needs. Stucky et al,16 in a
study of 19 obese burn and trauma patients, compared
the patients MEE as determined by indirect calorimetry
with their calculated needs using predictive equations.
The investigators found that the HBE with the recommended 20% injury factor overestimated patients caloric

needs in the acute phase of their injury. However, if the


injury factor was omitted, the HBE best represented the
patients MEE when compared with other predictive equations. In a study comparing indirect calorimetry with predictive equations in 36 obese patients requiring nutrition
support, the HBE with a stress factor of 1.5 for ICU
patients and 1.2 for ward patients best approximated indirect calorimety. The HBE predicted REE within 10% in
only half of patients.17 Currently, hypocaloric feeding of
obese ICU patients is recommended; in practice, it seems
to promote euglycemia and improve outcomes. However,
rigorous prospective studies are needed to elucidate the
best way to calculate calorie needs and to establish the
benefit of hypocaloric feeding.

Stroke
The conventional wisdom that stroke patients are initially
hypermetabolic has been challenged over the past decade.
Results of several studies support excluding a stress factor
from the HBE in order to avoid the complications of overfeeding, especially hyperglycemia from an excessive
caloric load. Bardutzky and colleagues18 evaluated 34
sedated, mechanically ventilated patients with ischemia
and hemorrhagic stroke by comparing their HBE with
their TEE as determined by continuous indirect calorimetry.18 The investigators reported that TEE was low during
the first 5 days after ICU admission following a stroke.
Linear regression analysis revealed a significant relationship between TEE and the HBE values without a stress or
activity factor (r2 = 0.9, P < .0001). The results demonstrated that patients have lower TEE following a stroke
than do other critically ill patients. The TEE did not differ
between acute cerebral ischemia or intracerebral hemorrhagic strokes. The HBE for basal energy needs appeared
to most accurately calculate the TEE for a stroke patient.
Finestone and colleagues19 evaluated energy expenditure
in 91 stroke patients from the time of their stroke to 90
days thereafter compared with matched controls. Seventysix (84%) had sustained ischemic strokes and 15 had
(16%) hemorrhagic strokes. The investigators measured
the REE prospectively on days 7, 11, 14, 21, and 90 by
indirect calorimetry and compared it with HBE (using an
adjusted weight for patients >125% ideal body weight).
The mean REE ranged from 107% 14.9% to 114%
12.9% of the % HBE for the stroke patients compared
with 112% 11.4% of the controls, which was not statistically different. The REE did not vary with stroke characteristics, but the investigators suggested that a larger
subgroup should be evaluated. Energy expenditure
increased by only 10%-15% above the HBE, and these
data dispute earlier notions that stroke patients exhibit
an initial hypermetabolic phase similar to traumatic
brain injury. These results indicated a lack of a severe

256 Nutrition in Clinical Practice / Vol. 26, No. 3, June 2011

hypermetabolic response phase acutely following either


type of stroke. Long-term energy expenditure following a
stroke will clearly depend on the patients capacity to participate in physical therapy during rehabiltion. The patient
who becomes nonambulatory and bedridden will experience a further decrease in energy expenditure.

