Điều Trị Bỏng Toàn Diện (Bản Expert Consult)

Critical care in the severely burned: organ support and management of complications
383
Intermittent mandatory ventilation
Intermittent mandatory ventilation (IMV) was developed to
allow spontaneous ventilation interspersed with volume-
cycled or time-cycled pressure control mechanical ventila­
tion. It was developed initially as a method to wean patients
from the ventilator by depending more and more on patient
effort for ventilation. The addition of a synchronized mode
(SIMV) to avoid placing a mechanical breath on top of a
spontaneous patient breath greatly improved this mode. It
has the advantage of maintaining some patient work in
breathing to preserve respiratory strength when mechanical
ventilation is required, and as a weaning tool to progres­
sively increase patient effort while reducing mechanical
support in preparation for discontinuing mechanical ventila­
tion. This method can be problematic in patients with low
Figure 33.3  Airway pressure curves illustrating the three mechanical functions: IN, initiation of the cycle; LIM, the preset limit (i.e. pressure or volume)
imposed on the positive pressure cycle; CYC, the function (i.e. time or volume) ending the cycle. Each mechanical function is governed by one of four
physical factors: volume, pressure, flow, and time. (a) A time-initiated, volume-limited mode. (b) A pressure-initiated (sub-baseline pressure produced by the
patient’s effort to breathe), volume-limited mode. (c) A time-initiated, volume-limited, time-cycled mode that extends inspiration beyond the time that the
volume is delivered. A plateau is reached after flow has stopped but before the ventilator cycles into exhalation. (Reprinted with permission from Shapiro BA, Lacmak
RM, Care RD, et al. Clinical application of respiratory care. St Louis, MO: Mosby Year Book; 1991)95
A
B
C
[IN]
Time
[LIM]
Vol.
[CYC]
Vol.
Pressure
[IN]
Press.
[LIM]
Vol.
[CYC]
Vol.
[IN]
Time
[LIM]
Vol.
[CYC]
Vol.
Figure 33.4  Airway pressure tracings of four volume-cycled modes. The
thick solid lines represent ventilator breaths. The thick dotted lines are
spontaneous breaths. The thin dotted lines illustrate the spontaneous
breathing pattern in the absence of ventilator breaths. IMV, intermittent
mandatory ventilation; SIMV, synchronized intermittent mandatory
ventilation. (Reprinted with permission from Shapiro BA, Lacmak RM, Care RD, et al.
Clinical application of respiratory care. St Louis, MO: Mosby Year Book; 1991)95
+10
+3
–3
0
+10
+3
–3
0
+10
+3
–3
0
+10
+3
–3
0
Control
mode
Assist
control mode
IMV
mode
SIMV
mode
Figure 33.5  Schematic illustration of pressure support ventilation. IN,
initiation by spontaneous breath; LIM limit (pressure); CYC, cycle (derived
from decreasing inspiratory flow); EX, expiration. (Reprinted with permission from
Shapiro BA, Lacmak RM, Care RD, et al. Clinical application of respiratory care. St Louis, MO:
Mosby Year Book; 1991)95
IN
EX
To patient
[IN]
Pressure
[LIM]
Pressure
[CYC]
Flow
pulmonary compliance, and the IMV mode may not allow
for sufficient spontaneous tidal volumes due to extremely
limited inspiratory capacity. The addition of pressure support
to augment spontaneous ventilatory efforts can be used
(Fig. 33.4).
Pressure support ventilation
Pressure support ventilation is a patient-triggered pressure-
limited flow-cycled ventilatory mode (Fig. 33.5). Each pres­
sure support breath is triggered by patient negative-pressure
effort, at which time a valve opens producing a high-flow
pressure-limited breath. The breath ends when the patient’s
inspiratory demand falls below a preset limit, allowing spon­
taneous respiration and complete patient control. It also
differs from the other modes in that it is flow-cycled as
opposed to volume- or pressure-cycled. Because this mode
is triggered and completed entirely by patient response, it
cannot be used in patients with decreased respiratory drive,
such as paralyzed patients and those who are heavily sedated.
This mode has a number of advantages because of improved
synchrony with patient effort. It can be used to provide full
ventilatory support by setting a flow and pressure such

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384
High-frequency percussive ventilation
High-frequency percussive ventilation (HFPV) is a pressure-
limited, time-cycled mode of ventilation that delivers subti­
dal pressure-limited breaths at a high frequency (400–800
beats/min) superimposed on a conventional inspiratory and
expiratory pressure-controlled cycle (10–30 breaths/min).
The purported advantages are to mobilize airway secretion
and casts for better pulmonary toilet, and to provide ade­
quate gas exchange at lower airway pressures. This method
of ventilation has been tested primarily in burned patients
with inhalation injury, and was first reported in 1989.28 In
this study, HFPV was used as a salvage therapy in patients
with inhalation injury and as primary therapy in another
group. Improvements in oxygenation and a lower rate of
pneumonia were seen. Another study documented an
improvement in mortality in burned patients with inhala­
tion injury treated with HFPV compared to historical
controls.29 Other outcomes in this study were significant
decreases in the work of breathing, and lower inspiratory
pressures in addition to improvements in oxygenation and
the rate of pneumonia. This method of ventilation seems to
be particularly efficacious in the treatment of inhalation
injury, particularly in comparison to HFOV.
A recent study was performed in severely burned ventilated
patients testing the effects of low tidal volume conventional
ventilator strategy against an HFPV ventilator strategy. This
study again found differences in improved oxygenation early
in the course, but no differences in mortality or other
outcome measures. However, the study did show that the
need for ventilator ‘rescue,’ defined as the need for changing
ventilator modes due to inadequate oxygenation or ventila­
tion despite maximizing the mode, was higher in the
ARDSnet group, thus favoring the use of HFPV in this popu­
lation (i.e. less rescue indicated). At the very least, these data
show that HFPV is useful in the population of burned
patients, and may in fact be beneficial by reducing the risk
of pulmonary failure at least in the short term.30
Airway pressure-release ventilation
Airway pressure-release ventilation (APRV) is a mode that
delivers continuous positive airway pressure with a time-
cycled pressure-release phase (to allow for expiration).
Advantages of APRV include optimization of mean airway
pressure, limitation of peak inspiratory pressures, and inte­
gration of spontaneous breathing independent of the venti­
latory cycle. These characteristics allow for an open lung,
with optimal alveolar recruitment and as a result, improved
ventilator–perfusion mismatching. This mode is best uti­
lized in patients who are permitted to breathe spontaneously
with negative pressure induced by diaphragmatic contrac­
tion, which aids in lung recruitment of areas that were
previously atelectatic. This is in contrast to conventional
positive-pressure ventilation, where positive pressure from
within the bronchus through the volume of air is distributed
preferentially down the path of least resistance to areas of
the lung that are already well aerated, predisposing them to
overdistension and barotrauma. Theoretically, this mode of
ventilation is the ideal lung-protective strategy. APRV gained
popularity in the late 1990s, and is becoming the preferred
mode of ventilation in many centers. Small prospective trials
suggest that APRV is associated with fewer ventilator days,
that an adequate tidal volume is delivered. It can also be
used effectively during weaning by reducing the pressure
incrementally to allow for progressively greater patient effort.
Caution must be exercised when reducing ventilatory support
so that a sufficient tidal volume is still delivered to maintain
adequate ventilation.
Inverse ratio ventilation
Inverse ratio ventilation is a mode of ventilation designed to
improve oxygenation at a given level of inspired oxygen.
Conventional ventilation uses the times of inspiration and
expiration at a ratio of 1 : 4 or 1 : 2, giving a longer time for
expiration, as it is generally a passive process. Inverse ratio
ventilation reverses this ratio to give a longer inspiratory
time (1 : 1 or 2 : 1) by using rapid inspiratory flow rates and
decelerating flow patterns during the inspiratory phase. The
effect of inverse ratio ventilation is to increase mean airway
pressures and thus recruit alveoli in an effect similar to PEEP.
Secondly, in severe lung disease, ventilation in the lung is
unequal due to peribronchial narrowing. Thus, some under­
ventilated alveoli that are actually open are not able to
exchange gases efficiently, increasing the intrapulmonary
shunt and reducing arterial oxygenation. Inverse ratio venti­
lation can improve this by selective air-trapping or intrinsic
PEEP in these compromised air spaces. Inverse ratio ventila­
tion can be done either in a volume-cycled or a time-cycled
pressure ventilation mode, but it is most commonly used
with pressure controlled ventilation to reduce peak airway
pressures.
The beneficial effects of inverse ratio ventilation have been
questioned. It may be that the same effect can be gained
simply by increasing peak airway pressures with PEEP or
peak inspiratory pressures. In fact, some studies have showed
no benefit of inverse ratio ventilation compared to conven­
tional volume ventilation in terms of oxygenation.24 These
studies did show some slight improvements in ventilation
(PaCO2). For this reason, inverse ratio ventilation cannot be
recommended except in the setting of ARDS refractory to
other therapies.
High-frequency oscillatory ventilation
High-frequency oscillatory ventilation (HFOV) is a mode of
ventilation that delivers subtidal, high-frequency oscillatory
breaths at a constant mean airway pressure (mPAW), other­
wise described as ‘CPAP with a wiggle.’ It is thought to main­
tain open alveoli by recruiting collapsed portions of diseased
lung and applying the equivalent of continuous positive
airway pressure used during conventional ventilation. Opti­
mizing mean airway pressure limits peak pressure, thereby
making this a ‘lung-protective’ mode. A recent randomized
prospective trial in adult patients with ARDS demonstrated
that HFOV resulted in brief improvements in oxygenation
although mortality and complication rates were not differ­
ent.25 In burned patients, one center reported early success
in reversing profound hypoxemia in patients with ARDS
while facilitating early excision and grafting with intraopera­
tive use.26 However, this same group recently showed that in
burned patients with inhalation injury this method often
failed secondary to hypercapnia rather than hypoxia.27 It
stands to reason, therefore, that this method might be tried
in those with oxygenation difficulties, and perhaps contin­
ued if hypercapnia is less of an issue.

Critical care in the severely burned: organ support and management of complications
385
small healthy areas of lung exist adjacent to diseased and
collapsed areas. In the conventionally treated group higher
tidal volumes and pressure are distributed only to open
healthy alveoli, therefore the barotrauma of high pressures
is delivered to this ‘healthy’ lung, thereby increasing the
damage there and worsening outcomes. In burned patients,
decreased chest wall compliance, presence of smoke inhala­
tion injury to the upper airways, and massive fluid admini­
stration are just a few variables that make effective gas
exchange challenging while optimally minimizing baro­
trauma. Prospective trials comparing modes of ventilation
to minimize VILI are lacking in the burn literature, making
it difficult to determine which approach is best suited to this
population. One study showed no statistically significant
differences in 61 burned patients between a pressure-limited
strategy and a conventional strategy for mortality, pulmo­
nary complications, or incidence of pneumothoraces.36 In
the trial comparing HFPV (a pressure-limited strategy) to an
ARDSnet-based conventional strategy, a lower incidence of
barotrauma was seen in the HFPV group. There was no dif­
ference in inflammatory markers between the two strate­
gies.30 It stands to reason that pressure-limited ventilation
strategies (either conventional or high frequency) might be
of benefit in burned patients in sufficiently powered studies.
One outcome that should certainly be accounted for is the
need for adjunctive therapies (rescue treatments), as implied
above.
Weaning from mechanical ventilation
Regardless of the mode of ventilation, almost all patients
surviving the initial insult will eventually need to be weaned
off the ventilator. Clinicians continue to debate the advan­
tages of weaning patients with various forms of mechanical
ventilation. Some clinicians prefer to use pressure support
ventilation (PSV) with or without SIMV because of the ease
with which the level can gradually be reduced. Others main­
tain that intermittent trials with abrupt cessation of venti­
lator support while maintaining endotracheal intubation
(’t-tube trials’) result in more rapid weaning.37 It must be
noted that weaning from ventilation depends upon the rate
at which the patient recovers from the condition requiring
mechanical ventilation and the aggression of the clinician
driving the weaning process. In practice, either method of
weaning from the ventilator (gradual weaning with pressure
support or intermittent t-tube or CPAP trials) will be success­
ful. What will certainly prolong the process are random
changes in ventilation parameters without a directed plan.
Monitoring of mechanical ventilation
For patients on mechanical ventilation, sedatives and para­
lytics for the endotracheal tube or other conditions often
impair the normal physiologic regulation of ventilation and
oxygenation. For these reasons, monitoring of ventilation
and oxygenation by the clinician is required.
Ventilation
Arterial CO2 tension remains the most accurate means of
assessing ventilation. This is typically measured by blood gas
analysis. After assessment of the pCO2, ventilatory settings
improved gas exchange, decreased atelectasis, improved
hemodynamic performance, and decreased sedative admini­
stration compared to conventional modes in non-burned
populations.31 Some recent data in trauma patients refutes
this, although this paper suffered from a significant lack of
statistical power.32 Nonetheless, this mode is being increas­
ingly used in burn units around the world, but to date no
prospective trials have been reported.
Inhaled nitric oxide
Nitric oxide (NO) is a short-lived gaseous product of
endothelial cells that is a powerful local vasodilator. Because
it is a gas, this product can be delivered through the endotra­
cheal tube to areas of ventilated lung where it can provide
localized pulmonary vasodilation. Thus, areas of ventilated
lung can receive more blood flow to reduce intrapulmonary
shunting and improve oxygenation. This compound has
been used extensively in neonates and children with hypox­
emic respiratory failure, with beneficial effect. It has also
been used in ventilated burned children to improve oxygena­
tion.33 Although nitric oxide therapy has received consider­
able attention as a potential therapeutic option in severe
pulmonary disease, no reports to date have documented
improved mortality or other clinical outcomes in spite of
improvements in oxygenation. For this reason, its use cannot
be recommended outside of rescue therapies or a clinical
trial.
Limiting ventilator-induced lung injury (VILI)
Ventilator-induced lung injury (VILI) is the result of injuri­
ous ventilator settings that lead to a combination of baro­
trauma, volutrauma, atelectrauma (repeated opening and
closing of alveoli), or chemotrauma (paracrine inflamma­
tory effects). VILI is a common complication of mechanical
ventilation and results in pneumothorax, pneumomediasti­
num, subcutaneous emphysema, interstitial emphysema, or
pneumatoceles. In a volume-cycled mode, large tidal volumes
along with elevated peak and plateau pressures have been
implicated in inducing VILI. It is conceivable that limiting
airway pressures may reduce morbidity. Early reports showed
no clear benefit of pressure-limited ventilation,34 which was
accomplished by giving lower tidal volumes more frequently
to maintain minute ventilation, and accepting a higher
PaCO2 value and lower arterial pH, which is termed permis­
sive hypercapnia. Criticism of these trials lay in their low
enrollment and lack of power to show differences. As an
answer to this critique, a large multicenter trial documented
improved survival and increased ventilator-free days in the
first 28 days in the ICU in patients with ARDS treated with
low tidal volumes (6 mL/kg predicted body weight) versus
traditional tidal volumes (12 mL/kg predicted body weight).
In fact, this study was stopped early by the data safety com­
mittee because of the benefits incurred to the treated group.35
Suspected reasons for the improvements seen in this trial
contrary to the earlier trials was the number of subjects
enrolled as well as the defined protocol to limit both tidal
volumes (volutrauma) and plateau pressures < 30 cmH2O
(barotrauma). Interestingly, this trial demonstrated decreased
inflammatory markers, specifically IL-6, in the low-tidal
volume arm suggesting a third possible mechanism of
benefit (chemotrauma). Theoretically, the low-tidal volume
strategy subscribes to the theory of ARDS, which dictates that

