Invited Review

Nutrition in Clinical Practice

Volume 00 Number 0
Energy Expenditure and Protein Requirements Following xxxx 2019 1–8

C 2019 American Society for

Burn Injury Parenteral and Enteral Nutrition

DOI: 10.1002/ncp.10390
wileyonlinelibrary.com

Amy K. Wise, MD; Kathleen A. Hromatka, MD; and Keith R. Miller, MD, FACS

Abstract
Severe burn injuries have long been known to have a profound effect on metabolic equilibrium that can persist after resolution
of the cutaneous injuries. Following burn injury, metabolism is a dynamic state resulting in the need for frequent interval
reassessment over the course of the care continuum. The acute phase of injury transitions to chronic alterations in macronutrient
utilization characterized by futile energy cycling and disproportionate catabolism of skeletal muscle. Protein supplementation
appears to be preferentially distributed to the burn wound rather than the skeletal muscle pool. Accurate assessment of caloric and
protein requirements is extremely difficult in these patients but is an essential step in efforts to attenuate functional impairment.
Indirect calorimetry should be utilized to determine caloric requirements, but trophic feeding strategies are preferred in the initial
resuscitative phase to prevent overfeeding while maintaining enteric and immune function. Controversy persists regarding optimal
protein targets, and weight-based estimates remain the norm. Exogenous protein and caloric provision performed in isolation is
insufficient to optimize outcomes and should be incorporated within a multidisciplinary approach to include muscle loading and
pharmaceutical adjuncts. (Nutr Clin Pract. 2019;00:1–8)

Keywords
burns; catabolism; hypermetabolism, protein; resting energy expenditure

Introduction but all have inherent limitations in practical application.5-8

Clinicians have long been battling hypermetabolism, loss of
lean body mass, and the resultant morbidity and mortality
that follows severe burn injury. As early mortality following
these injuries has decreased, a growing number of patients
return in follow-up with healing wounds but persistent
fatigue, inability to regain lost weight, and substantial
functional impairment.1,2 The exaggerated stress response
to injury manifests acutely in a variety of ways, including
tachycardia, insulin resistance, elevated body temperature,
loss of lean body mass, fatigue, and immunosuppression.
Coupled with elevated resting energy expenditure (REE)
and increased catabolism, these clinical conditions define
the persistent hypermetabolic state in which acute injuries
transition to a state of chronic illness. In polytrauma and
sepsis, these phenomena have been characterized as per-
sistent inflammation immunosuppression and catabolism
syndrome, but the degree and duration of hypermetabolism
observed in severe burn injuries is unique and dramatic.3,4
The determination of appropriate protein and energy
requirements following burn injury has proven extremely
difficult; however, understanding the profound metabolic
alterations in patients suffering burns is important to avoid
deleterious effects of both underfeeding and overfeeding
in the acute and chronic phases of treatment. Multiple
equations have been proposed to estimate these values,
Indirect calorimetry remains the most accurate method of
determining REE and is usually feasible in this subset of
patients. Clinicians must then determine the appropriate
timing and dosing of nutrition therapy dependent upon
the phase of illness. Recent large randomized controlled
trials (RCTs) in critically ill patients have challenged dogma
that early aggressive nutrition therapy improves outcomes
in the acute phase of critical illness.9-11 Arabi et al showed
no difference in mortality between a strategy of permissive
underfeeding vs standard enteral feeding during the first
14 days of admission in critically ill adults.10 Few trials,
however, include a substantial number of severely burned
patients, and optimal nutrition care of the seriously injured
From the Department of Surgery, University of Louisville,
Louisville, Kentucky, USA.
Financial disclosure: None declared.
Conflicts of interest: K. R. Miller serves on the faculty of the Nestlé
Nutrition Educational Fellowship. The other authors declare no
conflicts of interest with respect to authorship or publication of this
manuscript.
This article originally appeared online on xxxx 0, 2019.