Spinal Cord Injury


Early reports established a standard to predict energy
expenditure for spinal cord injury (SCI) by using the HBE
with a 1.2 activity factor and then again multiplied by 1.6
for an injury factor.20 It was assumed that the patient was
initially severely hypermetabolic because of the injury
itself. Two landmark studies evaluated energy expenditure
in the acute injury phase and the early rehabilitation phase,
and both suggested that the traditional use of stress factors
grossly overestimates patients caloric needs. Kolpek et al21
compared MEE, determined by indirect calorimetry, of
patients with severe head trauma and patients with SCI
and then compared those values with the predictive values
of the HBE. The overall mean MEE for the head injury
group was 2,385 171 kcal/d compared with 1,760 288
kcal/d for SCI (P = .06). The investigators reported that
during week 1, the SCI patients had MEE values that were
only 56% of PEE as calculated by the HBE. Overall, the
energy expenditure for SCI patients was only 94% of HBE
compared with 48% higher for head-injured patients.
Cox and colleagues22 observed 15 quadriplegic
patients who required only 22.7 kcal/kg/d compared with
27.9 kcal/kg/d in 5 paraplegic patients during the early
rehabilitation phase. These measured values as determined by indirect calorimetry were compared with several
predictive equations and found to be 10%-55% lower than
predictive equations. After an initial weight loss following
injury, the patients gained an average of 1.7 kg/wk. These
results suggested that calorie goals for individuals with
SCI should be reduced to avoid obesity. Following SCI,
muscle atrophy correlates with the severity and level of
cord injury. The level of SCI appears to significantly correlate with the extent of reduced caloric energy expenditure. More recently, Rodriguez et al23 evaluated 12 SCI
patients during the first 4 weeks following injury. The
investigators reported much lower MEEs by indirect
calorimetry compared with the traditional PEE for SCI as
determined by the HBE 1.6 (stress factor) 1.2 (activity factor). Their results were consistent with several
previous studies that found SCI patients to have drastically lower MEEs than reflected by predicted equations.
The investigators suggested eliminating the 1.2 activity
factor, reducing the stress factor for caloric prediction,
and not relying on nitrogen balance studies to predict
calorie needs.23 Rodriguez et al24 had reported in an
earlier study that 10 SCI patients experienced persistent

negative nitrogen balance for the first 7 weeks despite


aggressive nutrition support aimed at providing their PEE
(HBE 1.6 [stress factor] 1.2 [activity factor]) and at
least 2 g per kg of ideal body weight per day. The SCI
patients were compared with 20 matched controls with
multisystem trauma without SCI. Seventeen of 20 control
patients achieved positive nitrogen balance within 3 weeks
of admission while requiring an average of 2.3 g per kg of
ideal body weight per day and 110% of their PEE. The
investigators concluded that aggressive attempts to achieve
a positive nitrogen balance in the SCI population will possibly fail and likely result in drastic overfeeding.
Gater25 suggested modifying the interpretation of
BMI for SCI patients in order to define normal as
<22 kg/m2, overweight as 22-25 kg/m2, and obese as
>25 kg/m2. Groah et al26 examined the nutrient intake
and BMI of 73 community-dwelling individuals with SCI
for >1 year. Nearly 70% of the SCI population was overweight according to the adjusted BMI recommendations
suggested by Gater. Groah et al26 reported that intake of
several vitamins, minerals, and macronutrients did not
meet recommended levels or were excessively low, whereas
sodium and alcohol intake were elevated. The investigators also observed a high level of interest from the
patients in proper nutrition. Groah and colleagues advised
clinicians to encourage simple changes and to provide
nutrition counseling; patients should be advised to
increase fruits, vegetables, fiber, vitamins (especially vitamin D), and minerals, while decreasing overall fat and
refined carbohydrates. Monroe and colleagues27 evaluated the energy expenditure of 10 males with SCI, 9 with
paraplegia, and 1 highly functional man with quadriplegia, and compared the results with 59 age-matched, noninjured male control subjects. All participants were
evaluated 2 years or more following their SCI injury.
These patients were admitted to a metabolic ward for >2
days. One of these days was spent in a respiratory chamber to measure 24-hour resting, basal, and sleeping metabolic rates and spontaneous physical activities along with
the thermal effect of food. The investigators concluded
the individuals with SCI expended significantly lower
daily energy than the control subjects. The lower energy
expenditure in patients with SCI was explained by lower
levels of physical activity, lower resting metabolic rate,
and the thermic effect of food.27
Over the course of years following an SCI, individuals develop an altered body composition with reduced
lean body mass, reduced bone mineral density, and
increased fat mass.28,29 They are at risk of the traditional
obesity-related disorders such as diabetes and cardiovascular disease. The majority of people with SCI can benefit from nutrition counseling to prevent emerging
secondary conditions as they age. Rajan et al30 reviewed
several issues regarding the management of obesity in
individuals with SCI. The investigators suggested that

Patients With Potentially Hypometabolic Disease States / Magnuson et al 257

weight loss programs be designed that consider the barriers to dietary and physical activity unique to this population.30 Clearly, a well-designed long-term study is
necessary to evaluate the benefits of weight loss and sustained lower BMI in this population.