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386
oxyhemoglobin levels. The major limitations of this tech­
nique lie in the insensitivity to changes in pulmonary gas
exchange. Because of the shape of the oxyhemoglobin dis­
sociation curve, when the SaO2 exceeds 90% and the PaO2
is >60 mmHg, the curve is flat and changes in PaO2 can
change considerably with little change in SaO2. Regardless,
it is assumed that an SaO2 value >92% is indicative of ade­
quate oxygenation. An advantage to oxygen saturation meas­
urements that should not be overlooked is that it is a
continuous direct measure that is immediately available,
whereas blood gas measurement of PaO2 is by nature
intermittent.
A commonly used parameter to assess the adequacy of
oxygenation is the ratio of PaO2 to FiO2 (P/F ratio). As such,
the P/F ratio is one of the criteria utilized to diagnose acute
lung injury (ALI) and ARDS. A P/F ratio >300 along with
bilateral infiltrates seen in chest radiograph combined with
the absence of a cardiogenic cause of the infiltrates (deter­
mined either clinically or via pulmonary capillary wedge
pressure < 18 cmH2O) is required for the diagnosis of acute
lung injury.39 A P/F ratio <200 is required for a diagnosis of
ARDS. One major flaw when utilizing the P/F ratio is the fact
that mean airway pressure, a key determinant in oxygena­
tion, is not incorporated. Thus, two patients on two different
levels of ventilator support (one on minimal PEEP and
another on maximal PEEP) are indistinguishable based on
this parameter. To account this variable, the oxygenation
index may be used:40
Oxygenation Index OI
Mean airway pressure
mmH O
iO
/
(
)
(
(
)
)
=
×
2
2
F
PaO2
This parameter is particularly helpful in determining a
patient’s oxygenation status in relation to the level of ventila­
tor support: the higher the number, the worse the level of
oxygenation. Generally, an OI >20 should be a cause for
concern.
Initial ventilator settings to assure adequate oxygenation
are usually 40% oxygen in the inspired gas with 5 mmHg
PEEP. This amount of PEEP is used to mimic the normal
physiologic pressures in non-intubated subjects. When oxy­
genation begins to decline, initial maneuvers are to increase
the fractional inspired oxygen (FiO2) to >40% and possibly
to 100%. Concentrations of oxygen >60% are considered
toxic to airway epithelium, and other means to increase
oxygenation should be employed. This should consist ini­
tially of increasing the level of PEEP incrementally until the
desired level of oxygenation is reached while keeping the
FiO2 to <60%. Once a level of 15–20 mmHg of PEEP is
reached, other means of increasing oxygenation will need to
be employed. These consist of inverse ratio ventilation,
HFOV, HFPV, APRV with and without inhaled nitric oxide,
etc. which are described above.
Organ system failure and management
Etiology and pathophysiology
As stated earlier, it was hypothesized that organ dysfunction
commonly seen in the critically ill exists in a continuum
with SIRS. Certain patients with SIRS will go on to develop
multiple organ dysfunction syndrome (MODS), which is
characterized by non-fatal signs of organ system dysfunction,
to adjust minute ventilation can be made to reach the desired
level. Another method that has received attention of late is
expiratory end-tidal CO2 monitoring through infrared meas­
urement of CO2. This technique allows for continuous
online determination of end-tidal CO2, which is an estimate
of arterial PaCO2. For end-tidal CO2 to equate with PaCO2
an assumption of a low alveolar–arterial gradient must be
made; in patients with healthy lungs this gradient is only
2–3 mmHg. In certain trauma patients, particularly those
with head injuries, this gradient remains low and may be
used for continuous PaCO2 monitoring. However, in other
critically ill patients the alveolar–arterial gradient may be in
a state of flux, calling into question values received from an
end-tidal CO2 monitor. Factors affecting the alveolar–arterial
gradient include cardiac output, airway dead space, airway
resistance, and metabolic rate; each of these may change in
a severely burned patient, particularly those with inhalation
injury. For these reasons, end-tidal CO2 monitoring is not
recommended in burned patients for the estimation of
PaCO2.
In general, PaCO2 varies indirectly with minute ventila­
tion, and so this value must be considered when making
ventilator adjustments to alter PaCO2. Minute ventilation is
equal to tidal volume multiplied by respiratory rate. There­
fore, PaCO2 can be adjusted downward by increasing either
tidal volume or respiratory rate. In general, respiratory rate
should be set between 10 and 20 breaths and tidal volume
at 6 mL/kg initially. Adjustments can then be made in
minute ventilation to optimize PaCO2, which is usually
40 mmHg. When making these adjustments, it should be
noted that the respiratory rate cannot be increased above 40
breaths/min in those who are not neonates, and tidal volume
should be minimized to avert VILI.
When plateau airway pressures are >30 mmHg the venti­
lated lung is relatively non-compliant, indicative of ARDS or
pulmonary edema. In this situation, ‘permissive hypercap­
nia’ is a strategy that may be used to reduce barotrauma. This
strategy seeks to limit peak and plateau airway pressures by
reducing tidal volumes to allow for respiratory acidosis
(PaCO2 > 45 mmHg, arterial Ph < 7.30). This strategy was
used to some extent in the trial investigating the efficacy of
pressure-limited ventilation on improving outcomes in criti­
cally ill ventilated patients.
Oxygenation
Like the adequacy of ventilation, oxygenation has been clas­
sically determined using the partial pressure of O2 in arterial
blood. In general, a PaO2 value of 60 mmHg has been con­
sidered sufficient. Another frequently used monitor is pulse
oximetry, which is an optical measurement of oxygenated
hemoglobin in pulsatile vessels. Using differences in absorp­
tion of red and infrared light, the percentage of oxygenated
hemoglobin in the arteries can be calculated. Shortcomings
of this technique are that methemoglobin and carboxyhe­
moglobin are falsely measured as oxygen-saturated hemo­
globin, which is common initially in patients with smoke
inhalation injury. Otherwise, this is a very accurate technique
for the determination of oxygen content in arterial blood, as
97% of oxygen is carried to the tissues via hemoglobin. This
assertion has been corroborated by in vitro studies38 that
showed the accuracy of pulse oximetry to within 2–3% of

Critical care in the severely burned: organ support and management of complications
387
defense, wound healing, and other essential host functions.
Although cytokines in low physiologic concentrations pre­
serve homeostasis, excessive production may lead to wide­
spread tissue injury and organ dysfunction. Four of these
cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β
(IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) have
been most strongly associated with sepsis and multiple
organ failure in burns.41 The primary detraction to this theory
is that many patients, including burned patients, can develop
multiple organ failure without identified infection. It seems
that inflammation from the presence of necrotic tissue and
open wounds can incite a similar inflammatory mediator
response to that seen with endotoxin. The mechanism by
which this occurs, however, was not well understood, but
recent evidence suggests that this is due to activation of
the cytokine cascade through DAMPs (damage-associated
molecular pathways), which might in fact be antigens associ­
ated with liberated mitochondria from our own cells.42
Regardless, it is known that a cascade of systemic events is
set in motion either by invasive organisms or from open
wounds that initiates the systemic inflammatory syndrome
that may progress to multiple organ failure.
Another theory implicates prolonged tissue hypoxia and
the generation of toxic free radicals during reperfusion as the
primary mediator of end-organ damage. Deficits in resuscita­
tion then lead to areas of the microcirculation throughout
the body that receive inadequate nutrients and shift to anaer­
obic metabolism and formation of superoxides from ATP
metabolites. Localized tissue hypoxia might be related to
activation of microthrombosis locally with inadequate anti­
thrombotic response. This might be plausible, as some inves­
tigators showed levels of antithrombin III to be decreased
after severe burn.43 Drotrecogin-α is a purported treatment
that may have an effect on this mechanism, but only case
reports and small case series have been reported.44,45
The effects of the toxic products of oxygen free radical
formation are only now being elucidated. From in vitro
models and in vivo animal models, we know that tissues that
initially were in shock and are then reperfused produce
oxygen free radicals that are known to damage a number of
cellular metabolism processes. This occurs throughout the
body during burn resuscitation, but the significance of these
free radicals in human burn injury is unknown. It was found
that free radical scavengers such as superoxide dismutase
improve survival in animal models, but these results have
not yet been established in humans.
Oxygen free radicals oxidize membrane lipids, resulting in
cellular dysfunction. Endogenous natural antioxidants, such
as vitamins C and E, are low in patients with burns, suggest­
ing that therapeutic interventions may be beneficial.46 Serum
nitrate levels correlate well with multiple organ failure scores
in critically ill patients, implying a role for this constellation
of events in SIRS/MODS. Recent studies in burned patients
showed that levels of nitrates were associated with the sever­
ity of burn whereas those of antioxidants were not.47 This
might justify augmentation of antioxidants in those with
severe burns.
The last two theories revolve around the role of the gut in
the generation of organ failure, and the ‘two-hit’ theory
of multiple organ failure. For years, investigators have
implicated the gut as the ‘engine’ of organ failure, which is
associated with loss of gut barrier function and translocation
such as renal insufficiency or ventilator dependence. A subset
of these patients will go on to develop frank organ failure,
termed multiple system organ failure (MSOF), which often
leads to death (Fig. 33.6).6,7 What is required for the devel­
opment of SIRS is inflammation, which in the severely
burned emanates primarily from the burn wound. Factors
associated with progression from the systemic inflammatory
response syndrome to multiple organ failure are not well
explained, although some of the responsible mechanisms in
some patients are recognized. Occasionally, failure of the gut
barrier with penetration of organisms into the systemic cir­
culation may incite a similar reaction. However, this phe­
nomenon has only been demonstrated in animal models,
and it remains to be seen if this is a cause of human disease.
A number of theories have been developed to explain the
progression to multiple organ failure (Box 33.4). One of
these is the infection theory, which incriminates uncon­
trolled infection as the major cause. In the severely burned
patient these infectious sources most likely emanate from
invasive wound infection or lung infections (pneumonias).
As organisms proliferate out of control, endotoxins and
other antigens are liberated from Gram-negative bacterial
walls, and exotoxins from Gram-positive and Gram-negative
bacteria are released. Their release causes the initiation of a
cascade of inflammatory mediators called cytokines through
activation of PAMP (pathogen-activated molecular pathway)
receptors such as Toll-like receptors 2, 4, and 9,39 as well as
the recruitment of inflammatory cells which, if unchecked,
can result in organ damage and progression toward organ
failure.
Cytokines are a group of signaling proteins produced by a
variety of cells that are thought to be important for host
Figure 33.6  Progression to multiple organ failure. All severely burned
patients have the systemic inflammatory response syndrome (SIRS). A
subset of these will develop signs and symptoms of multiple organ
dysfunction syndrome (MODS). Still fewer will go on to develop multiple
system organ failure (MSOF).
SIRS
MODS
MSOF
Box 33.4  Theories for the development of multiple
organ failure
•
Infectious causes
•
Macrophage theory
•
Microcirculatory hypothesis
•
Endothelial–leukocyte interactions
•
Gut hypothesis
•
Two-hit theory

Total Burn Care
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388
Course of organ failure
Even with the best efforts at prevention, the systemic inflam­
matory syndrome that is ubiquitous in burn patients may
progress to organ failure. Experience with the severely burned
dictates that virtually all burned patients will display the
traditional signs and symptoms of SIRS, including tachycar­
dia, tachypnea, increased white blood cell count, etc. There­
after, various organ systems may begin to show signs of
dysfunction. Generally, these will begin in the renal and/or
pulmonary systems and progress in a systematic fashion
through the liver, gut, hematologic system, and central
nervous system. The development of multiple organ failure
does not inevitably lead to mortality, however, and effort to
support the organs until they recover is justified.
Renal system
Pathophysiology
Acute renal failure (ARF) is a potentially lethal complication
of burns. Despite substantial technical developments in
dialysis to replace the function of the kidneys, mortality
meets or exceeds 50% for all critically ill patients who
develop acute renal failure.52 Interestingly, mortality associ­
ated with ARF undergoing hemodialysis for frank failure in
the critically ill has not improved significantly for over 40
years. The same can be said for renal failure requiring dialysis
specifically in the severely burned. The cause of death in
these critically ill patients was not uremia because of advances
in dialysis, but primarily sepsis and cardiovascular and pul­
monary dysfunction.
With the advent of early aggressive resuscitation after burn,
the incidence of renal failure coincident with the initial
phases of recovery has diminished significantly in the severely
burned. However, a second period of risk for the development
of renal failure 2–14 days after resuscitation is still present,
and is probably related to the development of sepsis.53
Acute renal failure, usually in the form of acute tubular
necrosis (ATN), is characterized by deterioration of renal
function over a period of hours to days, resulting in the
failure of the kidney to excrete nitrogenous waste products
and to maintain fluid and electrolyte homeostasis. It may be
caused by a number of factors interfering with glomerular
filtration and tubular resorption. In burned patients, the
causes can be generally narrowed to renal hypoperfusion,
nephrotoxic insults from pharmacologic treatments (e.g.
aminoglycosides or intravenous contrast agents), or sepsis.
Ischemic renal failure is the more common of the two
causes, and is induced by hypoperfusion from an imbalance
between vasoconstrictive and vasodilatory factors acting on
the small renal vessels during low-flow states. Decreased flow
to the renal cells directly alters endothelial cell function,
reducing the production of and response to vasodilatory
substances. The renal medulla is the portion of the kidney
most sensitive to hypoxia, and the damage is initially to the
renal tubular cells. The outer medulla and proximal tubules
have high oxygen requirements, and the resulting ischemia
causes swelling of tubular and endothelial cells, with necro­
sis, apoptosis, and inflammation evident on histologic
examination. These changes lead to further vascular conges­
tion and decreased blood flow, leading to more cell loss and
further decrements in renal function.
of enteric bacteria and their toxic metabolites. Bacterial
translocation has been shown to occur after burn in
patients.48 These bacteria and their products then activate the
inflammatory cells described above, culminating in organ
failure. The relevance of gut-mediated bacterial translocation
to human disease, however, has been hotly debated. No
studies have shown clearly whether bacterial translocation is
the cause of SIRS/MODS, probably because so far, investiga­
tors have been unable to control bacterial translocation
effectively during shock in humans; thus, a cause and effect
relationship cannot be established. The ‘two-hit’ theory
ascribes a summation of insults to the development of organ
failure. Each of the insults alone is inadequate to cause the
response, but one or more of these insults can ‘prime’ the
inflammatory response system described above such that
another normally insignificant injury causes the release of
toxic mediators that end in multiple organ failure.
In the end, it is likely that some part of all of these theories
is a cause for MODS in patients with burns, and probably
the relative contribution of each is unique in each patient.
Therefore, a single solution is unlikely, which should be kept
in mind when devising strategies to improve care and
outcomes.
Diagnosis of sepsis
Presuming that sepsis has two potential causes, infection or
inflammation without infection, reliable detection of those
with some component of infection is warranted. Our diffi­
culty in severe burns is delimiting this, as traditional screen­
ing indicators for infection such as temperature and white
blood cell count are unreliable because of massive hyper­
metabolism and inflammation associated with recovery and
healing.49,50 Potential does exist for elevations in procalci­
tonin to be associated with a higher risk of infection, this
being linked to pathogen infection presumably through
PAMPs rather than DAMPs. An interesting study from Iran
examined the role of WBC, sedimentation rate, C-reactive
protein, and procalcitonin in diagnosing sepsis in the
severely burned. The authors found that procalcitonin was
the only test among them with any distinguishing capacity,
which in fact was quite accurate.51 We look for further studies
in the near future to further define this relationship.
Prevention
This brief outline of the potential pathophysiology and
causes of burn-induced critical illness and multiple organ
failure demonstrates the complexity of the problem. Because
different cascade systems are involved in the pathogenesis,
it is so far impossible to pinpoint a single mediator or system
that initiates the event. Thus, as the mechanisms of progres­
sion are not well known and specific treatments cannot be
accurately devised, it seems that prevention is likely the best
solution. The current recommendations are to prevent the
development of organ dysfunction, and to provide optimal
support to avoid conditions that promote its onset. In
burned patients this can be accomplished most reliably
through expeditious wound closure, rapid mobilization of
the patient, and prompt identification and treatment of early
infections.

