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B. T. Stewart
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Chapter 2
Pathophysiology
andHypermetabolic
Response toBurn
RoohiVinaik, DaliaBarayan, andMarcG.Jeschke
Introduction
Burn injuries represent one of the most severe forms of
trauma affecting more than two million people in North
America each year [1]. According to the World Health
Organization, there are an estimated 300,000 deaths per
year worldwide related to thermal injury [2]. In Canada,
there are approximately 43,000 emergency visits and over
2000 hospitalization per annum due to burn injuries [3].
R. Vinaik · D. Barayan
Sunnybrook Research Institute, Toronto, Canada
e-mail: roohi.vinaik@mail.utoronto.ca;
dalia.barayan@sri.utoronto.ca
M. G. Jeschke (*)
Hamilton Health Sciences, Hamilton, ON, Canada
McMaster University Hamilton, ON, Canada
e-mail: marc.jeschke@hhsc.ca
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
J. O. Lee (ed.), Essential Burn Care for Non-Burn Specialists,
https://doi.org/10.1007/978-3-031-28898-2_2
29
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R. Vinaik et al.
Outcomes have improved over the years due to establishment of specialized burn centers and improvements in resuscitation, dedicated burn-specific protocols, improved wound
coverage and infection control, and improved management
of inhalation injury [4]. However, burn patients still experience unacceptably high rates of morbidity and mortality
despite improved clinical care.
Poor outcomes in severe burns, or burns encompassing
more that 20% of the total body surface area (TBSA), are
attributable in part to the debilitating hypermetabolic stress
response, which is unrivaled in terms of its magnitude and
persistence [5]. Post-burn hypermetabolism is associated with
negative sequelae, including sepsis and multi-organ failure—
leading causes of death in burn patients [4]. Essentially, metabolic dysfunction in burns is characterized by two distinct
phases, an initial “ebb phase” during which metabolism and
tissue perfusion are decreased, and a following “flow phase”
defined by elevated resting energy expenditure (REE)
>110% of predicted REE [6]. The flow phase is accompanied
by pronounced muscle catabolism and lipolysis, loss of total
and lean body mass, and stress-induced diabetes, which eventually lead to physiologic exhaustion. However, although the
phenomenon of hypermetabolism has been well documented,
the mechanisms underlying this response are still not completely elucidated. An improved understanding of post-burn
hypermetabolism, accompanying changes, and management
are necessary to optimize patient care.
In this chapter, we define the hypermetabolic response
after burns, highlighting the key metabolic consequences. In
particular, we focus on glucose, lipid, and protein metabolism.
Then, we discuss the various organ systems affected by postburn hypermetabolism including the cardiac, renal, gastrointestinal, and immune systems. We conclude with a discussion
of management of hypermetabolism in the clinical setting,
namely focusing on how to calculate energy expenditure,
conservative measures such as nutritional supplementation
and early mobilization, and pertinent pharmacological
intervention.
Chapter 2. Pathophysiology andHypermetabolic…
31
What Is Hypermetabolism?
Several reports demonstrated that post-burn metabolic
changes occur in a biphasic fashion. Two distinct patterns of
metabolic regulation can be observed following injury [7].
The first phase is early shock hypometabolism (ebb phase),
which usually occurs within 48h post-burn. This response is
characterized by decreased cardiac output, oxygen consumption, and metabolic rate as well as impaired glucose
tolerance associated with the hyperglycemic state [8].
Within the first five days post-injury, however, these metabolic variables gradually increase to a plateau phase. This
second hypermetabolic phase (flow phase) is characterized
by a hyperdynamic circulation and increased metabolic rate
with resulting increases in body temperature, oxygen and
glucose consumption, CO2 production, and futile substrate
cycling [8]. Typically, patients are considered hypermetabolic when their REE is increased 10% or more above
normal [5]. This hypermetabolic stress response is initiated
to provide sufficient energy for maintaining organ function
and whole-body homeostasis under demanding trauma
conditions [4, 7–9].
While initially ubiquitous and essential, prolonged postburn hypermetabolism has negative consequences that are a
byproduct of pronounced metabolic derangements. For
example, elevated circulating levels of catecholamines, glucagon, and cortisol after injury stimulate excess release of free
fatty acids (FFAs) and glycerol from fat (450% increase in
triglyceride-fatty acid cycling), eventually resulting in organ
alterations associated with organ damage and dysfunction.
Increased lipolysis is further accompanied by increased glucose production by the liver (250% increase in glycolyticgluconeogenic cycling) and insulin release that is twice that of
controls in response to glucose load, indicative of profound
insulin resistance [10–14]. Stress hormones induce proteolysis
to increase availability of amino acids leading to cachexia (all
summarized in Fig. 2.1). The extent and duration of this
altered metabolic demand (discussed below) are directly
32
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R. Vinaik et al.