Amyotrophic Lateral Sclerosis


Amyotrophic lateral sclerosis (ALS) is a neurodegenerative condition of unknown cause that affects the upper
and lower motor neurons. This disease is rapidly progressive with a mean survival rate of only 2-4 years.31
Dysphagia, due to oropharyngeal muscle weakness, is one
of the first nutrition concerns exhibited by ALS patients.
Decreased nutrition intake resulting from dysphagia can
lead to malnutrition. Over time, many ALS patients will
require tracheostomy and intermittent positive pressure
ventilation secondary to the patients inability to spontaneously breathe. At this point, EN often becomes the
primary source of nutrition. Because of progressive muscle atrophy and weakness, it is thought that ventilatordependent ALS patients likely have a decreased energy
need. Siirala et al32 compared the measured indirect calorimetry values of ALS patients with their predicted REE
values using 5 different predictive equations. This study
found the mean MEE for these patients to be 33.6%
lower than the mean value calculated using predictive
equations. There is concern about overfeeding ventilatordependent patients because total body carbon dioxide
production is increased with storage of excessive carbohydrates, which in turn increases the need for ventilation.
Limited information is available regarding the nutrition
needs of patients with ALS, along with other conditions
that can lead to long-term ventilation, such as GuillainBarr syndrome and locked-in syndrome. Therefore, the
assessment of energy needs for patients receiving longterm ventilation is an area of interest that warrants further research.

Aging
It is assumed that as individuals age, their energy needs
decrease because of to a reduction in lean body mass.33
When determining the nutrition needs of older individuals, the clinician must consider the persons cognitive and
physical abilities. A decrease in these abilities often contributes to malnutrition in the aging population. Ahmed
and Haboubi34 reported that 16% of individuals >65 years
old are considered malnourished. However, these investigators also reported that 58% of Americans aged 65 years
and older have a BMI 25, which would classify them
as overweight with a need for reduced caloric requirements. Based on the large variation in malnourished

versus overweight elderly Americans, calculating energy


needs in this population becomes difficult. Most commonly, predictions of energy needs in elderly people are
made through use of equations such as the HBE. However,
use of the HBE in estimating energy needs for elderly
people has been criticized because of the lack of elderly
subjects in the original population studied. Compher et
al35 studied the energy expenditure of 61 African American
patients >65 years old who were admitted to a skilled
nursing facility. By comparing measured resting metabolic rate with BEE using the HBE, Compher et al concluded that the predictive equation underestimated the
patients nutrition needs. This study concluded that MEE
is the ideal way of determining energy needs for elderly
patients; however, if this measurement is not feasible, it
is suggested that this population requires an average of 25
kcal/kg/d.35 There is also indirect evidence suggesting that
the metabolic rate of individual organs is lower in older
compared with younger individuals. With aging, reductions in the mass of individual organs/tissues and in the
metabolic rate of tissue-specific organs contribute to a
reduction in resting metabolic rate, which in turn promotes changes in body composition favoring increased fat
mass and reduced fat-free mass.36