Critical care in the severely burned: organ support and management of complications
389
increase urinary sodium and decrease urine osmolality even
in prerenal conditions. In general, urine osmolarity and
urinary sodium concentrations are primarily used for these
determinations because of the ease of measurement. In
terms of clinical utility, renal dysfunction is often a mixture
of prerenal and intrinsic causes, making treatment decisions
difficult.
Should these tests reveal a prerenal cause, volume replace­
ment should ensue to prevent further renal ischemia. The
physical examination and invasive monitoring, if deemed
appropriate, should guide this volume replacement. The
decision to administer or remove fluids may prove difficult,
however, as both strategies have detrimental consequences if
followed inappropriately. Although volume replacement is
ineffective in restoring renal function once tubular necrosis
is established, it remains our most effective prophylactic
strategy, and is generally the place to start with the onset of
renal failure.
Owing to the wide variation in the definition of acute renal
failure, reporting an accurate incidence as well as resultant
outcomes has been problematic. In an effort to help resolve
this problem and standardize the classification of acute renal
failure (now referred to as acute kidney injury or AKI), the
Acute Dialysis Quality Initiative (ADQI) developed and
reported the RIFLE (Risk, Injury, Failure, Loss of function,
End-stage Renal Disease) criteria.58 More recently, the Acute
Kidney Injury Network (AKIN) proposed a modified version
of the RIFLE system because of a number of identified limita­
tions. These revised criteria are intended to simplify the defi­
nition and make it more clinically applicable. According to
the AKIN criteria, stage 1 AKI is defined by ‘an abrupt (within
48 hours) reduction of kidney function currently defined as
an absolute increase in serum creatinine of more than or
equal to 0.3 mg/dL, a percentage increase in serum creati­
nine of more than or equal to 50% (1.5-fold from baseline),
or a reduction in urine output (documented oliguria of
less than 0.5 mL/kg per hour for more than 6 hours).’
Stages 2 and 3 are the same as RIFLE – Injury and Failure,
respectively.59
In burned patients, investigators recently showed that the
incidence and outcomes of > 20% TBSA burned patients
with AKI using RIFLE criteria was 24% (12% Risk, 8% Injury,
and 5% Failure). Associated mortality was 14%, which
increased with increasing RIFLE class (7% normal, 13% Risk,
40% Injury, and 83% Failure). Renal dysfunction occurred
within 7 days in 55% of affected patients and completely
recovered in all survivors; pulmonary dysfunction was
After the initiating event, tubular function and GFR
decrease to reduce urine production. The progression of ARF
is commonly divided into three phases: initiation, mainte­
nance, and recovery, and can be oliguric (urine output
<400 mL/day) or non-oliguric (urine output >400 mL/day)
in nature. Patients with non-oliguric ARF have a better prog­
nosis than those with oliguric renal failure, probably due in
large measure to the decreased severity of the insult and the
fact that many have drug-associated nephrotoxicity or inter­
stitial nephritis.
Once ARF is established, pharmacologic improvement of
renal blood flow will not reverse the injury. Agents such as
dopamine, which was commonly used in the past to dilate
renal arterioles and increase renal blood flow via dopamine
receptors, have been shown to be mostly ineffective.54
Recently, the potent dopamine-1 receptor agonist fenoldo­
pam has garnered some interest as an agent to improve
renal perfusion and outcomes. A recent meta-analysis of
randomized controlled trials demonstrated that low-dose
fenoldopam (0.03–0.09 µg/kg/min) may be of benefit in
reducing the need for renal replacement therapy and hospi­
tal mortality when used in septic patients with either estab­
lished ARF or at high risk for ARF in a mixed ICU population.55
Its use in this setting has been reported in a non-controlled
study in burned patients, with improvement in renal func­
tion (increased urine output, decreased serum creatinine)
without any hypotension at the low dose.56 Further work will
need to be done in the burn population to fully determine
its efficacy.
Diuretic therapies, such as mannitol and loop diuretics,
have been used extensively in patients with acute renal
failure to increase urine flow, and protect the kidney from
further ischemic damage. Mannitol can reduce cellular swell­
ing in the proximal tubule and increase intratubular flow,
thus potentially decreasing intratubular obstruction and
further renal dysfunction. Mannitol has been previously rec­
ommended along with vigorous volume replacement and
sodium bicarbonate for the treatment of early myoglobinu­
ric acute renal failure. However, recent evidence suggests lack
of benefit and a call for re-evaluation of this practice.57 Loop
diuretics also increase intratubular flow rates, and can
convert an oliguric state to a non-oliguric state, thereby
making clinical management of renal failure easier. In
general, although patients with non-oliguric renal failure are
generally easier to manage from a volume standpoint, there
is no evidence that conversion from an oliguric to a non-
oliguric state improves outcomes.
The initial care of patients with ARF is focused on reversing
the underlying cause, and correcting fluid and electrolyte
imbalances. Renal failure is heralded by a decrease in urinary
output. Volumes of urine < 1 mL/kg/h may indicate the
onset of ARF. This failure may be due to prerenal causes,
which are typically decreased renal blood flow from hypop­
erfusion, or intrinsic renal causes, which are associated with
medications or sepsis. Differentiation between these etiolo­
gies can be made with laboratory examinations (Table 33.2).
Prerenal etiologies are associated with concentrated urine
(urine osmolarity >400 mmol/kg), decreased urinary sodium
concentrations, and decreased fractional excretion of sodium.
Intrinsic renal causes will be associated with more dilute
urine with higher sodium concentrations. These tests should
be performed before diuretics are used, as this treatment will
Table 33.2  Laboratory tests to distinguish prerenal from intrinsic
renal failure
Examination
Prerenal
Intrinsic renal
Urine osmolality (mmol/kg)
>400
<400
Urinary sodium (mEq/dL)
<20
>40
FENa (%)*
<1
>2
*FENa, fractional excretion of sodium, calculated as (U/PNa / U/PCr) × 100, where U
is urinary concentration, and P is plasma concentration. Na is sodium and Cr is
creatinine.

Total Burn Care
33
390
insulin, and sodium bicarbonate in the presence of meta­
bolic acidosis. Medications eliminated through the kidney
should be adjusted. Once the diagnosis of ARF is established,
consideration can be given to diuretic therapy or the early
initiation of continuous venovenous hemofiltration, espe­
cially if it is determined that the patient is volume over­
loaded. Reducing the volume of fluid given can also alleviate
volume overload in burned patients. These patients have
increased insensible losses from the wounds which can
be roughly calculated at 3750 mL/m2 TBSA wound plus
1500 mL/m2 TBSA total. Reducing the infused volume of
intravenous fluids and enteral feedings below the expected
insensate losses may alleviate some of these problems.
Reducing potassium administration in the enteral feedings
and giving oral bicarbonate solutions can minimize elec­
trolyte abnormalities. Almost invariably, severely burned
patients require exogenous potassium because of the height­
ened aldosterone response, which results in potassium
wasting; therefore, hyperkalemia is rare even with some renal
insufficiency.
Intermittent dialysis remains a viable replacement therapy
for severe ARF in the hemodynamically normal ICU patient,
although this may be changing. The indications for dialysis
are edema and volume overload or electrolyte abnormalities
not amenable to other treatments. In recent years, continu­
ous renal replacement therapies have emerged as yet an­
other option for critically ill patients with ARF (Fig. 33.7).
The advantages of continuous treatment over intermittent
include more precise fluid and metabolic control, decreased
hemodynamic stability, and the enhanced ability to remove
injurious cytokines. Disadvantages include the need for
anticoagulation and heightened surveillance. Bleeding pro­
blems are particularly prevalent in burned patients during
anticoagulation.
Peritoneal dialysis is another option for acute renal failure
in burned patients.64 Catheters can be placed at the bedside
with near-continuous exchanges to improve electrolyte and
volume overload problems. The capital required for this
treatment is minimal. Hypertonic solutions are used to
present in all. Sepsis was a possible aggravating factor in
acute kidney injury in 48%. They concluded that AKI is
common after severe burn, develops within days of injury,
and parallels other organ dysfunction.60 These data confirm
earlier studies showing that the development of renal failure
is associated with dismal outcomes; however, minor dys­
function does not necessarily correlate to progression and
mortality, giving hope to therapies designed to maintain
renal function after severe burn.
Another study examined the incidence of renal dysfunc­
tion in burned patients, defined by serum creatinine >
1.4 mg/dL; 39% of patients admitted to the ICU developed
renal insufficiency, of which 33% underwent renal replace­
ment therapy. Associated mortality in those with renal insuf­
ficiency was 44%; those who developed renal insufficiency
within 5 days of injury had higher mortality than those with
later onset. Of interest, all survivors regained normal renal
function later in their course.61 The next study investigated
early markers of renal dysfunction, and found that elevations
in urinary microalbumin and malondialdehyde (both 3–4-
fold) were present in all with eventual renal dysfunction.62
These may come to be indicators of risk for injury that can
be acted upon early in the course to prevent progression to
more severe degrees of failure and therefore improve out­
comes. The last study investigated the role of continuous
venovenous haemofiltration (CVVH) in the treatment of
renal dysfunction after severe burn. The investigators com­
pared a population of patients treated with high-volume
CVVH (at least 50 mL/kg/h) compared to non-treated his­
torical controls, and found that both 28-day mortality and
overall mortality were improved by 50% with this therapy.63
A multicenter randomized controlled trial comparing early
high-volume CVVH (70 mL/kg/h) to standard care is under
way in this high-risk population (ClinicalTrials.gov Identi­
fier: NCT01213914).
After ensuring adequate volume status, every effort should
be made to prevent other causes of renal injury. All nephro­
toxins should be discontinued or avoided. Hyperkalemia
that may develop can be treated with resins, glucose and
Figure 33.7  The probability of successful
weaning with intermittent mandatory ventilation,
pressure support ventilation, intermittent trials of
spontaneous breathing, and once-daily trials of
spontaneous breathing (Kaplan–Meier curves).
After adjustments for baseline characteristics (Cox
proportional hazards model), the rate of successful
weaning with a once-daily trial of spontaneous
breathing was 2.83 times higher than that with
intermittent mandatory ventilation (p < 0.006) and
2.05 times higher than that with pressure support
ventilation (p < 0.04). (Reprinted with permission from
Esteban et al. N Engl J Med 1995; 332-350. Copyright
Massachusetts Medical Society.)37
Duration of weaning (days)
Intermittent trials
Once-daily trial
Pressure support ventilation
Intermittent mandatory ventilation
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
0
2
4
6
8
10
14
12
Probability of successful weaning

Critical care in the severely burned: organ support and management of complications
391
management, suggesting that reducing the risk of further
harm is the most effective treatment for this condition at
present.
ALI and ARDS occur because of damage to the endothe­
lium and lung epithelium. It is speculated that the products
of inflammation, such as cytokines, endotoxin, comple­
ment, and coagulation system products, induce the changes
that are characteristic of ALI and ARDS. The acute phase of
ALI is characterized by an influx of protein-rich edema fluid
into the air spaces as a consequence of increased permeabil­
ity of the alveolar–capillary barrier. The importance of
endothelial injury and increased vascular permeability to
the formation of pulmonary edema is well established
(Fig. 33.8). Epithelial injury is also of great importance. In
fact, the degree of alveolar epithelial injury is an important
predictor of outcome.
Neutrophils are likely to play a role in the pathogenesis of
ALI. Histologic studies of lung specimens obtained early in
the course demonstrate marked accumulation of neutrophils
in the alveolar fluid. However, it must be stated that ALI and
ARDS develop in patients with profound neutropenia,66 and
some animal models of ARDS are neutrophil independent,
implying that neutrophils may be nothing more than
bystanders in the inflammatory process.
The effects of ventilator injury on the development and
progression of ALI and ARDS are now firmly established.
Previous studies focused on the potential damaging effects
of high oxygen concentrations on lung epithelium.67 Evi­
dence suggests that mechanical ventilation at high pressures
injures the lung,35 causing increased pulmonary edema in
the uninjured lung and enhanced edema in the injured
lung.68 Alveolar overdistension and cyclic opening and
closing of alveoli associated with high ventilatory pressures
is also potentially damaging to the lung.
After the development of ALI and ARDS, some patients
have a rapid recovery over a few days. Others progress to
fibrotic lung injury; the alveolar space becomes filled with
mesenchymal cells, extracellular proteins, and new blood
vessels. The finding of fibrosis on histologic analysis corre­
lates with increased mortality.69
remove fluid volume, and the concentrations of potassium
and bicarbonate are modified to produce the desired results.
The dwell time is usually 30 minutes, followed by drainage
for 30 minutes. This treatment can be repeated in cycles until
the problem is resolved. For maintenance, 4–6 such cycles a
day with prolonged dwell times (1 hour) is usually sufficient
during the acute phase. This treatment is known to occur in
burned patients, but has not received a significant amount
of study.
Pulmonary system
Mechanical ventilation in the severely burned generally takes
place for three reasons: airway control during the resuscita­
tive phase, airway management for smoke inhalation, and
for the development of acute lung injury and ARDS. The first
is for airway control early in the course with the develop­
ment of massive whole-body edema associated with the
great resuscitative volumes required to maintain euvolemia.
In this situation, the need for mechanical ventilation is not
due to lung failure per se, but instead to maintain the airway
until the whole-body edema resolves. Once this occurs,
usually 2–3 days into the course, extubation can be accom­
plished. Ventilator management during this phase is routine.
The second primary reason for mechanical ventilation is for
airway management early in the course of smoke inhalation.
Another chapter in this book will deal specifically with this
issue. The third is the development of hypoxemia. Severe
burns are known to be associated with hypoxemia and the
development of acute lung injury (ALI) and its more severe
counterpart, ARDS. The clinical manifestations are dyspnea,
severe hypoxemia, and decreased lung compliance with
radiographic evidence of diffuse bilateral pulmonary infil­
trates. These conditions exist as a continuum from ALI,
which is a mild form, to its most severe form, which is dense
ARDS. These conditions have been defined by the American-
European Consensus Conference Committee, and are listed
in Box 33.5. These definitions are relatively simple, and are
used in other critically ill populations. The rest of the discus­
sion will be related to ALI and ARDS.
Epidemiology and pathophysiology
ALI and ARDS occur as a result of injury to the lung, which
can be direct through smoke inhalation or pneumonia, or
indirect through mediators associated with sepsis. Until
recently, most studies of ALI and ARDS reported mortality
rates between 40% and 60%. Now, in trauma patients, the
most recent mortality rate for ARDS was 14%; in addition,
the incidence of ARDS fell by 50% in a matched patient
population.65 Thus, we can say conclusively that the inci­
dence has gone down; what has changed is the method of
Figure 33.8  Typical timeline for progression to ARDS. Patients are typically
intubated for airway compromise and operative intervention. At day 4 or 5
after severe burn, oxygenation will deteriorate, requiring higher inspired
concentrations of oxygen. These measures will soon fail with the
introduction of decreased lung compliance requiring higher inspired airway
pressures. Only then will infiltrates begin to appear on the chest X-ray (CXR).
Severe burn ±
smoke inhalation
Hypoxemia
Time
Day 0
Day 5
Day 7
Decreased lung
compliance
Lung infiltrates
on CXR
Box 33.5  Definitions of acute lung injury and acute respiratory
distress syndrome
•
Acute onset
•
Bilateral infiltrates on chest radiography
•
Pulmonary artery wedge pressure <18 mmHg
•
Acute lung injury (ALI) if PaO2/FiO2 is <30 but >200
•
Acute respiratory distress syndrome (ARDS) if PaO2/FiO2 is <200