Corresponding Author:
Keith R. Miller, MD, Department of Surgery, University of Louisville
550 South Jackson Street, Louisville, KY 40202, USA.
Email: krmill10@louisville.edu
2 Nutrition in Clinical Practice 00(0)
burn patient remains an area of medicine dotted with
question marks. Following the resolution of the acute phase,
futile energy cycling, and persistent assault on skeletal
muscle protein pools can result in significant functional
impairment and an indolent transition to chronic illness.12-14
During this period, even less is truly known regarding the
efficacy of nutrition support strategies.
The Hypermetabolic Response in Burn Patients
The Acute Phase Following Burn Injury
From a metabolic perspective, the fundamental response
to severe injury involves rapid diversion of resources with
increases in whole body oxygen consumption related to
underlying tissue injury and the requisite repair processes.15
Large total body surface area (TBSA) burn injuries are
therefore associated with substantial increases in REE.7
Investigators have attempted to explain the pathophysiology
of this hypermetabolic response following burn injury for
several centuries.
Early theories to explain hypermetabolism supported
the loss of external barrier function as the metabolic
driver. In 1953, Hardy et al published their findings on the
large volumes of insensible water loss in severely burned
patients.16 Rat models supported this as the primary source
of the hypermetabolic response.17,18 Subsequently, Zawacki
et al also proposed that hypermetabolism was the result
of evaporative losses and went on to test this theory by
measuring oxygen consumption and insensible weight loss
with and without the protection of a water impermeable
barrier covering the wounds. This study failed to detect
any significant differences between the 2 groups.19 In 1974,
Neely et al performed continuous indirect calorimetry (IC)
on 7 burn patients and demonstrated that rates of hyper-
metabolism correlated with both degree of exposure to
insensible water loss and body temperature but remained
significant in the absence of either variable.18 This suggested
that the explanation for the metabolic response to injury
extended beyond simple evaporative losses relevant only to
barrier disruption and was more systemic in nature.
Classically, 3 zones of burn injury including the zones of
coagulation (nonsalvageable), stasis (vulnerable yet salvage-
able), and hyperemia (usually survives) have been used to
describe regions of the burn wound.20 The tissues involved
directly by the burn incur tissue injury and cell death and
emit inflammatory mediators. Many mediators elicited from
the injury, including histamine, serotonin, and thrombox-
ane A2, result in increased permeability and vasoconstric-
tion, both locally and systemically, with further cytokine
activation.21 Following persistent capillary leak, plasma
oncotic pressure decreases, whereas interstitial oncotic pres-
sure increases, resulting in diffuse whole body edema.
This is often exacerbated by the tremendous volume of
crystalloid often required to maintain organ perfusion pres-
sures in the resuscitative portion of the acute phase of severe
burn injuries. Tangential activation of catecholamines and
glucocorticoids results in classic hyperdynamic physiology
consisting of tachycardia, increased cardiac output, and
hyperglycemia.22-24
Remote regional malperfusion to end organs secondary
to this physiology may further exacerbate the systemic
response, with septicemia and multiple organ failure as the
most common causes of death after burn injury.25 The gas-
trointestinal tract, in particular, appears to have the poten-
tial to be a potent contributor to the systemic inflammatory
response. Increased permeability due to gut barrier dysfunc-
tion as well as changes in intestinal microbiota may promote
translocation of pathogenic bacteria across the mucosal
membrane, putting patients at risk for bacterial sepsis,26-28
though the relationship between bacterial translocation and
infection has been challenged.29,30 The gut-lymph hypoth-
esis posits that although translocation may occur, it may
be macrophages and immune cells that have sequestered
bacterial products and circulated through the mesenteric
lymph that activate downstream inflammatory cascades,
with potential for systemic inflammatory response. Recent
theories suggest that erosion of the protective intraluminal
mucous layer and penetration of pancreatic proteases result
in a form of autocannibalization.31 These mechanisms
have been most closely examined in the setting of severe
trauma but are likely generalizable to systemic shock of any
etiology, including burns.