Cerebral Palsy
Patients with cerebral palsy (CP) pose a particular challenge in nutrition assessment. Patients with mild CP tend
to be obese compared with unaffected peers. However,
those with moderate to severe CP diverge significantly
from growth curves established for typical children: these
patients are shorter and lighter. The deviation from typical values becomes more pronounced in adolescence.
Patients with greatest observed growth as determined by
weight and tibial length are healthier: they use fewer
healthcare resources, spend fewer days in the hospital,
and have fewer school absences.37 But whether the
growth issues associated with CP are associated with
nutrition or with the underlying neurologic insult is not
clear, and increasing weight by offering a hypercaloric
diet is unlikely to improve functional status. Usual anthropometric measurements are not reliable in assessing the
nutrition status of patients with moderate to severe CP.
These patients have very low lean body mass: many do not
bear weight and their neurologic insult is often associated
with endocrine dysfunction. BMI therefore underestimates nutrition status. Kuperminc et al38 found that
clinical measurements of body composition were very
poor predictors of body fat in children with moderate to
severe CP. All indicators (BMI, arm circumference, triceps skinfold thickness) underestimated percentage of
body fat when compared with the gold standard, dualenergy x-ray absorptiometry. Johnson et al39 described

258 Nutrition in Clinical Practice / Vol. 26, No. 3, June 2011

high intramuscular fat content in the lower extremities of


children with spastic quadriplegia, a finding that has been
strongly associated with the chronic diseases of obesity.
REE appears to be lower across the spectrum of disability in patients with CP. Several studies of REE measured
by indirect calorimetry demonstrate that patients with CP
have significantly lower caloric requirements than anticipated using predictive equations. REEs in these studies
were generally about 75% of predicted requirements.40-42 A
recent study of TEE in mildly affected CP patients showed
decreased TEE compared with typical peers despite higher
energy expenditure with walking: 1,676 303 kcal/d versus 1986 499 kcal/d.43 These findings are consistent with
a prior report of adult energy expenditure by Johnson et
al44 in 1997. The observed dramatic reduction in energy
expenditure has been attributed to reduced physical activity, decreased cellular mass, or, more common, an inherent
function of the neurologic insult.40,43
Despite strong data regarding the body composition
and REE of patients with CP, the clinician must remember that patients with CP are at significant risk for malnutrition, and low anthropometric measurements should
be correlated with physical and laboratory findings in
patients without an enteral access. Pallor and poor
responsiveness, anemia, microcytosis, and hypoalbuminemia should raise the concern for undernutrition. Oral
motor dysfunction is reported in at least 50% and as many
as 90% of children with CP.45,46 Poor feeding skills are
strong predictors of early mortality.47 Caretakers routinely
report that feeding is time consuming and difficult. Reilly
et al,45 however, observed that mealtimes were in fact
significantly shorter than reported by parents and were
shortest for those children with the most severe oral
motor dysfunction, raising the possibility that patients
with the most severe dysfunction are least likely to get
needed nutrition in the absence of a gastrostomy tube.
Patients with gastrostomy tubes are at risk of increased
body fat and all its attendant morbidities. Sullivan et al48
prospectively followed a group of 40 children with CP: 22
fed by gastrostomy and 18 fed orally. All children had a
higher fat mass index and lower lean body mass than
typical reference children. Those patients receiving EN
had significantly larger triceps skinfold thicknesses (P =
.01) and higher fat mass index (P = .02) than those fed
orally at the beginning of the study, which likely reflected
the supplemental nasoenteral nutrition provided prior to
gastrostomy.48 The same group recently demonstrated
adequate growth without increase in fat mass index in a
cohort of 7 children fed a hypocaloric, micronutrient-rich
formula providing 50% of caloric needs anticipated by
predictive equations.49 Patients with CP benefit from
indirect calorimetry to determine nutrition needs. When
indirect calorimetry is not available, clinicians should
remember that most patients will have low REE and
TEE regardless of functional status and require frequent

evaluation during institution of nutrition recommendations to guard against overfeeding and obesity.