Total Burn Care
33
392
necessary to maintain homeostasis; and the NIH study had
more patients, and so may have been more sufficiently
powered to show differences between treatment groups.
Positive end-expiratory pressure has clearly been shown to
benefit patients with ALI and ARDS; however, the optimum
level has been controversial. The best effect of PEEP is to
increase functional residual capacity, or the number of open
alveoli at the end of expiration. However, the use of prophy­
lactic PEEP therapy in patients at risk for ALI showed no
benefit for the treatment group compared to controls.71
A study of PEEP therapy aimed at raising the level of PEEP
above the lower inflection point on pressure–volume curves
to prevent alveolar closure in addition to low tidal volumes
and pressure controlled inverse ratio ventilation showed
improved mortality compared to a control group managed
with conventional ventilation.72 Drawbacks to this study
were the unusually high mortality (71%) in the control
group, and improvements in mortality for the treatment
group compared to controls could only be determined at
hospital day 28, which was not appreciated at hospital
discharge.
Inhaled nitric oxide is an effective pulmonary vasodilator
with effects localized to ventilated areas of the lung, thus
directing more blood to the functional areas of the lung. The
conceivable effect, then, is to diminish the fraction of blood
shunted through the lungs without oxygenation, thereby
improving pulmonary venous oxygenation. Observational
studies suggest that inhaled nitric oxide might be beneficial
in the treatment of ARDS by improving oxygenation without
increased ventilatory pressures and reducing barotrauma.
However, randomized trials testing this hypothesis have
been disappointing. In the most recent large study, inhaled
nitric oxide therapy did not reduce mortality or reduce the
duration of mechanical ventilation. Improvements in oxy­
genation were seen, but the effects were not sustained.73 The
reported experience with this modality in burns is only
anecdotal.
Another modality commonly used in ICUs for refractory
hypoxemia is prone positioning. This is based on the ration­
ale that dependent areas of the lung in ARDS have the most
blood flow and the most edema, thereby leading to a greater
mismatch of blood flow and aerated lung, and greater shunt­
ing of blood past unaerated areas; hence blood returns to
the heart unoxygenated. By placing the patient in the prone
position for a prescribed period, the previously aerated lung
now receives a greater portion of blood flow as directed by
gravity. This approach almost always results in improved
oxygenation, but as with nitric oxide, has not been shown
to be of benefit for mortality in prospective trials.74 However,
two recent meta-analyses have demonstrated significant
mortality benefit in those with severe hypoxemia.75,76 Thus,
it appears that in certain subpopulations these types of thera­
pies may be considered after carefully balancing risk versus
benefit.
Glucocorticoids have been used in the treatment of ARDS
because of the inflammatory nature of the disease in a
number of trials, the results of which are for the most part
contradictory and equivocal. To add fuel to the fire, the most
recent large trial of glucocorticoid treatment of early severe
ARDS showed an improvement in ventilator days and MODS
scores.77 Others have shown benefit of glucocorticoid when
used in the later fibroproliferative phases of the disease to
In non-fatal cases of ARDS the lung heals by proliferation
of type II epithelial cells, which begin to cover the denuded
basement membrane and differentiate into type I epithelial
cells, thus restoring normal alveolar architecture and increas­
ing the fluid-transport capacity of the alveolar epithelium.
Alveolar edema is resolved by active transport of sodium
from the distal airspace into the interstitium by intact alveoli.
Soluble protein is removed primarily by diffusion between
alveolar cells, and insoluble protein is eliminated by endo­
cytosis and transcytosis by alveolar epithelial cells and
phagocytosis by macrophages.
The severely burned are unique among patients who
develop ALI and ARDS. Because direct injury to the lung
from smoke inhalation is common, often patients will
present with respiratory insufficiency and relative hypoxia
caused by increased capillary permeability, ciliary dysfunc­
tion, and interstitial edema associated with the chemical
injury of smoke. A few days later, the damaged and necrotic
respiratory mucosa begins to slough, causing bronchial plug­
ging and atelectasis, further worsening the clinical condition.
However, it is not usually until 4–8 days into the course of
injury that severe hypoxemia and ARDS develop in burned
patients, a scenario not unlike that in other types of patient
who develop ALI and ARDS, such as after abdominal sepsis
or multiple blunt trauma. It stands to reason that smoke
inhalation is associated with the development of ARDS, but
perhaps this association is related to the inflammation asso­
ciated with the injury in addition to that rendered by the
burn wound. In fact, it was shown that the degree of inhala­
tion injury was not associated with the development of
ARDS in burned patients.70 It may be, then, that smoke
inhalation and ALI/ARDS are two separate conditions which
are interrelated.
Treatment
The treatment of ALI and ARDS is largely supportive until
the healing processes described above can be accomplished.
A careful search for potential underlying causes should
ensue, including attention to potentially treatable causes
such as intra-abdominal infections, pneumonia, line sepsis,
and invasive burn wound infection. An improved under­
standing of the pathogenesis of ALI has led to the assessment
of several novel treatment strategies, including changes in
mechanical ventilation strategies, fluid management, sur­
factant therapy, nitric oxide treatments, and anti-inflammatory
strategies.
The most appropriate method of mechanical ventilation
for ALI and ARDS has been controversial for some time,
though the picture is becoming clearer; the ARDSnet study
provided much of this clarity.35 They reported a 22% decline
in mortality in patients with ALI and ARDS treated with tidal
volumes of 6 mL/kg compared to those treated with conven­
tional volumes of 12 mL/kg. In this study, peak airway pres­
sures could not exceed 30 cmH2O in the lower tidal volume
group, and a detailed protocol was used to adjust the frac­
tion of inspired oxygen and PEEP. These results were differ­
ent from those of previous smaller studies showing no
improvement with pressure-limited ventilation. Potential
reasons for the discrepancy between the NIH study and the
others are as follows: the NIH study had the lowest tidal
volume of the three studies, respiratory acidosis was allowed
in the NIH study, with sodium bicarbonate treatment if

Critical care in the severely burned: organ support and management of complications
393
heart in 1914. The relationship demonstrated in the Frank–
Starling curve justifies the use of preload augmentation
by volume resuscitation to increase cardiac performance.
However, when the end-diastolic volume becomes excessive
cardiac function can decrease, probably by overstretch of the
muscle fibers such that the contractile fibers are pulled past
each other, thereby reducing the contact required for con­
tractile force. The preload required to reduce cardiac func­
tion in experimental settings is in excess of 60 mmHg, which
is rarely encountered in patients.
Preload is estimated clinically either by central venous
pressure or by pulmonary artery wedge pressure.
Cardiac contractility
The force with which the heart contracts is referred to as
cardiac contractility. It is directly related to the number of
fibers contracting, and will be diminished in patients with
vascular occlusive disease of the myocardium who lose
muscle fibers due to infarction and ischemia, and in burned
patients during the acute resuscitation. Calculating the left
ventricular stroke work from pulmonary artery catheter-
derived values provides the best estimate of cardiac contrac­
tility, and can be calculated with the following formula:
LVSW
SV MAP
PCWP
=
−
×
(
)
.
0 0136
where LVSW is left ventricular stroke work, SV is the stroke
volume (cardiac index ÷ heart rate), MAP is mean arterial
pressure, and PCWP is pulmonary capillary wedge
pressure.
Afterload
Afterload is the force that impedes or opposes ventricular
contraction. This force is equivalent to the tension developed
across the wall of the ventricle during systole. Afterload is
measured clinically by arterial resistance as an estimate of
arterial compliance. Arterial resistance is measured as the
difference between inflow pressure (mean arterial) and
outflow pressure (venous) divided by the flow rate (cardiac
output):
SVR
MAP
CVP /CO
=
−
(
)
where SVR is systemic vascular resistance, MAP is mean
arterial pressure, CVP is central venous pressure, and CO is
cardiac output.
Heart rate and rhythm
For the heart to function properly the electrical conduction
system must be intact, so as to provide rhythmic efficient
contractions to develop sufficient force to propel blood
through the circulatory system. For example, if the heart rate
approaches 200 beats/min, the heart will not have time to
fill completely, thereby reducing myocardial fiber stretch and
reducing heart function. Also, if frequent premature ven­
tricular contractions are present, the heart will not perform
as well for similar reasons. Heart rate and rhythm are moni­
tored continuously as a routine in all critically ill patients
using electrocardiography.
Effects of burn on cardiac performance
Severe burns affect cardiac performance in a number of ways.
The first is to reduce preload to the heart through volume
loss into the burned and non-burned tissues. It is for this
good effect.78 It is likely that some population exists in which
glucocorticoid treatment is of benefit for those with ARDS
– however, we do not think it is burns. This type of therapy
may be treacherous in burned patients at risk for invasive
burn wound infection, but might be considered upon com­
plete burn wound closure.
Cardiovascular system
Principles
Treatment of cardiovascular responses after burn requires an
understanding of cardiovascular physiology and the effects
of treatment. One of the hallmarks of serious illness is the
direct link between cardiac performance and patient per­
formance. The four determinants of cardiac function and
hence tissue perfusion of blood at the whole body level are
the following:
•
Ventricular preload or end-diastolic muscle fiber length;
•
Myocardial contractility or strength of the heart muscle;
•
Ventricular afterload, or the degree of resistance against
which the heart must pump; and
•
Heart rate and rhythm.
A thorough comprehension of the effects of each of these
components on heart function is required in order to initiate
effective treatments for burned patients with cardiovascular
abnormalities.
Preload
Preload is defined as the force that stretches the cardiac
muscle prior to contraction. This force is composed of
volume that fills the heart from venous return. Because of
the molecular arrangement of actin and myosin in muscle,
the more the muscle is stretched with incoming venous
volume, the further it will contract. This is best demonstrated
on a Frank–Starling curve (Fig. 33.9), which was first
described by Otto Frank in a frog heart preparation in 1884;
Ernest Starling extended this observation in the mammalian
Figure 33.9  Frank–Starling curve. The solid line depicts the pressure–
volume relationship of the heart, showing that as pressure to the heart
(preload) increases, the volume pumped by the heart increases. Immediately
after burn, contractility diminishes, shifting the curve downward (dashed
line). It still must be noted that with this change, the volume pumped by
the heart still increases with increased pressure (preload), validating the use
of increased atrial pressure as a means of increasing cardiac output after
severe burn.
Pressure
Volume

Total Burn Care
33
394
Agents with primary effects on the α-adrenergic receptor
can be used to induce vasoconstriction and increase blood
pressure. These agents consist of norepinephrine and phe­
nylephrine, and can be used effectively during septic shock
or neurogenic shock to increase vascular tone. In burned
patients, it is felt that these agents will cause vasoconstriction
of the skin circulation and the splanchnic circulation to
preserve blood flow to major organs such as the heart and
brain. This redistribution in blood flow can cause conversion
of partial-thickness skin injuries to full-thickness and result
in ischemic injury to the gut. The use of specific vasoconstric­
tors must be weighed against these effects.
Another vasoconstrictive agent that is being used with
more popularity is vasopressin, which is a very potent vaso­
constrictor mediated through its own receptor independent
of the adrenergic receptors. Levels of vasopressin have been
shown to be low in septic shock, and physiologic replace­
ment at 0.02–0.044 U/kg/min without titration is used in
some burn units to increase mean arterial pressure to good
effect. Some investigators found that the use of vasopressin
in this condition increased blood pressure, decreased
heart rate, and spared norepinephrine dosing when used
concomitantly.79
Effects of β-blockade on cardiac performance
after severe burn
One of the responses to severe burn is a dramatic increase
in catecholamine production that has been linked to a
number of metabolic abnormalities, including increased
resting energy expenditure, muscle catabolism, and altered
thermoregulation. Propranolol, as a non-specific β-blocker,
has been used to reduce heart rate and myocardial work in
severe burns.80 Propranolol administration also reduces
peripheral lipolysis81 and muscle catabolism,82 which are
additional beneficial effects. Consideration should be given
to further trials with the use of propranolol to improve out­
comes in burned patients.
Gastrointestinal system
Pathophysiologic changes in the gut
The gastrointestinal response to burn is highlighted by
mucosal atrophy, changes in digestive absorption, and
increased intestinal permeability. Changes in gut blood flow
are related to changes in permeability. Intestinal blood flow
was shown to decrease in non-resuscitated animals, a change
that was associated with increased gut permeability at 5
hours after burn.83 This effect was abolished at 24 hours.
Systolic hypotension has been shown to occur in the first
hours after burn in animals with a 40% TBSA full-thickness
injury.
Clinical changes in the gut after burn
Given the changes in the gut to burn described above, it is
common to see some evidence of gut dysfunction after burn
evidenced by feeding intolerance84 and mucosal ulceration
and bleeding, particularly in the stomach and duodenum.
Enteral feeding is an important means of providing nutrition
to burned patients and has led to a decrease in mortality, but
at times the gut will not cooperate. Reduced motility and
ileus are common, at times requiring parenteral nutrition to
meet caloric needs. At present there is no specific treatment
reason that volumes predicted by resuscitation formulas
must be used to maintain blood pressure and maintain
hemodynamics. In addition, severe burn induces myocardial
depression characterized by a decrease in tension develop­
ment and velocities of contraction and relaxation. Cardiac
output is then reduced. These effects are most evident early
in the course of injury during resuscitation; however, they
are followed shortly thereafter by a hyperdynamic phase of
increased cardiac output caused primarily by a decrease in
afterload through vasodilation and an increase in heart rate.
Hemodynamic therapy: preload augmentation
When hypotension or other signs of inadequate cardiac
function (i.e., decreased urine output) are encountered, the
usual response is to augment preload by increasing intravas­
cular volume. This is a sound physiologic approach based
on the Frank–Starling principle, and should be the first
therapy for any patient in shock. Intravascular volume can
be increased with either crystalloid or colloid to increase the
central venous pressure and pulmonary capillary wedge pres­
sure to a value between 10 and 20 mmHg. The adequacy of
this therapy can be monitored by the restoration of arterial
blood pressure, a decrease in tachycardia, and a urine output
>0.5 mL/kg/h.
Some caution must be exercised when augmenting preload
for hemodynamic benefit in burned patients. Excessive
volume administration may lead to significant interstitial
edema and volume overload, with the development of
peripheral and pulmonary edema. These changes can lead
to conversion of partial-thickness burns to full-thickness
injuries in the periphery, and can cause significant respira­
tory problems. Judicious use of fluid administration after
hemodynamics are restored with spontaneous diuresis will
usually alleviate this problem; however, at times pharmaco­
logic diuresis will be required.
Hemodynamic therapy: inotropes
If volume replacement is insufficient to improve hemody­
namics in burned patients in shock, inotropes may be
required. These inotropes generally consist of adrenergic
receptor agonists, although phosphodiesterase inhibitors
that increase intracellular cAMP levels to increase myocyte
Ca2+ levels or digoxin that acts to increase myocyte Ca2+ levels
by inhibiting the Na+/K+ pump can also be used to improve
myocardial contractility.
Dopamine is a commonly used inotropic agent which has
both α- and β-adrenergic properties. The α effects are seen
primarily at higher doses (10–20 µg/kg/min), while the β
effects are seen at all doses. Therefore, dopamine can be
thought of as an ‘inoconstrictor,’ because it has both intropic
and vasoconstrictive properties. Other inotropes in this class
include epinephrine and norepinephrine. One caveat to the
use of these inoconstrictors is that myocardial oxygen con­
sumption increases, which may affect areas of the heart that
are ischemic. Dopamine has generally fallen out of favor of
late, to be replaced with more specific inotropes and vaso­
constrictors. Dobutamine is a commonly used inotrope
which has effects limited to β-adrenergic stimulation; thus,
cardiac contractility is increased without vasoconstriction.
The effect is to improve cardiac output generally without
specific splanchnic or renal effects.

Critical care in the severely burned: organ support and management of complications
395
the ICU did not find a benefit to keeping glucose in the
normal range, but a higher range might have been even more
beneficial.90 The caveat to this analysis was that on a post-hoc
basis, injured patients had better outcomes with the normal
glucose range rather than the higher.
In another landmark trial, cortisol levels were found to be
low in many critically ill patients and a mortality benefit
accrued with physiologic replacement with hydrocortisone.91
This study highlighted that hypocortisolemia is at least asso­
ciated with septic shock and hypotension, and that replace­
ment with hydrocortisone at 50 mg every 6 hours improves
outcomes. The same was seen in burned patients in the
ICU.92,93 It must be noted, however, that the benefits seem
to be limited to those with relative adrenal insufficiency
assessed by corticotropin stimulation, as seen in the
follow-up CORTICUS trial.94 Regardless, in the case of hypo­
tension not related to hypovolemia in burned patients, cor­
tisol levels and adrenal stimulation should be performed to
determine whether relative adrenal insufficiency exists, and
treatment with hydrocortisone should ensue.
Summary
Improved critical care of the severely burned has reduced
mortality over the past two to three decades. This has been
in part through the development of specialized units for the
care of burned patients which are equipped with the person­
nel and equipment to deliver state-of-the-art care. Better
understanding of the processes of critical illness and multi­
ple organ failure has led to effective prevention strategies and
treatment modalities. Further advances in the understanding
of mechanisms of the progression from SIRS to multiple
organ failure will engender new breakthroughs that can be
expected to further improve the outcomes of burned patients.
Further reading
Cartotto RC, Ellis S, Gomez M, et al. High frequency oscillatory
ventilation in burn patients with the acute respiratory distress
syndrome. Burns. 2004;30:453-463.
Chung KK, Wolf SE, Renz EM, et al. High-frequency percussive
ventilation and low tidal volume ventilation in burns: a
randomized controlled trial. Crit Care Med. 2010;38:1970-1977.
Harvey S, Stevens K, Harrison D, et al. An evaluation of the clinical
and cost-effectiveness of pulmonary artery catheters in patient
management in intensive care: a systematic review and a
randomised controlled trial. Health Technology Assessment.
2006;10:111-133.
Papp A, Uusaro A, Parviainen I, et al. Myocardial function and
haemodynamics in extensive burn trauma: evaluation by clinical
signs, invasive monitoring, echocardiography and cytokine
concentrations. A prospective clinical study. Acta Anaesthesiologica
Scandinavica. 2003;10:1257-1263.
Steinvall I, Bak Z, Sjoberg F. 2008 Acute kidney injury is common,
parallels organ dysfunction or failure, and carries appreciable
mortality in patients with major burns: A prospective exploratory
cohort study. Crit Care. 2008;12:R124-130.
for burn induced ileus, but it seems that early enteral feeding
will prevent some of these potential complications.
Stress ulceration of the stomach and duodenum, on the
other hand, can be prevented effectively with antacid therapy.
In the 1970s stress ulceration leading to life-threatening
hemorrhage was common. The mechanism of injury is
related to an imbalance between protective factors such as
mucus production, protective prostaglandin output and
bicarbonate secretion, and injurious factors such as decreased
blood flow and acid production. Gastric ulcers developed in
the watershed zones between capillary beds which are wors­
ened by gastric acid-induced injury. With today’s use of
standard critical care techniques with gastric acid suppres­
sion and expeditious wound closure, upper gastrointestinal
bleeding is relatively rare. When it occurs, treatment is con­
gruent with upper gastrointestinal bleeding in general,
through identification of the bleeding source and control
with local techniques or surgery if required.
In the past few years a condition termed abdominal com­
partment syndrome has arisen. This is associated with
massive volume resuscitation, which induces generalized
edema in a relatively limited abdominal compartment. It
eventuates in decreased gut blood flow and renal blood flow
causing oliguria and bowel ischemia.85 The tragedy is that
the early sign of this condition is low urine output, which is
commonly addressed by more intravenous fluid, which only
worsens the case. The associated physical finding is abdomi­
nal distension, and an estimate of intra-abdominal pressure
can be obtained by pressure monitoring of the bladder: pres­
sures >30 torr are concerning and should instigate further
investigation. Treatments are aimed at reducing intra-
abdominal pressures though catheter drainage,86 or decom­
pressive laparotomy may be considered. Unfortunately, in
those with burns >40% TBSA (those at highest risk for
abdominal compartment syndrome), decompressive lapa­
rotomy has a mortality rate approaching 100%.87 Therefore,
the best treatment for this condition is prevention through
judicious resuscitation.
Endocrinopathies
Hyperglycemia and insulin resistance are common in the
critically ill, and the burned patient is no exception. In 2001,
Greet van den Berge reported in a landmark trial that inten­
sive insulin treatment with continuous infusions of insulin
aimed at normalizing blood glucose levels between 80 and
110 mg/dL improved mortality, and reduced bloodstream
infections and acute renal failure.88 These studies were
among the first to show some benefit of a treatment for all
critically ill patients. Since this study, most intensivists
throughout the world have gone to a practice of glucose
control to a normal range through the use of insulin. This
may have other beneficial effects, as investigators have shown
anabolic benefit of insulin treatment in burned patients in
terms of muscle mass.89 The particular range to which glucose
should be controlled has not been firmly established,
however, as the latest large-scale study on glucose control in
 
