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* Metabolism Unit, Shriners Burns Institute, 610 Texas Avenue, Galveston, TX 77550, U.S.A.
2. Resting energy expenditure
3. Relationship of total energy expenditure (TEE) to REE
4. Sources of energy
5. Protein requirements
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
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.
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.
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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