Obesity
Any review of hypocaloric nutrition must address, however
briefly, overweight and obesity. Overweight (BMI >25 kg/m2)
and obesity (BMI >30 kg/m2) are epidemic: in the United
States, 34% of adults are obese and another 34% are overweight and at risk of obesity. Obesity is known to be associated with multiple comorbidities including type 2 diabetes,
hypertension, dyslipidemia, coronary artery disease, and
cancer, diseases associated with increased morbidity and
mortality during critical illness. It is hypothesized, therefore, that obesity must be a predictor of poor outcomes in
the ICU population. This has not been reliably borne out
in the literature. Two meta-analyses of 62,045 and 88,051
patients, both surgical and nonsurgical and spanning 2
decades, found no increase in ICU mortality among obese
patients compared with normal-weight patients,50,51 and
the analysis by Hogue et al51 reported decreased allhospital mortality for obese patients. Whether this is attributable to improved care, with particular attention to
control of nutrition and maintenance of euglycemia in the
critically ill obese patient, or to an inherent beneficial
effect of adipocyte activity on critical illness remains to be
elucidated.50
Reduction in BMI by as little as 5% has been shown to
improve comorbid disease in obese patients. It is predicted
that improved health will be tied to decreased mortality.
However, these gains have not been convincingly demonstrated. Obese patients requiring long-term nutrition support should receive hypocaloric nutrition in anticipation of
this benefit. Published guidelines recommend providing
500 kcal less than calculated or measured daily TEE for
patients with BMI 30-35 kg/m2 and 500-1,000 kcal less for
those with BMI >40 kg/m2.52 The HBE was shown by
ORiordan et al53 to be most representative of measured
REE in overweight and obese outpatients.

Clinical Considerations
The clinical conditions addressed here can result in an
energy expenditure lower than predicted by previous wisdom or by the patients prior basal levels. Failing to
reduce calories will result in weight gain and obesity.
Nutrition counseling should be a priority to maintain a
healthy BMI and avoid obesity and its attendant comorbidities, such as diabetes and cardiovascular diseases.
Several strategies should be used to maintain a healthy
weight for these patients. The gastrointestinal (GI) tract
should always be used if a person becomes unable to selffeed. Feeding the GI tract will maintain its physiological

Patients With Potentially Hypometabolic Disease States / Magnuson et al 259

function and reduce local and systemic infections. Enteral


access should be considered at the onset of inadequate
nutrient intake in order to minimize the risk of malnutrition. Several enteral formulas are commercially available
in a low caloric density for oral ingestion or for use with
a feeding tube. A complete nutrition assessment should
address these changes in caloric needs but also specifically focus on protein requirements. Diluting an enteral
product with water for the intention of decreasing the
caloric density can unintentionally diminish protein, and
decreased total caloric need is not synonymous with
decreased protein requirements. Providers cannot assume
that protein needs are diminished in direct proportion to
caloric needs. Nitrogen wasting and wound healing often
are present in these patients, and diluting their protein
can be detrimental. The reviewed population may require
reduced calories, but their protein needs will also vary
according to their baseline renal or liver function. The
presence of any skin breakdown or decubitus ulcers will
increase protein requirements. Groah et al26 reported that
vitamins and trace elements were not consumed at the
recommended levels. Vitamin and mineral intake should
be adjusted for concomitant diseases and any necessary
wound healing. In addition to appropriate calories, protein, vitamins, and minerals, other supplements such as
arginine are essential for wound healing.54 Once the
acute inflammatory process has digressed, serial albumin
and prealbumin levels can be helpful in adjusting protein
requirements.
Parenteral nutrition (PN) should be reserved only for
individuals who have a nonfunctional GI tract, and who
have been unable to receive EN for at least 7-10 days.
Several strategies can be used to reduce calories with PN
therapy. Diluting the final dextrose concentration to
approximately 10% or reducing the total carbohydrate
load to 130 g daily provides <500 kcal/d. Administering
low doses of parenteral lipid emulsions of 10 g/d or 50 g
once or twice weekly will also reduce the caloric load
without necessarily minimizing the amino acids.
Consulting with a clinical dietitian is imperative for a
full nutrition assessment and monitoring plan. These and
other practical strategies can help the patient and care
giver to optimize nutrition and prevent malnutrition while
avoiding unnecessary calories that lead to obesity, diabetes, and cardiovascular complications.