Access the complete reference list online at

Critical care in the severely burned: organ support and management of complications
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88. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin
therapy in the critically ill patients. New Engl J Med.
2001;345:1359.
89. Thomas SJ, Morimoto K, Herndon DN, et al. The effect of
prolonged euglycemic hyperinsulinemia on lean body mass after
severe burn. Surgery. 2002;132:341-347.
90. NICE-SUGAR Investigators. Intensive versus conventional glucose
control in critically ill patients. New Engl J Med. 2009;360:1283-
1297.
91. Annane D, Sebille V, Bellissant E, et al. Effect of low doses of
corticosteroids in septic shock patients with or without early
acute respiratory distress syndrome. Crit Care Med. 2006;34:
236-238.
92. Fuchs PC, Groger A, Bozkurt A. Cortisol in severely burned
patients: investigations on disturbance of the hypothalamic-
pituitary-adrenal axis. Shock. 2007;28:662-667.
93. Winter W, Kamolz L, Donner A, et al. 2003 Hydrocortisone
improved haemodynamics and fluid requirement in surviving
but not non-surviving of severely burned patients. Burns.
2003;29:717-720.
94. Sprung CL, Annane D, Keh D, et al. CORTICUS Study Group.
Hydrocortisone therapy for patients with septic shock. New Engl J
Med. 2008;358:111-124.
95. Shapiro BA, Lacmak RM, Care RD, et al. Clinical application of
respiratory care. St Louis, MO: Mosby Year Book; 1991.

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Burn nursing
Debra A. Benjamin, Mary Jaco, Eric Koch
Introduction
The care of the patient with a burn injury is most challenging
for the nurse. Care begins with the immediate resuscitation
of the patient in the emergency department and continues
until the patient is completely rehabilitated. During the
initial resuscitation, the role of the nurse is to assess and
monitor the patient’s hemodynamic alterations. Fluid resus­
citation and nursing management of fluid resuscitation are
adequately discussed earlier in this book. Therefore, this
chapter will cover other areas where the nurse’s care and
management are crucial.
Acute care
Nurses operate in an age of accountability where quality and
resource utilization drive healthcare. The public demands
and deserves the best possible outcome. Evidence-based
practice (EBP) integrates providers’ clinical expertise with the
best evidence. It helps nurses structure how to make accurate
and timely decisions. It improves the odds of doing the right
thing at the right time for the patient. Closing the gap
between research and practice affects all aspects of medical
care. Workplaces must support the use of EBP by creating
structures and processes, building the infrastructure to
support EBP.
Practicing nurses today need strong and effective clinical
leadership. In addition, in today’s settings, every nurse must
be a leader herself/himself, using knowledge and skills to
make decisions, and accepting accountability for competent
care and safe patient outcomes. Transformational leader­
ship is a method well suited to nursing in the clinical envi­
ronment. It repositions staff nurses from the bottom of the
organization pyramid to the center. Each nurse emerges as a
leader as the clinical situation demands. Power is not given
away, but rather partnerships develop between nurses at
the bedside, and management. Management becomes a
partner and resource as opposed to a controlling force. This
provides attractive work environments for professional
people recognizing the contributions of each individual
and giving value to the power necessary for each partner to
participate fully.
Pulmonary priorities
Inhalation injury continues to be the most serious and
life-threatening complication of burn injury today. Early
diagnosis and treatment greatly impact the outcome of care.
Impaired gas exchange is a potential problem for patients
who have face and neck burns and/or inhalation injury.
Inhalation injury may include carbon monoxide poisoning,
upper airway injury (heat injury above the glottis), lower
airway injury (chemical injury to lung parenchyma), and
restrictive defects (circumferential third-degree burn around
the chest). Upper airway edema causes respiratory distress
and is the primary concern during the initial 24–48 h post-
burn phase. Tracheobronchitis, atelectasis, bronchorrhea,
pneumonia, and adult respiratory distress syndrome (ARDS)
may occur during the acute, post-burn stage either related or
unrelated to inhalation injury.
Nursing care of a patient with inhalation injury begins
with a detailed history of the accident. Inhalation injury is
suspected when the accident occurred in a closed space.
Close observation of the patient and frequent respiratory
assessments are made throughout the initial and acute phase
post-burn. Initially, the patient is observed for hoarseness
and stridor, which indicate narrowed airways. Emergency
equipment is placed at the bedside to facilitate intubation if
necessary. Observing the frequency of cough, carbonaceous
sputum, and increased inability to handle secretions
may indicate possible inhalation injury and the potential
for impaired gas exchange. Other important observations
include respiratory rate, breath sounds, and the use of acces­
sory muscles to aid in respiratory effort, nasal flaring, sternal
retractions, increased anxiety, and complaint of shortness of
breath. Disorientation, obtundation, and coma may be due
to significant exposure to smoke toxins such as carbon mon­
oxide or cyanide. These conditions are managed emergently
with 100% oxygen.
Bronchoscopy may be done early to diagnose inhalation
injury as well as facilitate airway clearance. Humidified
oxygen should be readily available and applied to patients
who have evidence of impaired gas exchange (especially
pediatric patients). Aggressive nasotracheal suction may be
indicated if the patient has difficulty with managing secre­
tions either because of the increased amount of secretions
and/or the decreased effectiveness of the cough. In addition,
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00034-5
CHAPTER 34 
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develops over time. These skills must be taught by experi­
enced nurses to new burn nurses. Assessment of burn wound
takes place in the hydrotherapy area, operating room, and at
the bedside.
Wounds may consist of eschar, pseudoeschar, skin buds,
autograft, donor sites, hypermature granulating tissue, blis­
ters, and exposed bone and tendons. Besides the many kinds
of possible wounds, there are many topical antibacterial
agents available for managing wounds. These choices raise
many decisions for the team to address. Topical antimicro­
bial creams and ointments include mafenide acetate, silver
nitrate, silver sulfadiazine, petroleum and mineral oil-based
antibacterial products, and Mycostatin powder. Wounds may
be treated in the open fashion (topicals without dressings)
or closed fashion (topicals with dressings or soaks). There
are several techniques for applying dressings to different
areas of the body, that need to be able to withstand exercise,
ambulation, and moving around in bed. Biological dressings
such as homograft or heterograft may be used as temporary
wound coverage. Dressings may also be synthetic or biosyn­
thetic or silver impregnated. Selection is based on the present
condition of the wound and the expected outcome.
Secondary goals of wound care are to promote healing
and to maintain function of the affected body part. These
goals are accomplished by preventing wound infection,
treating wound infection, preventing graft loss and tissue
necrosis, providing personal hygiene, and maintaining
correct positioning and splinting throughout hospitaliza­
tion. To prevent burn wound infection, the burn nurse must:
cleanse the wound with soap and water; debride the wound
of loose necrotic tissue, crusts, dried blood, and exudate;
apply topicals or dressings and ensure dressing changes are
done/ordered. The nurse must inspect the wound for evi­
dence of infection: cellulitis, odor, increased wound exudate,
and/or changes in exudate; changes in wound appearance;
and increased pain in the wound. The physician should be
notified so that changes in wound care can be made. Cul­
tures and biopsies may be ordered to identify the type
and count of organisms and treat with a specific systemic
antibiotic, topical dressing, soak, or a combination of all
three treatments. The wound is often the source of blood­
stream sepsis. The five cardinal signs of sepsis are: hyperven­
tilation, thrombocytopenia, hyperglycemia, disorientation,
and hypothermia.6
Preventing graft loss is another wound care challenge for
nursing. Usually the patient returns from the operating room
in a position that is maintained for 3 or 4 days. Any interac­
tion with the patient during this time of graft immobiliza­
tion requires creativity and care in order to prevent shearing
of the graft. Postoperative dressings on the thighs and back
are protected with polymycin, fine-mesh gauze to prevent
soiling by feces and to minimize cleanup. The dressings are
continuously monitored for increased drainage and odor,
which would indicate possible wound infection. If infection
is suspected, then the postoperative dressings may be
removed early for a closer inspection of the wound.
Donor sites will also require additional care to prevent
infection. Of course, the care postoperatively depends on the
coverage of the donor site. If the donor site is covered with
fine-mesh gauze, the initial care is to ensure homeostasis and
adherence of the gauze to the wound. Therefore the post-op
pressure dressing remains intact for 6–12 h and is then
aggressive pulmonary toilet, including turning, coughing,
and deep breathing, up and out-of-bed rocking in mother’s
arms may be done regularly and frequently. Elevation of the
head of the bed, unless contraindicated, will also support
and possibly improve ventilation. Trends and changes
should be correlated with laboratory results and shared with
the team.
Another complication is circumferential third-degree
burns around the chest and neck, which often cause
restrictive defects. The increased amount of edema com­
bined with decreased chest excursion may greatly decrease
tidal volume. This condition may progress and can become
life-threatening, in which case chest escharotomy may be
necessary to release the constricting eschar. The procedure
may be done at the bedside or in the operating room. Equip­
ment includes sterile drapes, scalpel, and electrosurgical unit
(to control bleeding).
Intubation and mechanical ventilation may be required to
improve gas exchange. Tube placement should be checked
and documented frequently and verified daily by X-ray.
Securing the endotracheal tube requires a standard tech­
nique for stabilization and prevention of pressure necrosis.
Adequate humidity is necessary to prevent secretions from
drying and causing mucous plugging. Remember to provide
pre/post-suctioning hyperoxygenation. Sterile technique is
used when suctioning to prevent infection. Attention to the
details of oral hygiene will provide comfort for the patient
and may reduce the occurrence of ventilator-associated
pneumonia related to colonization in the oral pharynx.1
Criteria for extubation depend on why the tube was
inserted initially, but, overall, stable vital signs and hemody­
namic parameters will support the plan for extubation. The
patient should be awake and alert in order to protect the
airway; therefore, pain medications may be reduced before
extubation. Ventilatory measurements and blood gas analy­
sis should be within normal limits.
Immediately following extubation, the nurse must be alert
for signs and symptoms of respiratory distress, administer
suction as needed, monitor blood gas measurements, provide
optimal positioning for ventilation, as well as provide reas­
surance and support to decrease anxiety.
Age, burn size, and the presence of inhalation injury and
pneumonia have been identified as major contributors to
mortality.2 Thus, vigilant nursing care (frequent nursing
assessments, aggressive pulmonary toilet, etc.) combined
with anticipating potential problems and being prepared to
deal with the problems will add to the team effort and pos­
sibly improve the patient outcome.
Burn wound care
The primary goal for burn wound management is to close
the wound as soon as possible. Prompt surgical excisions
of the eschar and skin grafting have contributed to reduced
morbidity and mortality in severely burned patients.3–5
Wound care in the burn unit has become an art of burn
nursing practice. It can be extremely challenging and com­
plicated and, for a new nurse, it can be the most difficult and
misunderstood part of burn nursing. The complexity exists
because of the variety of wound types that require different
interventions in relation to time post-burn or time postop­
erative. Wound assessment and care is a learned skill that

Burn nursing
399
removed. The focus of managing the donor site is to keep
the wound dry. If grafts/donor sites are on the back or backs
of the legs, the patient is placed in a Clinitron bed for 4–5
days to promote drying. If the donor site remains wet, addi­
tional drying techniques (hair dryers, external heaters) may
be used periodically during the day.7
If the donor site is covered with a synthetic or biological
dressing, the same principles apply. Basically, apply a pres­
sure dressing to ensure adherence to the wound for a short
period of time postoperative and then expose to the air to
support drying of the wound. A bed cradle is used to keep
bed linen from contacting the wounds. The location of the
graft, donor site, and eschar may all be on the same extrem­
ity, which again requires creativity to accomplish all three
interventions of care.
Nurses must always be vigilant when it comes to skin
assessment; early detection and prevention is the key ingre­
dient in preventing pressure ulcers in major burn patients.
Pressure ulcers are no longer treated as a burn wound. There
is evidence to support nursing practices in the prevention of
pressure ulcers in burn patients. Burn patients have many
risk factors that predispose them to develop pressure ulcers.
Initially, hypovolemic shock with blood flow shunted away
from the skin to preserve vital organ function is a factor.
Additional injuries may increase the risk for pressure ulcers,
such as: inhalation injury, which may require intubation and
use of paralytic agents to manage the airway. Fluid resuscita­
tion may contribute to massive edema in both burned and
unburned areas. The edema is maximized at about 2–3 days
post-burn, which also decreases the blood flow to the skin
and adds weight to all parts of the body.
Maintaining systemic hydration can continue to be a
problem long after the patient has received adequate resus­
citation for burn shock. Continued fluid therapy to replace
fluid loss through the burn wound is essential. If systemic
hydration is not maintained, even normal skin may be at
risk. To complicate this situation, the quantity of fluid lost
through the burn wound may increase the moisture on
normal skin adjacent to the burn wound. This moisture may
cause the normal skin to break down and predispose the
skin to further compromise.
Surgical care
The perioperative setting combines a number of profession­
als with different levels of experience and expertise, all
directed towards patient care. Each team member has a spe­
cialized role: the surgeon provides surgical intervention; the
surgical technician supports the surgeon; the anesthesiolo­
gist or CRNA provides life support functions, and the circu­
lating nurse’s role is to provide safe patient care by ensuring
that all team members adhere to professional standards and
guidelines. The perioperative nurse is a professional regis­
tered nurse who provides nursing care to patients in the
preoperative, intraoperative and postoperative phases of
surgery. Perioperative burn nursing care can be described as
hot, intense and demanding. Burn nursing in fact, represents
one of the profession’s most challenging specialties.
Once surgery is completed, perioperative nurses provide
postoperative care and assessment. This phase of nursing
care can also be challenging for the nurse caring for the
patient during the immediate postoperative period. Nursing
care and plan for care depends on many factors: amount of
blood loss, surgical time and the site and extent of excision
and grafting. The post-anesthesia nurse caring for the burn
patient must be knowledgeable as to the medications and
procedures used during surgery, to provide appropriate safe
nursing care.
Many burn-injured patients will make repeated trips to the
operating room for surgical excision of the burn wound and
grafting, with graft taken from unburned areas. These pro­
cedures may require the patient to be anesthetized for long
periods of time. Patients are at risk for pressure ulcers in the
operating room; proper positioning and the use of pressure-
reducing devices is essential to reduce the risk of pressure
ulcer formation. During these operative procedures the
patient may lose large quantities of blood resulting in
decreased tissue perfusion and patient may develop shock.
Vasopressors, antibiotics, and fluid resuscitation are the
usual treatments for shock. The low-flow states and the use
of vasopressors may also result in decreased tissue perfusion
and increased risk of pressure ulcer formation.
Post-surgery, the patient is often immobilized with large
bulky dressings and splints to protect the graft. These dress­
ings need to be applied with enough pressure to stop the
bleeding from the grafted wound and the donor site. But if
the dressings are applied too tightly, or if edema develops
after dressing application, this may cause increased pressure
on the skin.
Throughout the acute phase of care the burn patient is
predisposed to pain and anxiety. Pain in the burn wound
and fear of pain causes patients to try not to move. Careful
titration of anxiolytics and narcotics can result in an alert
patient who is relatively pain free but this requires intense
attention to detail from the nursing staff.
To prevent wound bed desiccation, soaks are used to main­
tain moisture in the grafted wound and to aid in decreasing
wound colonization with bacteria. This moisture, when in
contact with adjacent normal skin, may increase the risk of
tissue breakdown.
Inadequate nutrition prior to or after the burn injury
is potentially a significant problem. The hypermetabolic
response in the burn-injured patient leads to protein malnu­
trition if caloric intake is compromised. To reduce the risks
of systemic infection and to promote wound healing, enteral
hyperalimentation is most frequently used and the patient
is fed by nasogastric or nasojejunal tubes.
In summary, burn patients are among the high-risk popu­
lations for pressure ulcer development. The physiology of
the burn injury combined with many of the therapies and
treatments used during hospitalization impacts the burn
patient’s risk for pressure ulcers.
All patients, except those with skin grafts postoperatively,
will benefit from a bath or shower. Large acute burns are
placed on a shower cart and the wounds are gently showered
with warm water. The overhead heater is on and the room
temperature is 85°F (29°C) or above. Large acute burns are
not immersed in a tub of water to prevent auto contamina­
tion and electrolyte imbalance.8 Hydrotherapy can be used
for careful assessment of the wounds, as well as personal
hygiene such as shampoo, mouth care, face care, and peri­
neal care.
Hydrotherapy is an excellent opportunity for patient and
family teaching about wound care and dressing application.