Insulin resistance and hyperglycemia follow injury and
often persist beyond the acute phase of injury in both
adult and pediatric burn patients.24,32,33 Glycemic control
with insulin infusion has been demonstrated to improve
outcomes in pediatric burn patients,34 and glycemic control
has become the norm in all critically ill patients.35 Acceler-
ated gluconeogenesis and peripheral insulin resistance con-
tribute to the observed hyperglycemia. Substrate is initially
provided by glycogen stores, which are readily depleted in
the first few hours following injury. In the inflammatory
setting, pyruvate dehydrogenase, which serves as the key
gatekeeper to the Krebs cycle, is inhibited, and carbohydrate
metabolism is shunted toward anaerobic pathways, resulting
in lactate production.36-39 Lipogenesis is inhibited, and
mitochondrial β-oxidation of fat may be impaired, resulting
in the inability to utilize fat during this period.40 As a result,
proteolysis (predominately from lean body mass) becomes a
primary contributor for ongoing substrate provision. Early
work in critically ill trauma patients suggests that both
protein synthesis and catabolism are increased but that the
increase in proteolysis is far greater than the increase in syn-
thesis, resulting in an overall negative nitrogen balance.41-43
Hypermetabolism is partially attributable to increased
adenosine triphosphate (ATP) turnover in fundamental
processes, including protein synthesis, gluconeogenesis, and
Wise et al
urea production. Yu et al demonstrated that these pro-
cesses explain approximately 60% of the hypermetabolic
response.44 The time frame by which the assault on skele-
tal muscle occurs is swift. A 2018 study by Puthucheary
et al demonstrated decreased intramuscular ATP 1 day
following an inflammatory insult, potentially related to
the intentional redirection of substrate to fulfill alternative
fuel requirements.40 Skeletal muscle becomes a source of
amino acids both as precursors for gluconeogenesis and
later as substrate for the healing of burn wounds.42 This
was demonstrated in vivo by Gore et al who used labeled
phenylalanine with serial biopsies to show net movement
of phenylalanine out of skeletal muscle with net movement
into burn wound tissue.43
Exogenously administered protein/amino acids appear
to transition to the burn wound rather than to the skeletal
muscle protein pool. This was demonstrated by observed in-
creases in fractional synthesis rates (FSRs) in burn wounds
without concurrent increases in skeletal muscle FSRs with
amino acid administration.45 This same phenomenon was
demonstrated again 1 year following the initial injury.46
Although these studies were performed in the pediatric
population, similar findings have been reported in the
acute phase in critically ill (though not specifically burned)
adults.47,48 This highlights the importance of how protein
is utilized throughout the course of recovery, initially as
substrate for ongoing metabolism and later in the chronic
setting as building blocks for tissue repair.
Transition from Acute to Chronic Phases
of Illness
The timing and nature by which these metabolic alterations
downregulate or shift back toward normal are not well
understood, but this does not occur rapidly. The acute in-
flammatory response lasts 4–5 weeks in severe burn injuries,
at which time some inflammatory markers trend toward
normal.49,50 Stanojcic et al prospectively followed 1288
adult burn patients and found that REEs were significantly
increased and prolonged in burn patients with >40% TBSA
compared with smaller burns. They also demonstrated a
significant increase in serum fats, triglycerides, and free fatty
acids that remain elevated throughout the entire hospital
stay.49 This is also demonstrated within the pediatric liter-
ature with a well-demonstrated long-term change in protein
balance, which lasts between 9 and 12 months after burn
injury, as well as a longer-term change in growth rate.12,13
In the acute phase, early excision of burn wounds and
grafting or coverage has been accepted as an important prin-
ciple to improve survival in patients without inhalational
injury.51 Unfortunately, this does not appear to immediately
correct alterations in REE, even when utilized in con-
junction with nutrition support.52,53 Many inflammatory
markers trend toward normal after several weeks, depend-
3
ing upon the depth and size of the burn.49,50 Although
the patients may be more hemodynamically stable during
this phase, hypermetabolic alterations persist. Stanojcic
et al demonstrated a significant increase in serum fats,