F . Schematic depicting key post-burn hypermetabolic
alterations
related to the degree of burn injury quantified based on total
body surface area (TBSA) with partial- and full-thickness
burns [15–17].
Magnitude andDuration
A recent comparison of genomic alterations in white blood
cells (WBCs) following acute lipopolysaccharide (LPS) exposure, blunt trauma, and severe burns demonstrated that gene
expression returns to normal within 24 h of LPS exposure
[18] and one month after blunt trauma [19]. However, the
WBC genome of burn patients uniquely remains altered for
up to one-year post-injury—the furthest time point studied.
The duration of the genomic response to burn trauma parallels that of the metabolic perturbations induced by the injury
[1, 20, 21]. Within the first few months after burn, metabolic
rate increases ~40–80% above normal and remains elevated
for up to one-year post-injury [22]. Although both polytrauma [23] and sepsis [24] also trigger a similar metabolic
Chapter 2. Pathophysiology andHypermetabolic…
response, the degree of this hypermetabolic state is less than
that of burns and resolves more promptly. For patients with
>40% TBSA full-thickness burns, resting metabolic rate at
thermal neutral temperature (30°C) has been shown to surpass 140% of normal at admission and is reduced to 130%
once wounds are fully healed, to 120% at 6 months, and then
to 110% at 12 months post-injury [25]. While this hypermetabolic response decays significantly in the first 6 months after
burn, more recent studies have revealed that severely burned
patients can remain hypermetabolic for up to 3years postinjury [22, 26, 27].
The magnitude and persistence of this stress response
depend not only on burn size, age, and body composition but
also the patient’s preprogrammed genetic response to an
insult. Inhalation injury or another insult such as an infection
can further accentuate and prolong the increased metabolic
rate after injury [15]. Unfortunately, persistent hypermetabolism after burn trauma is a major concern as it is associated
with a profound catabolic state in almost every organ system
of the body [22, 28] (Fig.2.1). To date the cellular and molecular mechanisms underlying burn-induced hypermetabolism
have not been fully identified and despite improved clinical
care, the detrimental sequelae of this complex response are
major contributor to post-burn morbidity and mortality.
33
Biomarkers andMediators
As discussed above, marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion
are involved in initiating the acute hypermetabolic response
and its ensuing catabolic state after injury [1, 29–37] The rise
in these catabolic hormones is accompanied by a decrease in
the normal endogenous activity of anabolic agents, primarily
human growth hormone and testosterone, which together
combine to result in a large net protein loss [38, 39]. Cytokines
such as interleukin 6 (IL-6) and tumor necrosis factor (TNF),
endotoxin, neutrophil-adherence complexes, reactive oxygen
34
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R. Vinaik et al.
species, nitric oxide, and coagulation as well as complement cascades have also been implicated in mediating and
maintaining the post-burn hypermetabolic state [28]. Once
these cascades of events are initiated, their mediators and byproducts further drive the persistent and increased metabolic
rate accompanied by alterations in glucose, lipid, and amino
acid metabolism [40]. This self-perpetuating process is speculated to drive an entire spectrum of metabolic abnormalities
that are observed after severe burn injury. Thus, management
of burn-induced hypermetabolism remains a clinical priority.
If left untreated, this protective stress response becomes auto
destructive, ultimately causing vast cachexia, multi-organ failure, and even death [1–11, 13, 14]. In the ensuing section, we
will discuss some of the key metabolic sequelae after burns
in detail, along with the specific organ systems targeted in
thermal injuries.
Metabolic Consequences: Glucose, Lipids,
Amino Acids
Glucose Metabolism
Glucose homeostasis in healthy subjects is tightly regulated.
Under normal circumstances, post-prandial elevations in circulating glucose levels stimulate pancreatic β-cells to release
insulin—a potent anabolic hormone. Insulin release promotes peripheral glucose uptake into skeletal muscle and
adipose tissue and suppresses glucose production (i.e., gluconeogenesis) in the liver, thereby restoring blood glucose concentrations [41, 42]. However, post-burn metabolic alterations
cause significant shifts in energy substrate metabolism in
order to provide glucose—a major fuel source to vital organs.
In order to satisfy the high energy demands of the post-burn
hypermetabolic state, glucose levels are markedly increased
by (1) releasing the above-mentioned stress mediators, primarily glucagon and cortisol, to oppose the anabolic actions
of insulin, (2) activating hepatic gluconeogenesis to increase
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