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400
As the patient gets closer to discharge, families are required
to do more of the care. The trend for earlier release from the
hospital poses additional challenges for nursing, since it
reduces the time available to prepare the patient for dis­
charge. The better the patient and families are educated, the
better the outcome will be. Early involvement with patient
and family helps identify potential obstacles at discharge
and facilitates care coordination in the discharge process.
Metabolic and nutritional support
Hypermetabolism, or metabolic stress, is the direct response
to a burn injury. The amount of stress increases proportion­
ally to the extent of the injury and strongly influences a
patient’s nutritional requirements. This response can magnify
the normal metabolic rate by 200%. Malnutrition, starva­
tion, and delayed wound healing will result if calories are
not provided consistently to meet nutritional requirements.
Children require more calorie and protein replacement than
adults, because they have additional nutritional demands to
support growth and development.
Monitoring output and managing nutritional intake are
among nursing’s primary responsibilities. An accurate record
of intake and output is critical to patient care because poten­
tial problems can be detected early and alternate options of
care can be individualized to help the patient achieve his/
her goals. Accurate weights, daily or as ordered, are also
important. Remember to record whether dressings, splints,
or linens are included in the weight. Obviously, including
additional elements does not reflect an accurate weight, but
trends in weight either up or down may be identified and
may be helpful in the overall management of the patient.
Typically, when patients cannot consume enough calories
by mouth, then enteral feedings are begun. Sometimes
enteral feedings are started before the patient is given the
option of eating because the amount of calories is so great
and/or the condition of the patient is unstable. Parenteral
nutrition is used when enteral fails. The goal is to provide
adequate nutrients, calories, and protein. A nasogastric tube
is inserted initially and used to decompress the stomach
until bowel sounds return. Then tube feedings are started at
a very low volume per hour to act as a buffer against ulcer
formation. The nasogastric tube allows for checking hourly
gastric residuals, gastric pH, and guaiac. If the gastric pH falls
below 5, or if the guaiac is positive, Maalox and Amphojel
are given every 2 h, alternately every hour.
Aspiration of stomach contents is a potential complication
and always a concern. Gastric residuals are checked before
suctioning to prevent the patient from vomiting and possi­
bly causing aspiration. Another precaution is to keep the
head of the bed elevated. A Dobhoff tube is also inserted
initially, and feedings are begun as soon as 6 h post-burn.
The rate starts slow and is advanced as tolerated to meet the
calculated amount of nutritional replacement. Tube feedings
continue until the patient can take the required amount of
calories by mouth.
Another potential problem with both tubes is dislocation;
therefore, it is important to check placement periodically
throughout the day. When gastric residuals start climbing, it
may be because the Dobhoff tube has slipped into the
stomach or the patient is septic. Tube feedings may become
contaminated and become a source of infection for the
patient leading to significant morbidity. Routine procedures
should be established to prevent this occurrence and care
should include sterilization of the blender and limiting to
4 h the amount of time that tube feedings can be hung at
the bedside. The tubing and container should be changed
every 4 h.
Sometimes when patients are encouraged to begin taking
food by mouth, it will help to stop the tube feedings during
the day and feed only at night. Not scheduling painful activi­
ties around meal-time and providing frequent mouth care
will also contribute to improved oral intake.
Regular bowel patterns are expected in the post-burn
period. Patients are given many medications during hospi­
talization that may contribute to either diarrhea or consti­
pation. Patients are expected to have at least one bowel
movement per day. If not, then a bowel evacuation regimen
should be initiated. If diarrhea is the problem and the
volume exceeds 1500°mL/day, then bulking agents and/or
antidiarrhea medication may be useful to promote routine
bowel elimination.
The importance of monitoring and documenting the many
parameters of intake and output cannot be overemphasized.
Established clinical protocols and guidelines facilitate the
implementation and evaluation of the nutritional program.
Other strategies to support the hypermetabolic phenom­
enon of the burn patient are to keep the room temperature
above 85°F (29°C) and to keep the room door closed to
prevent drafts. Also frequent rest periods must be provided
during the day. Nursing generally makes the schedule of
activities for the day, so including frequent rest periods is
just as important as anything else that needs to be done
during the day. Adequate sleep during the night is also very
important: it often this that makes the difference between a
good day and a bad day. A quiet comfortable environment
without sensory overload (lights and noise) is essential for
the patient to sleep.
Nurses are the grand communicators of progress and/or
problems. Nurses work closely with dietitians, physicians,
patients, and families to ensure that optimal metabolic and
nutritional support is achieved during the post-burn period.
Pain and anxiety assessment and management
The expected outcome for pain and anxiety management is
for the patient to achieve a balance between successful par­
ticipation in activities of daily living and therapies and being
comfortable enough to rest and sleep as needed. The ulti­
mate goal is for the patient to be satisfied with the pain
management plan as it is implemented. Assessment of pain
and anxiety provides a baseline for evaluation of pain and
anxiety relief measures. Pain and anxiety scales are essential
to quantify painful episodes and to evaluate effectiveness of
medication. Knowing when and how much to intervene is
guided by knowing the baseline pain and anxiety rating for
the individual. Patients and families should be given infor­
mation upon admission on how to use the assessment scales
and to identify an acceptable level of pain and anxiety.
Intravenous administration of opioids and anxiolytic
agents is essential to manage pain and anxiety during the
initial stage of injury due to the altered absorption and cir­
culation volume following a major burn injury. A PCA
(patient-controlled analgesia) pump is useful on children

Burn nursing
401
older than 5 years of age and adults. It is important to
manage background pain as well as procedural pain for
which medication should be given 15–30 min prior to a
painful procedure. Constipation is frequently a complica­
tion of pain management; thus, a bowel management
program should be instituted at the same time. Relaxation,
guided imagery, music therapy, hypnosis, and therapeutic
touch are adjunct techniques to complement analgesia and
reduce anxiety.9 Emotional support and patient and family
education decrease fear and anxiety, thereby enhancing the
pain management plan.10
Patient/family education
In order for nurses to be competent teachers, they must be
competent practitioners with solid theoretical foundations.
Continuing education to maintain competency is key for
clinical staff because of their role as educators of patients
and families. Reinforcement of the educational process
(assess, plan, implement, evaluate, and document), charac­
teristics of patient population, updates on educational strat­
egies, age-appropriate interventions, and ways to evaluate
learning are topics that will sharpen educator competency.
Discharge planning and education begins upon admis­
sion. It begins with a thorough assessment of the patient’s
life prior to the injury. Identifying knowledge deficits and
barriers to education, prioritizing strategies for education,
providing supplemental educational handouts and/or classes
as well as developing a plan for evaluating the effectiveness
of the teaching opportunity are integral parts of the educa­
tional process.
Assessment provides essential information for planning an
educational program to meet the specific individual needs
of each patient and family. It is also done periodically during
different stages of the educational process to determine if the
plan remains valid or changes need to be made.
The assessment findings become part of the educational
plan, in that the plan is tailored to meet the needs and con­
cerns of the patient and family. The plan includes the learn­
ing objectives, the strategies for education, and the learning
materials. All of these parts of the educational goal are agreed
upon by the patient/family and the educator.
Implementation of the plan is the next step, followed by
a thorough evaluation of the effectiveness of learning and/
or determination of whether the education goal is being
accomplished. Alterations in the original plan may be
needed any time during the educational process depending
on unforeseen situations or changes in conditions that were
not anticipated.
The benefits are many. This process ensures communica­
tion of educational topics among the team members, pro­
vides a historical account of education, and documents
progress and/or changes in the plan. It benefits the patient
and family by making them competent in their role as care
provider when discharged from the hospital. Knowledge
allays anxiety about the unknown and aids in compliance
with recommended care after discharge, improving the
long-term outcomes.11 Patients and families can be empow­
ered to become active participants in the burn care team
early in the post-burn course through a well-structured edu­
cational plan.
Rehabilitation of the burn-injured patient
A major burn is one of the most devastating injuries, both
physically and emotionally, known to man. After weeks of
being an invalid, undergoing repeated surgeries, fighting
infection, having the body ravaged by the metabolic conse­
quences of injury, and enduring pain and anxiety, the patient
now faces months of continued physical therapy to regain
the level of function that they had known before the injury.
Most patients who have sustained a major burn will con­
tinue to have a higher than normal metabolic rate for over
a year and thus find that they do not have the stamina to
easily regain their lifestyle.12 In addition to the catabolic
effects of burn injury, being hospitalized and in bed with
minimal activity for many weeks or months causes bone
weakening and loss of muscle. Children are more prone to
fractures.13 Although these patients must continue to exercise
to prevent contractures, they may not have the physical
strength or endurance necessary to actively participate in
such programs. Likewise, these patients frequently become
depressed; as they face an altered self-image and a forced
physical dependence on others. They fear that they will never
look normal and that they will not be able to return to a
normal life. For the adult, the concerns of whether they will
be able to return to work or have to change their occupation
is also a factor. What is the role of the nurse at this phase of
treatment? Although nurses have been very involved in the
care of the patient in the early phases of care, many nurses
do not see a role for themselves at this stage. The transition
from the hospital to home care is often difficult for both the
patient and family. It is important prior to discharge that the
patient and family be educated in the care of wounds and
healed skin before they leave the hospital. They also need
information about the normal depression that occurs post-
hospitalization and resources in their home community to
which they have access. This is where the nurse case manager
becomes an integral part of the patient care team. Nurse case
managers who are hospital based can begin to work with the
patient and family soon after admission to assess the patient’s
future needs and coordinate these with outside agencies
to ensure that the transition goes smoothly. Often, case
managers from workmen’s compensation carriers or health
maintenance organizations (HMOs) are involved during the
early phase as well. Coordination of activities between case
managers is important to provide seamless care. With chil­
dren, it is important for the nurse case manager to begin
working with the school nurse or community health nurses
to provide for this seamless transition in care.
Although the rehabilitation therapist plays an important
role in providing referrals to community therapists and psy­
chologists, and social workers frequently make referrals to
community mental health providers, the nurse case manager
should be involved in the overall coordination of these and
other services to foster a unified approach. The free flow of
communication between all providers is necessary for
optimal rehabilitation of the patient.
Work-hardening programs for adults
Work-hardening programs have been shown in adults to
more rapidly return the patient to their optimum level of
functioning.14

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402
These programs may be available through community
rehabilitation facilities, vocational rehabilitation agencies,
HMOs hospitals or health centers with cardiac rehabilitation
programs or through workmen’s compensation carriers. The
major concern for the nurse case manager and the burn team
is which patients need these programs and at what point
the patient will benefit the most from such intensive
programs.
Assessment
Burn patients, like those recovering from coronary heart
disease and surgery, find themselves deconditioned. Even
3 weeks of bedrest in a healthy subject can result in a 25%
decrease in maximal oxygen consumption. Thus, burn
patients who are hospitalized for 2 or more weeks may need
to be considered for such programs. Burn patients should be
first assessed for risk factors associated with coronary heart
disease. Such risk factors include:
•
age and sex
•
elevated blood lipids
•
hypertension
•
cigarette smoking
•
physical inactivity
•
obesity
•
diabetes mellitus
•
diet
•
heredity
•
personality and behavior patterns
•
high uric acid levels
•
pulmonary function abnormalities
•
ethnic race
•
electrocardiographic abnormalities during rest and
exercise
•
tension and stress.
Cardiac stress testing is usually recommended prior to
beginning an exercise program. If the patient has several risk
factors, the exercise program can be tailored to fit the patient’s
needs.15
Planning
What is available? Often the major issue is what is available
and who will pay for this care. When an adult is injured on
the job, this is often arranged and paid for by the compensa­
tion carrier, since they have a vested interest in returning the
patient to work as soon as possible.
Implementation
Once the details are worked out the next hurdle is to get
buy-in from the patient and family. Some programs require
the patient to be in a facility some distance from their home;
this may present issues for both the patient and family.
Similarly, if the program is in the local community, daily
visits to the rehabilitation facility may pose transportation
issues, especially if the patient is unable to transport him or
herself. These details can usually be worked out with coop­
eration of all caregivers and the family involved. Motivation
and determination are often the most difficult factors to
overcome. This is especially true if the patient is suffering
from depression. The nurse case manager can be very
instrumental in rallying the burn team and caregivers in the
community to help the patient and family to see this as a
way to return the patient to more normal function.
Evaluation
Success in such programs requires that all involved have the
same goals and that these goals result in measurable out­
comes. The goal of such programs is not only to increase the
patient’s tolerance to exercise but also to improve their psy­
chological and social functioning and to return the patient
to work or to the same level of functioning pre-injury.
Extensive exercise in children
Children may suffer from the same deconditioning as adults,
especially if they have suffered 40% or greater burns. Cucuzzo
et al. have shown that children with greater than 40% burns
have bone demineralization.16 Treatment of these patients
with long-term anabolic steroids and intensive exercise pro­
grams can return the patient’s metabolic status and bone
re-mineralization to normal much sooner.
Assessment
Children seem to do better if they are at least 6 years old
when they begin the exercise program. The best time to start
such a program is approximately 6–9 months post-burn.
With most patients this is after they have had 2–3 months
away from the hospital after discharge from their initial
injury. Like adults, individualized programs considering
their current general state of health are necessary. When
children enter these intensive exercise programs it is impor­
tant for the parent or a responsible adult member of the
family to be involved. This may be a significant factor in
when the patient is able to start such a program. Similar
results can be obtained in younger children through active
play and exercise accompanied by music therapy. The use of
activities set to music can increase stamina and actively
stretch scar tissue and increase joint mobility.
Planning
Although cardiac rehabilitation programs and the like may
be readily available in most major towns and cities in this
country, often they do not take children. Children’s hospitals
often have rehabilitation units or outpatient programs for
children that can offer similar programs to the adult cardiac
programs. Children’s hospitals are usually found in major
cities; thus, these programs may not be as accessible as pro­
grams for adults. In some communities, school-age children
may be able to obtain help within the school sport pro­
grams, especially if they have qualified athletic trainers. Chil­
dren aged 4–6 may have more difficulty finding programs
outside of children’s hospitals. Some early childhood inter­
vention and pre-kindergarten programs may be available for
younger children.
Another question is who pays for this care? Unlike the
adult with insurance or workman’s compensation insurance,
children are often without funding for this rehabilitative
care. State programs for children with special needs (e.g.
Title V programs) are one avenue to explore. Other sources
of funding may come from private or public charities,