triglycerides, and free fatty acids that remained elevated
throughout the entire hospital stay, potentially as a result of
prolonged dysfunction in β oxidation at the mitochondrial
level and alterations in the metabolic activity of adipose
tissue.49 Alterations in the immune response persist as
demonstrated by aberrations noted in the leukocyte tran-
scriptome at 90 days postinjury.54 The dysregulation of
muscle and protein kinetics can last for years following
severe burns, as manifested clinically by fatigue, poor wound
healing, and ongoing loss of lean body mass and bone
density.46,55
Catabolism of lean muscle is a well-documented phe-
nomenon after burn injury.42,43,56 Muscle loss can be sub-
stantial over this interval, with amino acids from skeletal
muscle redistributed for wound healing.12,43 Clinically, this
phenomenon appears to persist after full healing of the burn
wound. Hart et al demonstrated that 9 months following
full clinical healing of the burn wound, children continued
to have a net negative protein balance as well as continued
loss of lean body mass. These trends persisted for 9–12
months, at which point building of lean body mass and
neutralization of the ratio of protein synthesis to protein
breakdown was observed.12 These data were paired with
an earlier study of 80 severely burned children in whom
growth in both height and weight was significantly below
that expected for their ages for 2 years following a severe
burn, despite early excision and wound coverage.13
It appears that loss of muscle mass is not distributed
equally throughout the body but occurs more significantly
in the upper extremities. Simultaneously, there is an increase
in total body fat, which is largely in the trunk.57 Loss of
lean body mass can be attributed both to the catabolic state
induced by burn injury in addition to resultant immobil-
ity. Animal studies have demonstrated that both burned
and unburned rats that were not ambulating experienced
decreased lean muscle mass when compared with both
burned and unburned ambulatory peers.14 Isotope studies
and serial muscle biopsy in severely burned children have
not demonstrated increased protein synthesis in the skeletal
muscle 1 year following injury, despite exogenous protein
provision.46 This highlights the futility of nutrition support
strategies when utilized in the absence of aggressive muscle
loading and potential adjunctive measures.
Although muscle has thus far been the focus, alterations
in adipose may also contribute to persistent critical ill-
ness. Stimulated by the catecholamine surge in addition
to cytokine activation, there are biochemical structural
changes noted in white adipose tissue.58 In a process
known as “browning,” adipose tissues display increased
mitochondrial density and presence of uncoupling protein
4 Nutrition in Clinical Practice 00(0)
1, which is a mediator for driving the energy of mitochon-
drial respiration to thermogenesis. Accelerated browning
of white adipose tissue has been demonstrated in burn
patients when compared with controls, with exaggerated
responses observed in burns >40% TBSA.49 The degree and
persistence of these structural changes in adipose may be an
additional factor in prolonged debility following severe burn
injuries.59,60 Just as muscle wasting occurs in this setting, so
too does adipose wasting, and the metabolic influence of
adipose cannot be ignored.61
Determining Energy and Protein Requirements
Caloric Requirements
Clinicians must derive a plan for nutrition therapy that
reflects the changing needs of the healing burn patient. IC
has long been considered the gold standard to determine
energy requirements.5 In practice, however, IC was used
routinely in only 66% of burn centers surveyed in 2007.62
For awake patients, continuous IC may be impractical, as
it requires measurement of both volume and the oxygen
and carbon dioxide content of inhaled and exhaled gas
via tight fitting masks.55 In practice, therefore, calorimetric
measurements are obtained over short static periods, and
the frequency in which it is used varies significantly between
centers.62 In ventilated patients, accurate measurement of
REE via IC is further complicated by inability to account for
leaks in the ventilator circuit or around endotracheal tubes,
instability of delivered oxygen concentrations, and inability
to fully separate inspired and expired gases.6 Functional
application of IC may be further limited by inconsistent
availability of the expertise to interpret the metabolic cart
for clinical purposes.
