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R.R. WOLFE*
* Metabolism Unit, Shriners Burns Institute, 610 Texas Avenue, Galveston, TX 77550, U.S.A.
Abstract
1. Introduction
2. Resting energy expenditure
3. Relationship of total energy expenditure (TEE) to REE
4. Sources of energy
5. Protein requirements
Acknowledgements
References
The response to severe
burn injury requires conscientious nutritional support. This
should be provided by the enteral route whenever clinically
possible. Onset of nutritional support should not begin until the
shock response is adequately resuscitated and the patient is
clinically stable. Patients should be kept in a warm environment
with occlusive dressings over the wounds to minimize heat loss,
thereby reducing caloric requirements. Optimal caloric intake is
best determined by measurements of resting energy expenditure
(REE) in the fed state and multiplying that value by 1.2 to
account for the small amount of activity. If direct measurement
of REE is not possible, then the basal energy expenditure as
predicted by Harris and Benedict can be multiplied by 1.5 to get
an average value for caloric requirement. This level of intake
should be modified according to the individual response. At least
50% of non-protein calories should be carbohydrate and 20% fat;
the source of the remainder of the calories is probably not
important. Protein intake should be about 1.5 g protein/kg/d in
adults, but may be as high as 2.0 or even 2.5 g protein/kg/d in
small children.
Injuries as severe as a
third degree burn over 10% of the body surface have minimal
effect on metabolic regulation or food intake. Consequently,
whereas such injuries may be extremely painful and require
skilled medical care for optimal recovery, they do not present a
significant nutritional problem. On the other hand, severe burn
injury over 30% of the body surface or more results in a
pronounced metabolic response that has prolonged nutritional
implications. The understanding of the nature of this response
and the consequent changes in nutritional requirements is
important not only for the optimal treatment of such patients,
but also because many aspects of the response to burn injury can
serve as a more general model of the so-called 'stress response'.
This is because the extent of injury is quantifiable and the
state of critical illness is maintained for a long enough time
(often weeks) to enable nutritional and metabolic studies.
2.1. Mechanism of hypermetabolism
2.2. Prediction of resting energy expenditure in burned patients
Resting energy expenditure
(REE) after burn injury can be as much as 100% above that
predicted from standard tables for size, age, sex and weight.
Although some debate persists regarding some aspects of the
genesis of this phenomenon, increased heat loss from the burn
wound and increased beta adrenergic activity are probably both
important factors. Burned skin loses its effectiveness as a
barrier to water loss, leading to increased evaporative heat loss
via the wound (CALDWELL, BOWSER and CRABTREE, 1981). In addition,
radiation heat loss is increased from burn wounds (CALDWELL,
HAMMELL and DOLAN, 1966), presumably due to high blood flow to
the burn wound (AULICK et al., 1972). Occlusive dressings
can significantly lower the radiation heat loss from burn wounds,
but evaporative heat loss is not reduced significantly (CALDWELL,
BOWSER and CRABTREE, 1981). Consequently, patients with large
burns that are treated with occlusive dressings will nonetheless
have a high rate of water turnover (GORAN et al., 1990),
meaning that fluid and electrolyte requirements are likely to be
high to maintain normal urine output and plasma concentrations of
electrolytes. Despite persistent increased evaporative loss via
the wound, occlusive dressings can greatly minimize heat loss.
Also, maintenance of a high room temperature (approximately
90°F) and humidity will further minimize heat loss and thus
energy expenditure. Within this context of clinical care, the
metabolic response of burn patients becomes similar to that of
patients with other forms of critical illness.
The role of
adrenergic stimulation in causing burn hypermetabolism is more
controversial than the role of increased heat loss. It has been
observed that beta adrenergic blockade can significantly reduce
metabolic rate in patients treated without occlusive dressings
(WILMORE et al., 1974), but both acute and chronic beta
blockade in burned children treated with excisional therapy and
occlusive dressings has not been found to reduce energy
expenditure (HERNDON et al., 1988). It therefore seems
unlikely that adrenergic blockade can play a significant role in
minimizing caloric requirements in patients treated with modern
techniques.