Conclusion
Clinical conditions associated with a hypometabolic state,
such as SCI, stroke, ALS, and CP, create a unique challenge for clinicians to assess and manage nutrition support needs. The literature is sparse, but several cases and
small studies have reported that people with these clinical
conditions have decreased energy requirements. Nutrition

assessments and monitoring plans are imperative to avoid


protein and micronutrient malnutrition. A tendency for
obesity, resulting from several factors besides limitations
in physical activity, is a constant challenge for this population. Many of these patients also experience physiologic
changes, with reductions in lean body mass and increased
fat mass, which make it crucial to follow strategies to
avoid obesity and related complications such as diabetes
and cardiovascular disease.

References
1. Buchholz AC, Pencharz PB. Energy expenditure in chronic spinal
cord injury. Curr Opin Clin Nutr Metab Care. 2004;7:635-639.
2. van den Berghe G. Intensive insulin in critically ill patients. N Engl
J Med. 2001;345:1359-1367.
3. Ott L, McClain C, Young B. Nutrition and severe brain injury.
Nutrition. 1989;5:75-79.
4. Miles JM. Energy expenditure in hospitalized patients: implications for nutritional support. Mayo Clin Proc. 2006;81:809-816.
5. Liggett SB, Renfro AD. Energy expenditures of mechanically ventilated nonsurgical patients. Chest. 1990;98:682-686.
6. Pirat A, Tucker AM, Taylor KA, et al. Comparison of measured
versus predicted energy requirements in critically ill cancer
patients. Respir Care. 2009;54:487-494.
7. Swinamer DL, Phang PT, Jones RL, Grace M, King EG. Effect of
routine administration of analgesia on energy expenditure in critically ill patients. Chest. 1988;93:4-10.
8. McCall M, Jeejeebhoy K, Pencharz P, Moulton R. Effect of neuromuscular blockade on energy expenditure in patients with severe
head injury. JPEN J Parenter Enteral Nutr. 2003;27:27-35.
9. Dempsey DT, Mullen JL, Fairman R, Crosby LO, Spielman G,
Gennarelli T. Energy expenditure in acute trauma to the head with
and without barbiturate therapy. Surg Gynecol Obstet. 1985;160:
128-134.
10. Fried RC, Guenter PA, Stein TP, et al. Barbiturate therapy reduces
nitrogen excretion in acute head injury. J Trauma. 1989;29:
1558-1564.
11. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the
management of severe traumatic brain injury, XII: nutrition. J
Neurotrauma. 2007;24(suppl 1):S77-S82.
12. Bitzani M, Matamis D, Nalbandi V, Vakalos A, Karasakalides A,
Riggos D. Resting energy expenditure in brain death. Intensive
Care Med. 1999;25:970-976.
13. Martindale RG, McClave SA, Vanek VW, et al. Guidelines for the
provision and assessment of nutrition support therapy in the adult
critically ill patient: Society of Critical Care Medicine and
American Society for Parenteral and Enteral Nutrition: executive
summary. Crit Care Med. 2009;37:1757-1761.
14. McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the
Provision and assessment of nutrition support therapy in the adult
critically ill patient: Society of Critical Care Medicine (SCCM)
and American Society for Parenteral and Enteral Nutrition
(A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2009;33:277-316.
15. Dickerson RN, Boschert KJ, Kudsk KA, Brown RO. Hypocaloric
enteral tube feeding in critically ill obese patients. Nutrition.
2002;18:241-246.
16. Stucky CC, Moncure M, Hise M, Gossage CM, Northrop D. How
accurate are resting energy expenditure prediction equations in
obese trauma and burn patients? JPEN J Parenter Enteral Nutr.
2008;32:420-426.
17. Anderegg BA, Worrall C, Barbour E, Simpson KN, Delegge M.
Comparison of resting energy expenditure prediction methods with

260 Nutrition in Clinical Practice / Vol. 26, No. 3, June 2011

measured resting energy expenditure in obese, hospitalized adults.