For these reasons, clinicians have attempted to con-
struct accurate predictive equations to replace IC at the
bedside. Suman et al compared IC measurements with 3
predictive equations in pediatric burn patients: the Food
and Agriculture/World Health Organization/United Na-
tions University, Schofield, and Harris-Benedict. These 3
predictive equations were developed based on data from
healthy children and fail to account for the hypermetabolic
response. On average, IC measured the REE at 152% of
the 3 predictive equations, highlighting both the degree
of hypermetabolism and the need for population-specific
predictive equations.6 Dickerson et al identified 43 primary
literature methods of calculating energy needs in adult
burn patients.7 The Curreri formula, one of the earliest
examples, was created specifically to calculate energy re-
quirements among burn patients by studying 9 patients and
calculating backwards to determine the number of calories
needed to avoid measured weight loss.63 The formula fell
out of favor, however, as it tends to overestimate caloric
requirements.55 In a 1989 survey of dietitians in adult burn
centers, the Curreri formula was used to help assess energy
requirements by 60% of respondents, but when this survey
was repeated in 2007, only 4.2% of respondents still used
the Curreri formula.62 The Toronto formula, developed in
1988, considers many variables, including body temperature,
TBSA, and number of days postburn.64 This equation,
however, was found to underestimate energy requirements
when compared with IC. In fact, Dickerson et al found
that none of the published equations reliably predicted
energy expenditures within 20% of that measured by IC.7
Hence, predictive equations remain unreliable in the setting
of burn injury and can both dramatically overestimate or
underestimate caloric requirements. For this reason, IC
remains the gold standard.65
Protein Requirements
When it comes to the determination of protein require-
ments in the setting of burn injury, there is no corollary
to IC. Instead, calculation of nitrogen balance is used
to assess protein requirements via a variety of methods,
including urinary nitrogen assays, labeled radio isotope
studies, and visceral protein levels. Historically, urinary
nitrogen assays have been the gold standard in nitrogen
balance calculations. Regular use, however, is limited by
the need for continuous collection and analysis. Urinary
measurement following burn injury is further complicated
by the massive protein losses from the burn wound.66 These
losses are generally accounted for by employing estimates
or correction factors, which may be insufficient, especially in
burns.67 Regular use of radioisotope studies is not feasible in
the intensive care unit (ICU) outside of the research setting.
Visceral protein levels are of no utility in the acute and
postacute setting. Minimal changes in visceral proteins have
been observed despite achieving positive nitrogen balance in
a recent study, concluding that visceral proteins should not
be used as nutrition markers in burn patients.68 Fluid shifts
and hepatic reprioritization toward the production of acute-
phase reactants rather than visceral proteins has been well
described in critical illness from multiple etiologies. These
markers are predictors of morbidity and mortality but do
not correlate reliably with nutrition status.69
Isotope studies, though not practical for clinical use, have
successfully provided baseline data for the development of
estimates to achieve protein balance in study populations.
Evidence suggests that it is possible to increase whole
body protein synthesis without alteration of whole body
catabolism with exogenous substrate. This was demon-
strated with the administration of parenteral nutrition
(PN) with 1.7 g/kg/d of protein in blunt trauma patients
compared with controls.56 Further isotope studies in burn
populations revealed conflicting evidence regarding the up-
per limit of benefit for protein supplementation. Wolfe et
al used a crossover study to compare supplementation of
Wise et al
a low-protein diet (1.4 g/kg/d protein) with a high-protein
diet (2.2 g/kg/d). Within this study, there was variation in
protein synthesis based on the method of assessment, but
measurement of labeled isotopes suggested there was no
additional benefit in protein synthesis with higher protein
diets.70
Conversely, the use of nitrogen balance assays appears
to demonstrate a dose-dependent response to protein sup-
plementation. Dickerson et al examined trauma patients
by monitoring nitrogen balance following injury and found
that net positivity was observed in 29% of patients receiving
1–1.49 g/kg/d, 38% of patients receiving 1.5–1.99 g/kg/d,
and 54% of patients receiving >2 g/kg/d.71 If positive
nitrogen balance alone is sufficient to maintain lean body
mass and curtail the hypermetabolic response, patients will
require >2 g/kg/d to achieve this end point.