A large body of data has
enabled the development of predictive equations to estimate REE.
For example, in a study incorporating 127 observations in 56
burned children, it was found that predicted basal energy
expenditure (PBEE) obtained from the Harris-Benedict equation,
body surface area and body weight, correlated significantly with
REE (CURRERI et al., 1974). On the other hand, neither
days post-burn nor burn size was significantly correlated with
REE in that or other studies of patients treated with excisional
therapy and occlusive dressings (e.g., GORAN et al., 1991).
In an uncomplicated recovery from an injury, one would anticipate
a progressive decrease of REE over time until the PBEE is
reached. In burn injury, this is rarely the case because periods
of severe critical illness can occur as much as weeks after
injury, thereby disrupting a direct relation between days
post-injury and REE. With regard to the lack of relation between
burn size and REE, it is important to realize that a relation has
never been shown to exist at burn sizes greater than 40% Even the
Brooke Army Base studies, widely referred to as the basis for
formulas for caloric requirements (e.g., CURRERI et al., 1974),
showed no relationship between burn size and REE if smaller burns
were excluded from data analysis. Thus, equations predicated on
burn size overestimate caloric requirements in patients with
large burns (WOLFE, 1981). These are precisely the patients least
able to tolerate caloric excess.
The single most powerful predictor of REE in burn patients is PBEE. In the paper of CURRERI et al.,(1974), it was found that in fed patients, on average, REE = 1.29 X PBEE. However, there was considerable variation about this average relation. Only 75% of the predictions were within ± 30% the measured value, and 10% of the measured values varied by more than 45% from the predicted value. Thus, an accurate determination of REE can only be obtained in any given individual patient by direct measurement.
The
extensive studies of REE, performed at the Brooke Army Base in
the 1970's (e.g., WILMORE et al., 1974), led to the
conclusion that REE in adults might be 200-300% greater than
predicted basal values. However, these patients were treated
neither with early excision of burned tissue nor occlusive
dressings. These points are of importance, because studies
performed in adults treated with early excision and occlusive
dressings have consistently found lower values in adult patients
than those reported from the Brooke studies. Although the data
base in adults treated with early excision and occlusive
dressings is not extensive, the same general observations have
been made as in children (GORAN et al., 1991): the PBEE is
the most important predictor of REE; burn size is not related to
REE; the average REE (in the fed state) is about 1.3 times
greater than PBEE; and there is a large individual variability
between PBEE and REE. In virtually all studies of children and
adult patients, REE was lower than 2 X PBEE.
Knowledge of the
relationship between TEE and REE is essential if REE measurements
are to have any value in predicting caloric requirements. This
relationship was documented in a recent study in 15 burned
children in whom TEE was determined by the doubly-labelled water
technique, and REE was determined by indirect calorimetry (GORAN
et al., 1990b). TEE was 1.33 ± 0.27 times PBEE and 1.18 ±
0.17 times REE in the fed state. Importantly, TEE was
significantly correlated with measured REE (r2 =0.92),
but not with PBEE. If the average activity factor, calculated as
the difference between TEE and REE, was incorporated into a
predictive equation based on the measured value of REE cited
above, then it was found that the average energy requirement to
maintain energy balance is 1.55 X PBEE. This value is
significantly lower than those commonly used for patients with
large burns. The caloric intake required to ensure that 95% of
patients achieve energy balance is approximately equal to 2 X
PBEE. Expressed differently, 2 X PBEE will provide excess caloric
intake to all but 5% of patients, and in some patients the excess
may be 70% or more above actual requirement. It is therefore
reasonable to aim for the average energy intake (1.5 X PBEE), and
to adjust that rate either up or down as dictated by tolerance in
terms of blood glucose and triglyceride concentrations, as well
as body weight changes over time. Although the above data were
generated in children, they are very similar to the value for
predicted TEE in adults described earlier (GORAN et al., 1991).
The need to monitor individual tolerance is particularly
important in critically ill patients, who may be intolerant of
even maintenance levels of energy intake.