Burn nursing
403
school-mandated programs, or vocational rehabilitation
programs for the older teenager.
Implementation
Motivating the child and parent can be a major task. Often
the parent and child have spent weeks or months during the
acute phase of care away from home. If there are other chil­
dren in the home or if the parent normally works outside
the home, the parent may not feel that he/she can be away
from home an additional 2–3 months. The child may also
not want to leave the safety of the home environment. Thus
motivating the child and parent is often difficult. Helping
the parent see this as a valuable program will require the
whole burn team to work together with the patient and
family.
Evaluation
The outcome of these programs for the child can be meas­
ured in increased exercise tolerance and improved psycho­
logical and social adjustment. A major function of these
programs is to convince the child and parent that the patient
is a normal child and can succeed mentally and physically.
If the child returns home and can keep up with his/her peers,
this alone improves the child’s self-esteem.
Reconstructive care
Assessment
The role of the nurse in the reconstructive surgery phase is
to be an advocate for the patient and family. Education of
the patient and family throughout the course of burn care is
also an important nursing function. Many people have unre­
alistic expectations for reconstructive surgery. The nurse’s
role in the outpatient clinic or physician’s office is to listen
to the patient and family and to understand their hopes and
expectations. Often when the surgeon discusses what should
or could be done to improve the patient’s appearance or
function, the patient and family member are reticent to ask
questions or to describe what they want. Patients’ priorities
are often different from the surgeons and this leads to dis­
satisfaction. Most surgeons prefer to wait until the scar has
matured to begin reconstructive surgery. Occasionally, if the
scar tissue is interfering with function, correction of the scar
will be attempted. This is especially true in children where
scar tissue may cause bone deformity if left until it has
matured. In children, some reconstructive procedures are
best postponed until the child has matured. Usually, surgery
is best accepted by the child at the beginning of high school
or just prior to starting further education. Although it is dif­
ficult to continue to be supportive of the patient and family
during the scar maturation process, the nurse’s role is one of
education, support, and encouraging the patient to continue
with exercise, splints, and pressure garments, if ordered.
Planning
Once again, the nurse case manager can be instrumental in
helping the family find the funding and resources to provide
reconstructive surgery for the patient. If the patient is working
or in school, planning the procedures should accommodate
the patient’s school or work schedule as much as possible.
For children, funding through Services for Children with
Special Needs may be available. Working with insurance
companies and HMOs can be tricky if the surgery is pre­
sented as cosmetic rather than corrective surgery.
Implementation
Preparing the patient for surgery is the responsibility of the
nurse and physician. Providing the patient with realistic
expectations is often difficult. Many times, immediately
after the surgery, the area will look worse and the patient
may feel dissatisfied and depressed. Preoperative prepara­
tion of the patient and family may allay some of these
issues. Surgery, itself, is frightening enough for the patient
and family. In children, this can be especially frightening
because it may bring up memories of their original burn
treatment and the pain associated with this treatment. Post­
operatively, the nurse’s role is to teach the patient and
family how to care for the wound to prevent infection and
further scarring.
Evaluation
Whose body is it anyway! A line from a famous play actually
sums up the evaluative process for reconstructive surgery. As
professionals, we may see great improvement in the patient’s
condition after surgery. But if the patient is not satisfied with
his or her appearance, little has been gained by the surgery.
This is the reason that the patient and family must have
realistic expectations prior to surgery.
Further reading
Baxter CR. Fluid volume and electrolyte changes in the early
post-burn period. Clin Plast Surg. 1974;1(4):693-703.
Carleton SC, Tomassoni AJ, Alexander JK. The cardiovascular effects of
environmental trauma. Cardiol Clin. 1997;13(2):257-262.
Demling RH. Fluid replacement in burned patients. Surg Clin North
Am. 1987;67(1):15-30.
Demling RH. Pathophysiologic changes after cutaneous burns
and approaches to initial resuscitation. In: Martyn JA, ed. Acute
management of the burn patient. Philadelphia: WB Saunders;
1990.
Gordon MD, Gottschlich M, Helvig EL, et al. Review of evidence-
based practice for the prevention of pressure sores in burn
patients. J Burn Care Rehabil. 2004;25:388-410.
 
Access the complete reference list online at

Burn nursing
403.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Hixon S, Sole M, Kir T. Nursing strategies to prevent ventilator
associated pneumonia. AACN Clinical Issues. 1998;9(1):1-15.
2. Shirani KZ, Pruitt BA Jr, Mason AD. The influence of inhalation
injury and pneumonia on burn mortality. Ann Surg. 1987;205:
82-87.
3. Tompkins RG, Burke JF, Schoenfield DA, et al. Prompt eschar
excision: a treatment system contributing to reduced burn
mortality. Ann Surg. 1986;204:272-281.
4. Herndon DN, Gore D, Cole M, et al. Determinants of mortality
in pediatric patients with greater than 70% full thickness total
body surface areas of thermal injury treated by early total excision
and grafting. J Trauma. 1987;27:208-212.
5. Tompkins RG, Remensnyder JP, Burke JF, et al. Significant
reductions in mortality for children with burn injuries through
the use of prompt eschar excision. Ann Surg. 1988;208:577-585.
6. Ramzy PI. Infections in burns. In: Wolf SE, Herndon DN, eds.
Burn care. Austin, TX: Landes Bioscience; 1999:73-80.
7. Dziewulski P, Barret J. Assessment, operative planning and surgery
for burn wound closure. In: Wolf SE, Herndon DN, eds. Burn care.
Austin, TX: Landes Bioscience; 1999:19-51.
8. Carrougher G, Gretchen G. Burn wound assessment and topical
treatment. In: Carrougher G, ed. Burn care and therapy. St Louis:
Mosby; 1998:133-165.
9. Patterson DR. Non-opioid based approaches to burn pain. J Burn
Care Rehabil. 1995;16:372-376.
10. Marvin JN. Pain assessment versus measurement. J Burn Care
Rehabil. 1995;16:348-357.
11. Falvo DR, Donna R. Effective patient education. Gaithersburg, MD:
Aspen; 1994.
12. Hart DW, Herndon DN, Klein G, et al. Attenuation of
posttraumatic muscle catabolism and osteopenia by long-term
growth hormone. Ann Surg. 2001;233:827-834.
13. Klein GL. Bone loss in children following severe burns: increase
risk for fractures in osteoporosis. Osteoporosis Update 1999.
Xian, PR, China: Proceedings of the Third International Congress
on Osteoporosis; 1999:63-68.
14. Zeller J, Strum G, Cruse C. Patients with burns are successful in
work hardening programs. J Burn Care Rehabil. 1993;14:189-196.
15. Adams RB, Tribble GC, Tafel AC, et al. Cardiovascular
rehabilitation of patients with burns. J Burn Care Rehabil.
1990;11:246-255.
16. Cucuzzo N, Ferrando A, Herndon D. The effects of exercise
programming vs traditional outpatient therapy in the
rehabilitation of severely burned children. J Burn Care Rehabil.
2001;22:214-220.

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Special considerations of age:
the pediatric burned patient
Jong O. Lee, William B. Norbury, David N. Herndon
Introduction
The incidence of burn injuries has declined steadily over the
past two decades. Approximately 1.25 million people are
burned in the United States every year, of which one-third
are children;1 60 000–80 000 patients sustain severe enough
burns to require hospital admission;2 30 000 children
require hospital admission for treatment of their burn inju­
ries.1 About 4000 burn patients die each year,2 and approxi­
mately 1000 of them are children.3
House fires injure or kill over 10 000 people per year.
House fires are among the leading causes of burn-related
deaths in children. Children between 0 and 5 years of age
are at a greater risk, as a disproportionate number of fire
deaths occur in homes. Deaths among preschool children
are at a rate of more that twice the national average (29.6
deaths/million children), or an average of 20% of the total
percentage of all home fire deaths.
Scalds are common in children less than 3 years old. Scald
injuries may be due to household accidents or deliberate
abuse. These may include spilling hot coffee or water, chil­
dren reaching up to countertops, pulling pot handles or
cords attached to cooking appliances and spilling the con­
tents onto themselves, unknowingly putting body parts
under a hot water faucet or climbing into a hot tub, and
intentionally or unintentionally being placed into or brought
in contact with a hot substance by another individual.
Improvements have been made in the reduction of mor­
bidity and mortality related to burns over the past few
decades. Advances in fluid resuscitation, early surgical exci­
sion and grafting of the burn wound, infection control, treat­
ment of inhalation injury, nutritional support, and support
of hypermetabolic response to burns have contributed to a
50% decline in burn-related deaths and hospital admissions
in the United States.2 This overall improvement in mortality
is most perceptible in children. In 1949, Bull and Fisher
reported the expected 50% mortality rate for 49% total body
surface area (TBSA) burn in children aged 0–14.4 This has
improved to 50% expected mortality in 98% TBSA burn in
the same population group.5
In a review of 103 children with >80% TBSA burns over a
15-year period, it was found that 69 patients survived, with
an overall mortality of 33%. Mortality was greatest in
children under 2 years of age and in burns >95% TBSA
(Figs 35.1 and 35.2).6 Another major predictor of mortality
was the length of delay to intravenous (IV) access (Fig. 35.3).
Patients that received resuscitation fluids within the first
hour had a significantly higher chance of survival.6 The mor­
tality rate also increased significantly with inhalation injury,
sepsis and multiorgan failure. In no pediatric patient, no
matter how large the burn, how young, or with what type of
inhalation injury, could it be accurately predicted at the time
of admission whether they would live or die.6
The burn injury produces overwhelming physiological and
psychological challenges to a child. The unique anatomical
and physiological attributes of the child require the attention
of physicians who are trained not only in burn care but also
in the specifics of pediatric care. The most obvious differ­
ences between adults and children are size and body propor­
tions. Shorter lengths, tighter angles, and smaller diameters
of various anatomical structures and spaces make certain
manipulations more difficult. These differences require the
provision of special equipment and supplies, which reflect
the configurations of pediatric anatomy. In addition to ana­
tomical differences there are also many physiological differ­
ences between children and adults, which must be considered
and will be discussed concerning the treatment of the pedi­
atric burn patient.
Initial evaluation
A patient must be immediately removed from the source of
burn, and clothing and jewelry removed immediately as
these items can prolong the burning process. Pouring cool
water onto the burn can cause hypothermia in large burns
and should be avoided. After the burning process is stopped,
the patient should be kept warm by covering with a sterile
(if available) or clean sheet or blanket. If the burn is chemi­
cal, the patient should be removed from the chemical imme­
diately and the burn wound should be irrigated with copious
amount of water for at least 30 minutes. If chemical is
powder, it should be brushed off first prior to irrigation.
Burn patients should be treated as a trauma patient and
any potential life-threatening injuries should be identified
and treated. The airway should be assessed first. Oxygen
100% should be administered and oxygen saturation moni­
tored using pulse oximetry. If inhalation injury is suspected,
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00035-7
CHAPTER 35 
Access the complete reference list online at

Total Burn Care
35
406
a long transfer to a burn center. A radial arterial line may not
be reliable in pediatric patients with extremity burns and
may be difficult to secure. A femoral arterial line may be
more reliable and easier to secure.
A bladder drainage catheter is placed to monitor urine
output as a measure of successful resuscitation. A nasogastric
tube is placed in all patients with major burns, as they can
develop gastric distension or ileus.
Persistent tachycardia should alert a clinician to a missed
injury or under-resuscitation. Accurate and rapid determina­
tion of burn size and depth is vital to the proper manage­
ment of burn injury.
Resuscitation
There is a systemic capillary leak after a large burn, which
increases with burn size. Capillary usually regains compe­
tence 18–24 hours after burn injury. IV access should be
established immediately for the administration of resuscita­
tive fluid. Increased delays to commencement of resuscita­
tion of burned patients result in worse outcomes and should
be avoided.6 Therefore it is crucial that IV access be obtained
as early as possible, even though such access may be difficult
to obtain. Owing to the small circulating volume in children,
delays in resuscitation for periods as short as 30 minutes can
result in profound shock. Peripheral IV access is preferred,
and it may go through burned skin if necessary. IV access
should be well secured. When peripheral IV is not available
because of severe extremity burns, a central venous line may
be placed. Children with large burns should have two large-
bore IV lines for fluid administration. The presence of
two IV lines also provides a safety margin if one infiltrates,
to allow continued resuscitation while another line is
re-established. Either internal jugular, subclavian or femoral
lines can be obtained, but femoral venous access may be
easier to obtain in edematous patients.
arterial blood gas and carboxyhemoglobin levels should be
obtained, as pulse oximetry readings will be falsely normal
in patients with elevated carboxyhemoglobin levels, as
carboxyhemoglobin is read as oxyhemoglobin by the pulse
oximeter.
Tachypnea, stridor, and hoarseness indicate an impending
airway problem due to inhalation injury or edema, and
immediate intubation should be considered. A full-thickness
circumferential chest burn can interfere with ventilation.
Chest expansion should be observed to ensure adequate air
movement. If the patient is on a ventilator, airway pressure
and PCO2 should be monitored. If ventilation is compro­
mised, escharotomy of the chest should be performed to
improve ventilation.
A blood pressure measurement may be difficult in patients
with burned extremities. These patients may need an arterial
line to monitor their blood pressure, especially if they require
Figure 35.1  Mortality in burns >80% total body surface area for various
ages.
Mortality (%)
70
60
50
40
30
20
10
0
0–2
11–18
3–10
Age (years)
Figure 35.2  Mortality for increasing burn size.
Mortality (%)
70
80
60
50
40
30
20
10
0
80–85
86–90
91–95
96–100
Surface area burn (% of total BSA)
Figure 35.3  Time to intravenous access in survivors and non-survivors.
Mortality increases with delays in starting an intravenous line and instituting
volume resuscitation.
Percent receiving intravenous access
80
100
60
40
20
0
0–1
1–4
>4
Time to intravenous access (hours)
Survivors
Non-survivors

Special considerations of age: the pediatric burned patient
407
When vascular access is unobtainable the intraosseous
route is a viable option. Fluid volumes in excess of 100 mL/h
can be administered directly into the bone marrow.7
Intramedullary access can be utilized in the proximal tibia
until IV access is accomplished. A 16–18 gauge bone marrow
aspiration needle, spinal needle, or commercially available
intraosseous needle can be used to cannulate the bone
marrow compartment. Although previously advocated only
for children younger than 3 years of age, intraosseous fluid
administration can be safely performed in all pediatric age
groups.8 The anterior tibial plateau, medial malleolus, ante­
rior iliac crest, and distal femur are preferred sites for intra­
osseous infusion. The needle should be introduced into the
bone, avoiding the epiphysis, either perpendicular to the
bone or at a 60° angle, with the bevel facing the greater
length of bone (Fig. 35.4). The needle has been properly
inserted when bone marrow can be freely aspirated. The
needle should be well secured to prevent inadvertent removal.
Fluid should be allowed to infuse by gravity drip. The use of
pumps should be discouraged in case the needle is dislodged
from the marrow compartment.
Fluid losses are proportionally greater in children owing
to their small body weight to body surface area ratio. Normal
blood volume in children is approximately 80 mL/kg body
weight and in neonates 85–90 mL/kg, compared to an adult
whose normal blood volume is 70 mL/kg. Evaporative water
losses in a 20% TBSA burn in a 10 kg child are 475 mL or
59% of the circulating volume, whereas the same size burn
in a 70 kg adult causes the loss of 1100 mL or only 22% of
blood volume. The commonly used ‘rule of nines’, useful in
adults and adequate in adolescents, does not accurately
reflect the burned body surface area of children under 15
years of age (Fig. 35.5). The standard relationships between
Figure 35.4  Intraosseous line placement in the proximal tibia (a) and distal
femur (b). (Redrawn with permission from Fleisher G, Ludwig S, eds. Textbook of pediatric
emergency medicine, 2nd ed. Baltimore: Williams & Wilkins; 1988: 268.)
A
B
Figure 35.5  The ‘rule of nines’ altered for the anthropomorphic differences of infancy and childhood.
19%
15%
13%
17%
17%
18%
18%
18%
18%
10%
32%
15%
15%
9½%
9½%
9½%
32%
9½%
9½%
32%
9½%
36%
9%
9%
1–4
5–9
10–14
Adult
(Rule of nines)