To date, there are no large RCTs demonstrating im-
proved outcomes solely related to protein administration
in the setting of burn injury. An observational study by
Allingstrup et al, which included ICU patients experiencing
sepsis and patients with >15% TBSA burns, demonstrated
that ICU mortality was increased in those patients who
received low protein and amino acid supplementation (at
approximately 1 g/kg/d) compared with those who received
high protein (approximately 1.7 g/kg/d); however, subgroup
analysis of burn-specific patients was not performed.72
There does appear to be an association with higher protein
administration and improved outcomes in a mixed group
of critically ill and burned patients, but there is no clear
evidence of causation.
Given our inability to identify a perfect end point by
which to assess protein requirements in the critically ill
patient, let alone in the severely injured burn patient, it
is important to revisit the objective of protein provision
in the setting of burn injury. The primary goal is to
spare the preexisting lean body mass protein pool while
allowing for increased whole body protein synthesis. As
previously discussed, exogenous protein does not appear
to be incorporated within skeletal muscle to a great extent
but rather serves as substrate for wound healing.45,46 The
goal then becomes to provide sufficient protein to meet
these requirements, limiting mobilization of skeletal muscle
mass for these purposes. The quantity of protein required
to accomplish this objective remains in question, as does
the plausibility of accomplishing this goal with protein
provision alone.
Clinicians are left to utilize weight-based targets to
predict protein requirements in the setting of burn injury.
Traditionally, protein has been replaced at rates ranging
widely from 1.0 to 2.5 g/kg/d with significant institutional
variation. Body weight calculation strategies to guide pro-
tein replacement also vary. Some sources recommend re-
placement based on fat-free mass, whereas others use actual
body weight or ideal body weight.73 In children, protein
5
provision is typically more aggressive, and the International
Society of Burn Injury recommended 3 g/kg/d in this patient
population.74 The 2016 recommendations from the Amer-
ican Society for Parenteral and Enteral Nutrition empha-
sizes the importance of protein to optimize wound healing
and promote the maintenance of lean body mass. To this
end, they recommend 1.2–2 g/kg/d of protein in the general
critical care population but 1.5–2 g/kg/d protein in burn
patients specifically. It should be noted that because of the
paucity of data regarding this issue, this recommendation is
based upon expert consensus.65
Practical Recommendations Based
on Available Evidence
Futile energy and protein cycling highlight questions re-
garding how exogenously provided substrate is utilized in
the setting of injury and chronic illness. Despite ongoing
controversy and the relative paucity of burn-specific data,
clinicians must develop nutrition support plans for burn
patients both in the acute and chronic phases of care. Rec-
ommendations and treatment objectives are summarized in
Table 1.
Caloric provision in the acute setting should not be overly
aggressive, as multiple RCTs have shown no benefit of full
nutrition support compared with permissive underfeeding
during the acute phase of critical illness.10,11 Extrapolating
to burn injuries and acknowledging the futile carbohydrate
and fat metabolism seen in burn injuries, we believe the goal
in the setting of the acute resuscitative phase of severe burns
should focus on attempts to mitigate the immune response
through the “non-nutrition” benefits of enteral nutrition. As
discussed earlier, the gut can become a perpetrator of the
immune response in the setting of systemic malperfusion.
This response may be attenuated through the provision of
trophic enteral nutrition. Chen et al randomized 19 severe
burn patients to receive enteral nutrition vs PN starting
within 24 hours after injury and increasing to caloric goal by
the third postinjury day. The study demonstrated increased
motility, reduced permeability, decreased inflammatory me-
diators, and preserved mucosal barrier function in those
receiving enteral nutrition when compared with PN, further
supporting the enteral route as preferable to the parenteral
route.75 Trophic feeds should be initiated early (within 6
hours) in the setting of burn injury, and this has been
demonstrated to be potentially beneficial and well tolerated
in multiple studies.76-78 In addition, similar to severe acute
pancreatitis, retrospective review shows that there may be a
therapeutic window in the setting of burn injury whereby
gastrointestinal tolerance can be improved.79 Therefore, if
enteral nutrition is not initiated early, tolerance may remain
an issue throughout the duration of acute illness.