JPEN J Parenter Enteral Nutr. 2009;33:168-175.
18. Bardutzky J, Georgiadis D, Kollmar R, Schwarz S, Schwab S.
Energy demand in patients with stroke who are sedated and receiving mechanical ventilation. J Neurosurg. 2004;100:266-271.
19. Finestone HM, Greene-Finestone LS, Foley NC, Woodbury
MG. Measuring longitudinally the metabolic demands of stroke
patients: resting energy expenditure is not elevated. Stroke. 2003;
34:502-507.
20. Long CL SN, Geiger JW, Schiller WR, Blakemore WS. Metabolic
response to injury and illness: estimation of energy and protein
needs from indirect calorimetry and nitrogen balance. JPEN J
Parenter Enteral Nutr. 1970;3:352-356.
21. Kolpek JH, Ott LG, Record KE, et al. Comparison of urinary urea
nitrogen excretion and measured energy expenditure in spinal cord
injury and nonsteroid-treated severe head trauma patients. JPEN J
Parenter Enteral Nutr. 1989;13:277-280.
22. Cox SA, Weiss SM, Posuniak EA, Worthington P, Prioleau M,
Heffley G. Energy expenditure after spinal cord injury: an
evaluation of stable rehabilitating patients. J Trauma. 1985;25:
419-423.
23. Rodriguez DJ, Benzel EC, Clevenger FW. The metabolic response
to spinal cord injury. Spinal Cord. 1997;35:599-604.
24. Rodriguez DJ, Clevenger FW, Osler TM, Demarest GB, Fry DE.
Obligatory negative nitrogen balance following spinal cord injury.
JPEN J Parenter Enteral Nutr. 1991;15:319-322.
25. Gater DR Jr. Obesity after spinal cord injury. Phys Med Rehabil
Clin N Am. 2007;18:333-351, vii.
26. Groah SL, Nash MS, Ljungberg IH, et al. Nutrient intake and
body habitus after spinal cord injury: an analysis by sex and level
of injury. J Spinal Cord Med. 2009;32:25-33.
27. Monroe MB, Tataranni PA, Pratley R, Manore MM, Skinner JS,
Ravussin E. Lower daily energy expenditure as measured by a
respiratory chamber in subjects with spinal cord injury compared with control subjects. Am J Clin Nutr. 1998;68:
1223-1227.
28. Zehnder Y, Luthi M, Michel D, et al. Long-term changes in bone
metabolism, bone mineral density, quantitative ultrasound parameters, and fracture incidence after spinal cord injury: a crosssectional observational study in 100 paraplegic men. Osteoporos
Int. 2004;15:180-189.
29. Spungen AM, Adkins RH, Stewart CA, et al. Factors influencing
body composition in persons with spinal cord injury: a crosssectional study. J Appl Physiol. 2003;95:2398-2407.
30. Rajan S, McNeely MJ, Warms C, Goldstein B. Clinical assessment
and management of obesity in individuals with spinal cord injury:
a review. J Spinal Cord Med. 2008;31:361-372.
31. Silva LB, Mourao LF, Silva AA, et al. Amyotrophic lateral sclerosis:
combined nutritional, respiratory and functional assessment. Arq
Neuropsiquiatr. 2008;66(2B):354-359.
32. Siirala W, Olkkola KT, Noponen T, Vuori A, Aantaa R. Predictive
equations over-estimate the resting energy expenditure in amyotrophic lateral sclerosis patients who are dependent on invasive
ventilation support. Nutr Metab (Lond). 2010;7:70.
33. Chernoff R. Issues in geriatric nutrition. Nutr Clin Pract.
2009;24:176-178.
34. Ahmed T, Haboubi N. Assessment and management of nutrition in
older people and its importance to health. Clin Interv Aging.
2010;5:207-216.