Carbohydrate intake
provides nutritional benefit in terms of oxidation as an energy
substrate (WOLFE, ALLSOP and BURKE, 1979), some suppression of
glyconeogenesis (WOLFE, ALLSOP and BURKE, 1979), and as a
consequence of the insulin response suppressing protein breakdown
(SHANGRAW et al., 1989) and possibly stimulating synthesis
(GORE et al., 1990). On the other hand, a variety of
detrimental effects resulting from excess glucose intake,
including extreme hyperglycemia, pulmonary overload, and hepatic
fat deposition, limit the amount of carbohydrate that can safely
be given to critically ill patients. Therefore, some fat should
also be given, not only to enable total caloric requirement to be
met, but also to prevent essential fatty acid deficiency if
nutritional support will be prolonged for weeks. It is reasonable
to provide at least 50% of calories as carbohydrate and 20% as
fat. In most cases it probably makes little difference whether
the remaining 30% of non-protein calories are provided as
carbohydrate or fat.
There has
been considerable recent activity assessing the optimal form of
carbohydrate and fat. Thus, both xylitol and fructose have been
proposed as alternative carbohydrates, but little compelling
evidence has been obtained supporting an advantage of these
compounds over glucose, given that both must first be converted
to glucose in the liver before peripheral metabolism is possible.
A wide variety of fats have been recently advocated, including
fish oil, medium-chain triglycerides, 'structured lipids' in
which medium- and long-chain fatty acids are incorporated into
the same triglyceride molecule, and triacetin. Future research
will be necessary to determine if any of these forms of fat offer
distinct advantages over long-chain fatty acids.
Major trauma, burns and
sepsis have in common a rapid net catabolism of body protein, as
well as a redistribution of the nitrogen pool within the body.
Muscle protein breakdown is accelerated, whereas certain rapidly
produced so-called 'acute-phase' proteins are produced at an
increased rate in the liver, wound repair requires amino acids
for protein synthesis, and increased immunological activity may
also require accelerated protein synthesis. The magnitude of the
net catabolism of muscle may be so pronounced that maintenance of
lean body mass is an unreasonable goal in a critically ill
patient. Nonetheless, provision of dietary protein and/or amino
acids is essential for minimizing net protein catabolism.
Furthermore, it seems likely that a higher-than-normal intake of
protein may be useful. Even the mild stress of simple bed-rest
increases the protein requirement to maintain N balance (STUART
et al., 1988). However, it is also clear that there is a
limit to the extent to which increased protein intake can
ameliorate net protein catabolism in a previously well-nourished
critically ill patient. Protein intake greater that 1.5 g
protein/kg/d has not been shown to provide any advantage (e.g.,
WOLFE et al., 1983) and can result in increased
concentrations of urea and ammonia. Consequently, it is
recommended that protein be provided to adults at a rate between
1.2 and 1.5 g protein/kg/d. Data quantifying protein requirements
in children are lacking. However, since they would normally
require more protein than adults in order to support growth, it
is reasonable to assume that a higher protein intake might be
useful. Thus, it is not uncommon to give as much as 3 g
protein/kg/d to burned pediatric patients. Nonetheless, at this
time there is no compelling evidence that there is any advantage
to providing more than 2 g protein/kg/d. Protein containing a
well-balanced mixture of amino acids would seem to be the most
advantageous for both adults and children. Formulations enriched
with branched-chain amino acids have been promoted, but clinical
trials have failed to show a clinical advantage in most
critically ill patients, particularly when concentrations of
other amino acids in the unbalanced formulation be come
rate-limiting for protein synthesis. More recently, research has
focused on the importance of glutamine intake in critically ill
patients. Since both oral and enteral formulations have omitted
glutamine entirely, it is not surprising that some beneficial
effects have been found with the addition of glutamine,
particularly in terms of improving N balance (which may reflect
repletion of the free intracellular glutamine pools). However, it
is not yet clear if there is any advantage in terms of protein
synthesis to adding glutamine in an amount in excess of its
normal contribution to protein composition. Other specific amino
acids, such as arginine and histidine, have also been promoted as
having specific, unique 'pharmacologic' effects, but convincing
experimental evidence in humans supporting these claims is not
yet available.
This work has been
supported by NIH grant DK 33962 and a grant from Shriners
Hospital.
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