Most patients will tolerate trophic feeding without
complication, but serial clinical evaluation is essential to
6 Nutrition in Clinical Practice 00(0)
Table 1. Recommendations and Treatment Objectives Relative to Phase of Illness Following Severe Burn Injury.
Phase of illness Time period Treatment strategy
Acute
Initial First 0–72 Burn wound assessment
resuscitative hours Targeted resuscitation
Organ replacement therapy
Escharotomies
Topical barrier/antimicrobial
Consider therapeutic adjuncts
Stabilization Days to weeks Burn wound reassessment
(post-acute) Early excision/grafting
Topical therapy
Rehabilitation/therapy
Chronic Weeks to Burn wound reassessment
(recovery) months/years Topical therapy
Rehabilitation/therapy
IC, indirect calorimetry; LBM, lean body mass.
identify intolerance characterized by abdominal disten-
sion, pain, and worsening hemodynamic lability. Nutrition
support should be withheld if necessary based on these
parameters.80 Determining exact caloric goals and require-
ments is likely less important during this acute resuscitative
phase, and the avoidance of overfeeding should be the
priority. As clinical course progresses and the patient moves
toward the stabilization portion of the acute phase, tube
feeding regimens can then be advanced as clinically toler-
ated to initial targets in the 25–30-kcal/kg/d range.65 At this
point, we recommend individualizing caloric goals utilizing
frequent IC measurement. Multiple studies have shown that
tube feeding regimens, both gastric and postpyloric, can be
continued in the operating room through what may be the
multiple debridement and grafting procedures required in
the setting of large burns.81,82 We agree with current expert
consensus guidelines recommending protein supplementa-
tion goals of 1.5–2 g/kg/d to provide adequate substrate
for wound healing. Ongoing research suggests that higher
targets may be beneficial, but evidence is inconclusive at
this time.71 Cointerventional therapies should be employed,
including early excision and grafting, glycemic control, and
goal-directed resuscitation. Adjunctive therapies including
β-blockade, anabolic steroids, and glycemic control have
been studied as a means to truncate the acute phase and
may be considered.83-85 This is best achieved in the setting
of a multidisciplinary burn care team,86 including early
initiation of physical therapy and maintaining mobility to
preserve lean muscle mass.
Although the acute phase lasts 4–5 weeks, metabolic
derangements continue into the chronic phase of the dis-
ease process, and ongoing nutrition support with both
caloric and protein supplementation is appropriate on an
individualized basis.
Nutrition Goals
Caloric Protein Treatment objective
Trophic Trophic Maintain gut barrier
Attenuate immune response
Encourage enteral tolerance
Support microbiome
Per IC >2 g/kg Minimize LBM losses
Support wound healing
20–25 kcal/kg/d >2 g/kg Recover lost LBM
Conclusion
The physiologic and metabolic response to severe burn
injury is dramatic and unique. Early enteral nutrition is
still appropriate, but trophic strategies are acceptable in the
initial resuscitative portion of the acute phase. Following
transition from the resuscitative phase, IC remains the
standard with regard to determination of caloric require-
ments. In our opinion, protein supplementation should be
targeted to maintain adequate substrate for wound healing
while preserving lean body mass, with current consensus
guidelines supporting 1.5–2 g/kg/d. Adjunctive measures
should be considered in an attempt to truncate the acute
phase of injury in order to minimize mobilized protein
from the lean mass pool. Finally, nutrition support should
utilized as part of a multidisciplinary approach.
Statement of Authorship
K. R. Miller contributed to conception/design of the work;
K. R. Miller, K. A. Hromatka, and A. K. Wise drafted the
manuscript, critically revised the manuscript, and agree to be
fully accountable for ensuring the integrity and accuracy of the
work. All authors read and approved the final manuscript.
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