35. Compher C, Cato R, Bader J, Kinosian B. Harris-Benedict equations


do not adequately predict energy requirements in elderly hospitalized African Americans. J Natl Med Assoc. 2004;96:209-214.
36. St-Onge MP, Gallagher D. Body composition changes with aging:
the cause or the result of alterations in metabolic rate and macronutrient oxidation? Nutrition. 2010;26:152-155.
37. Himmelmann K, Beckung E, Hagberg G, Uvebrant P. Bilateral
spastic cerebral palsyprevalence through four decades, motor
function and growth. Eur J Paediatr Neurol. 2007;11:215-222.
38. Kuperminc MN, Gurka MJ, Bennis JA, et al. Anthropometric
measures: poor predictors of body fat in children with moderate to
severe cerebral palsy. Dev Med Child Neurol. 2010;52:824-830.
39. Johnson DL, Miller F, Subramanian P, Modlesky CM. Adipose tissue infiltration of skeletal muscle in children with cerebral palsy. J
Pediatr. 2009;154:715-720.
40. Azcue MP, Zello GA, Levy LD, Pencharz PB. Energy expenditure
and body composition in children with spastic quadriplegic cerebral palsy. J Pediatr. 1996;129:870-876.
41. Stallings VA, Zemel BS, Davies JC, Cronk CE, Charney EB.
Energy expenditure of children and adolescents with severe disabilities: a cerebral palsy model. Am J Clin Nutr. 1996;64:627-634.
42. Bandini LG, Puelzl-Quinn H, Morelli JA, Fukagawa NK.
Estimation of energy requirements in persons with severe central
nervous system impairment. J Pediatr. 1995;126(5 pt 1):828-832.
43. Bell KL, Davies PS. Energy expenditure and physical activity of
ambulatory children with cerebral palsy and of typically developing
children. Am J Clin Nutr. 2010;92:313-319.
44. Johnson RK, Hildreth HG, Contompasis SH, Goran MI. Total
energy expenditure in adults with cerebral palsy as assessed by
doubly labeled water. J Am Diet Assoc. 1997;97:966-970.
45. Reilly S, Skuse D, Poblete X. Prevalence of feeding problems and
oral motor dysfunction in children with cerebral palsy: a community survey. J Pediatr. 1996;129:877-882.
46. Sullivan PB, Juszczak E, Lambert BR, Rose M, Ford-Adams ME,
Johnson A. Impact of feeding problems on nutritional intake and
growth: Oxford Feeding Study II. Dev Med Child Neurol.
2002;44:461-467.
47. Strauss DJ, Shavelle RM, Anderson TW. Life expectancy of children with cerebral palsy. Pediatr Neurol. 1998;18:143-149.
48. Sullivan PB, Alder N, Bachlet AM, et al. Gastrostomy feeding in
cerebral palsy: too much of a good thing? Dev Med Child Neurol.
2006;48:877-882.
49. Vernon-Roberts A, Wells J, Grant H, et al. Gastrostomy feeding in
cerebral palsy: enough and no more. Dev Med Child Neurol.
2010;52:1099-1105.
50. Akinnusi ME, Pineda LA, El Solh AA. Effect of obesity on intensive care morbidity and mortality: a meta-analysis. Crit Care Med.
2008;36:151-158.
51. Hogue CW Jr, Stearns JD, Colantuoni E, et al. The impact of obesity on outcomes after critical illness: a meta-analysis. Intensive
Care Med. 2009;35:1152-1170.
52. Klein S. Medical management of obesity. Surg Clin North Am.
2001;81:1025-1038, v.
53. ORiordan CF, Metcalf BS, Perkins JM, Wilkin TJ. Reliability of
energy expenditure prediction equations in the weight management clinic. J Hum Nutr Diet. 2010;23:169-175.
54. Brewer S, Desneves K, Pearce L, et al. Effect of an argininecontaining nutritional supplement on pressure ulcer healing in
community spinal patients. J Wound Care. 2010;19:311-316.

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