Total Burn Care
35
408
appropriate electrolyte and fluid management. Children of
under 1 year of age may require more sodium supplementa­
tion because of higher urinary sodium losses. Potassium
losses are usually replaced with oral potassium phosphate
rather than potassium chloride, as hypophosphatemia is fre­
quent in this population.10 Calcium and magnesium losses
also must be supplemented.
Intravenous resuscitation fluid should be isotonic and
replace lost electrolytes. Lactated Ringer’s is the most com­
monly used resuscitation solution for the first 24 hours post
burn. Children less than 1 year of age should also receive a
separate maintenance fluid containing dextrose solution in
addition to resuscitation fluid to prevent hypoglycemia as
their glycogen stores are limited.
Assessment of resuscitation
The routine clinical signs of hypovolemia in adult burn
patients, such as low blood pressure and decreased urine
output, are late manifestations of shock in the pediatric
patient, and tachycardia is omnipresent. Children have
remarkable cardiopulmonary reserve, often not showing
clinical signs of hypovolemia until more than 25% of the
circulating volume has been lost and complete cardio­
vascular decompensation is imminent. Pulse pressure,
mental status, distal extremity color, and capillary refill
reflect volume status. Capillary refill is a good indicator of
volume status in pediatric burn patients. Decreased capillary
refill should warn a clinician of imminent cardiovascular
collapse. Measurement of arterial blood pH with base deficit
or lactic acid is of particular importance in this age group,
reflecting decreased tissue perfusion. Improvement in base
deficit or lactic acid shows successful resuscitation.
Children frequently develop a reflex tachycardia after
even the most trivial injury due to an overexuberant
body surface area and weight in adults do not hold true in
children, as infants possess a larger cranial surface area and
a smaller area in the extremities than adults. Most routinely
used resuscitation formulas were developed using adult
patients and are almost exclusively weight-based. Since the
linear relationship between weight and body surface area
does not exist in children, use of these formulas in children
results in under- or over-resuscitation (Table 35.1).
Pediatric burn patients should therefore be resuscitated
using formulas based on body surface area, which can be
calculated from height and weight using a standard nomo­
gram (Fig. 35.6) or formulas (Table 35.2). The most com­
monly used resuscitation formula in pediatric patients calls
for the administration of 5000 mL/m2 TBSA burned plus
2000 mL/m2 TBSA for maintenance fluid given over the first
24 hours after burn, with half the volume administered
during the initial 8 hours and the second half given over the
following 16 hours.9 The subsequent 24 hours, and for the
rest of the time their burn wound is open, require 3750 mL/
m2 TBSA burned or remaining open area plus 1500 mL/m2
TBSA for maintenance requirements. The fluid requirement
decreases as a patient achieves more wound coverage and
healing. As in the adult patient, resuscitation formulas offer
a guide for the amount of fluid necessary for replacing lost
volume in children, and the amount of fluid should be
titrated according to the patient’s response.
Hyponatremia is a frequently observed complication
in pediatric patients after the first 48 hours post burn. Fre­
quent monitoring of serum sodium is necessary to guide
Table 35.2  Formulas for calculating body surface area (bsa)
Dubois formula
BSA (m2) = ht (cm)0.725 × wt (kg)0.425 × 0.007184
Jacobson formula
BSA (m2) = [ht (cm) + wt (kg) − 60]/100
Table 35.1  Resuscitation by the Parkland formula only compared to maintenance fluid requirements alone
Calculated needs
Replacement burn loss
Example
% Burn
Resuscitation*
Maintenance†
mL
mL/kg/%
1 year old
15
600
800
−200
−1.33
10 kg
30
1 200
800
400
1.33
0.48 m2 BSA
60
2 400
800
1 600
2.67
90
3 600
800
2 800
3.11
4 years old
15
990
1 200
−210
−0.85
16.5 kg
30
1 980
1 200
780
1.58
0.68 m2 BSA
60
3 900
1 200
2 760
2.79
90
5 940
1 200
4 940
3.33
12 years old
15
2 400
2 250
1 150
1.92
40 kg
30
4 800
2 550
2 550
2.12
1.13 m2 BSA
60
9 600
2 250
7 350
3.06
90
14 400
2 250
12 150
3.38
*4 mL/kg/% burn.
†2000 mL/m2 BSA.

Special considerations of age: the pediatric burned patient
409
Figure 35.6  Standard nomogram for the
determination of body surface area based on
height and weight. The example depicted is for a
child of 100 cm in height and 23 kg in weight.
(Reprinted with permission from Eichelberger MR, ed.
Pediatric trauma: prevention, acute care and rehabilitation.
St Louis: Mosby Year Book; 1993: 572.)
240
220
200
190
180
170
160
150
140
130
120
110
100
90
80
70
60
50
40
30
90
2.0
180
160
140
130
120
110
100
90
80
70
60
50
45
40
35
30
25
20
18
16
14
12
10
9
8
7
6
5
4
3
1.9
1.8
1.7
1.6
1.5
1.4
1.3
1.2
1.1
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
80
70
50
60
40
30
20
15
10
9
8
7
6
5
4
3
Weight
in pounds
Surface area
in square
meters
2
0.10
0.15
0.20
0.25
0.30
0.35
0.40
0.45
0.50
0.55
0.60
0.70
0.80
0.90
1.00
1.10
1.20
1.30
13
14
15
16
17
18
19
20
22
24
26
28
30
35
40
50
60
70
45
55
65
75
85
80
90
15
10
9.0
8.0
7.0
6.0
5.0
4.0
3.0
2.5
2.0
1.5
1.0
25
20
30
40
50
60
70
80
cm
in
m2
lb
kg
Height
For children of
normal height
for weight
NOMOGRAM
SA
Weight
catecholamine response to the trauma or anxiety. Systolic
blood pressures <100 mmHg are common in children
younger than 5 years of age (Table 35.3). Young children
with immature kidneys have less tubular concentrating
ability than adults, and urine production may continue in
spite of hypovolemia.
An indwelling urinary drainage catheter is essential for
burns >20% during resuscitation. During the early phase of
resuscitation, urine output should be assessed as frequently
as every 15 minutes and the resuscitation fluid titrated
appropriately. Fluid administration should be titrated to
achieve a urine output of 1 mL/kg/h in children and 2 mL/
kg/h in infants. Other endpoints for resuscitation should
also be followed, such as heart rate, blood pressure, capillary
refill, and mental status. Initial fluid boluses should be
administered in amounts appropriate for the size of the child
and should represent no more than 25% of the total circulat­
ing volume (20 mL/kg).
Over-resuscitation must be avoided as it can lead to pul­
monary edema, right heart failure, abdominal compartment
syndrome, extremity compartment syndrome, and cerebral
edema in burn patients. Of particular concern is the develop­
ment of cerebral edema. Care should be taken in order to
maintain elevation of the head of the bed, particularly during
the initial 24–48 hours post burn, and to avoid hypercarbia.
Although children possess a large cardiopulmonary reserve,
a child’s heart is less compliant, and stroke volumes plateau
at relatively low filling pressures, shifting the Starling curve
to the left. Cardiac output is almost completely dependent
upon heart rate, and the immature heart is more sensitive to

Total Burn Care
35
410
One successful approach is to attach the ET tube with tape
around the back of the head, both above and below the ears.
An additional piece of tape over the top of the head, secured
to the tape behind the head, will prevent accidental extuba­
tion in most children.12
Inhalation injury
Inhalation injury remains one of the primary contributors
to burn mortality.13 The mortality rate of children with iso­
lated thermal burns is 1–2%, but increases to approximately
40% in the presence of inhalation injury.14,15 The incidence
of and mortality from inhalation injury both increase with
increasing burn area.15 Carbon monoxide poisoning coupled
with hypoxia is the most frequent cause of death due to
‘smoke inhalation.’ Any patient with a flame-related injury,
particularly if confined in a closed space, should be evalu­
ated for an inhalation injury. If inhalation injury is sus­
pected, arterial blood gas and carboxyhemoglobin level
should be obtained and the patient should be placed on
100% oxygen. As with adults, the only definitive method to
diagnose an inhalation injury is through direct visualization
of the airway with fiberoptic bronchoscopy. Signs of poten­
tial inhalation injury include facial burns, singed nasal
vibrissae, carbonaceous sputum, abnormal mental status
(agitation or stupor), respiratory distress (dyspnea, stridor,
hoarseness, wheezing), or elevated carboxyhemoglobin level
>10%, especially in a closed-space fire.16,17 The initial car­
boxyhemoglobin level should be calculated from the time
the admission level is drawn, back to the time of the burn
injury. A carboxyhemoglobin level >60% has a >50% chance
of mortality (Table 35.4).
Treatment modalities for inhalation injury include airway
maintenance, clearance, and pharmacological management
(Table 35.5). Further care is mainly supportive and includes
ventilator support as needed, vigorous pulmonary toilet,
humidification of inspired air, and antibiotics for docu­
mented infection. A group of children treated with a regimen
of nebulized heparin and acetylcysteine showed a significant
decrease in reintubation rates, atelectasis, and mortality
compared to a control group.18
Hypermetabolism
Profound hypermetabolism is a classic feature of children
with large burn injury. Children with burns demonstrate a
profound increase in metabolic rate. No other disease state
volume overload. Cardiac output can be measured using a
PiCCO monitor (pulse contour cardiac output), based on
transpulmonary thermodilution, which is less invasive than
a Swan–Ganz catheter and only requires a thermodilution
arterial catheter and a central venous line. Transthoracic or
transesophageal echocardiograms should be used early to
assess cardiac function in patients who are not responding
to conventional therapy. Children are particularly prone to
the development of edema from both vasogenic and hydro­
static sources. Vasogenic edema occurs in the early post-burn
period when vascular integrity is impaired. The maintenance
of intravascular osmotic pressures reduces the likelihood of
edema development. Salt-poor albumin can be expected to
remain in the intravascular space if administered more than
8 hours post burn in amounts necessary to maintain serum
albumin levels at >2.5 g/dL. Albumin deficit can be calcu­
lated using the formula:
[ .
/
/
)] [
(
)
]
2 5
3
g dL
current serum albumin (g dL
wt kg
−
×
×
The deficit can be administered as 25% albumin and given
in divided doses.
Evaluation and management of airways
Airway evaluation and management must be given priority
in pediatric patients. Children are more prone to obstruction
owing to the smaller aperture of the trachea. Equal amounts
of airway edema in pediatric and adult airways result in
significantly disproportionate increases in amounts of resist­
ance and decreases in cross-sectional area. A 1 mm increase
in the tissue thickness of a 4 mm diameter pediatric trachea
results in a 16-fold increase in resistance and a 75% decrease
in cross-sectional area. The same edema in an adult airway
would increase the airway resistance threefold and reduce
airway area by 44%.11
Potential hemorrhage and edema make emergency intuba­
tion difficult. Early intubation should be considered when a
long transfer is anticipated, severe inhalation injury is
present, or a patient has a large burn which likely will
develop airway edema with a large amount of fluid resuscita­
tion. Concurrent placement of an endotracheal tube over the
bronchoscope should be considered at the time of bronchos­
copy. A readily available estimate of airway diameter is the
width of the patient’s little finger, an age-based formula
(age + 16)/4 or the use of Broselow tape.
The ET tube must be well secured. In a child, exudative
wounds and moist dressings can make this task difficult.
Table 35.3  Normal pediatric vital signs
Age
Minimum heart
rate (beats/min)
Systolic BP
(mmHg)
Respirations
(breaths/min)
Minimal
hemoglobin (g/dL)
Minimal hematocrit
(%)
<2 years of age
100–160
60
30–40
11.0
33.0
2–5 years of age
80–140
70
20–30
11.0
33.0
6–12 years of age
70–120
80
18–25
11.5
34.5
>12 years of age
60–110
90
16–20
12.0
36.0

Special considerations of age: the pediatric burned patient
411
Pharmacological agents have been used to attenuate cata­
bolism in burn injury. To minimize erosion of lean body
mass, administration of anabolic hormones such as recom­
binant human growth hormone, insulin, insulin-like growth
factor-1 (IGF-1), (IGF-1)/IGF-binding protein-3 (IGFBP-3);
anabolic steroids such as testosterone and synthetic ana­
logue oxandrolone; and adrenergic antagonists such as pro­
pranolol have been used in pediatric burn patients. These
agents contribute to maintenance of lean body mass and
promote wound healing.27–33
Thermoregulation
A hypothalamic reset induced by various inflammatory
cytokines and pain causes elevation of core body tempera­
ture after a major burn even in the absence of infection. Burn
patients strive for temperatures of about 38°C. Depressed or
‘normal’ temperatures are more likely indicative of over­
whelming sepsis or exhausted physiological capabilities to
maintain temperature. Routine methods of heat conserva­
tion are inadequate owing to the extensive heat loss through
convection and evaporation after major burn. Infants and
toddlers, with their increased body surface area to volume
ratios and lower muscle mass for shivering, are particularly
susceptible to hypothermia.
Every effort should be made to reduce the heat loss
experienced by pediatric patients. Ambient temperatures
and humidity should be maintained at 30–33°C and 80%,
respectively, in order to reduce energy demands and evapora­
tive water losses. Bathing or showering should be completed
expeditiously, avoiding undue environmental exposure.
Hypothermia produces numerous consequences. The
heart is particularly sensitive to temperature, and ventricular
arrhythmias are not uncommon. Hypothermia also increases
the susceptibility of the myocardium to changes in electro­
lyte concentrations. The oxyhemoglobin dissociation curve
is shifted to the left by lowered body temperature, impairing
peripheral oxygenation. In extreme cases, hypothermia pro­
duces central nervous system and respiratory depression,
coagulopathy, and loss of peripheral vasomotor tone.
Nutritional support
Nutritional support becomes an essential part of treatment
of acute burn patients during their hospitalization. Early
enteral nutrition is used to accomplish nutritional support
of the hypermetabolic response in severely burned patients.
Early enteral nutrition preserves gut mucosal integrity and
improves intestinal blood flow and motility.34 Early institu­
tion of enteral feeding can also abate the hypermetabolic
response to burn.34,35 Patients with smaller burns are placed
on a high-protein, high-calorie diet to support their meta­
bolic response. Those with larger burns >30% TBSA are
placed on enteral feedings to supplement their diet.
Feeding tubes can be placed beyond the pylorus and
enteral nutrition can be initiated within few hours of admis­
sion. Most children will tolerate enteral feedings as early as
1–2 hours post burn. Several studies have demonstrated the
efficacy of early alimentation and the additional salutary
effects.36,37 Enteral feedings can be given through a flexible
silastic nasoduodenal or nasojejunal feeding tube, bypassing
the stomach, which may experience ileus.
produces as dramatic an effect on the metabolic rate as burn
injury.19,20 This hypermetabolism slows wound healing and
prolongs generalized weakness. Prolonged hypermetabolism
can lead to loss of lean body mass and increased morbidity.
Marked wasting of lean body mass occurs within a few weeks
of injury.
The hypermetabolic response increases with increasing
burn size. There is an upregulation of catabolic agents, such
as catecholamine, cortisol, and glucagons,21 which induces a
hyperdynamic cardiovascular response, increased oxygen
consumption, energy expenditure, proteolysis, lipolysis, and
glycogenolysis, loss of lean body mass and body weight,
delayed wound healing, and immune depression.22–25
Cytokine levels increase after burn injury and normalize
only at 3–6 months post burn.26 Larger burn injuries are
characterized by more pronounced and persistent inflamma­
tory responses, indicated by higher concentrations of proin­
flammatory cytokines that promote more severe catabolism.26
Sex hormones and endogenous growth hormone levels
decrease around 3 weeks post burn.26
Table 35.4  Carbon monoxide poisoning
Carboxyhemoglobin
(%)
Symptoms
0–10
Normal
10–20
Headache, confusion
20–40
Disorientation, fatigue, nausea, visual
changes
40–60
Hallucination, combativeness, convulsion,
coma, shock state
60–70
Coma, convulsions, weak respiration and
pulse
70–80
Decreasing respiration and stopping
80–90
Death in less than 1 hour
90–100
Death within a few minutes
Table 35.5  Airway maintenance, clearance, and pharmacological
management
Turn side to side
q 2 h
Sitting or rocked in chair
As soon as physiologically
stable
Ambulation
Early
Chest physiotherapy
q 2 h
Suctioning and lavage (nasal/oral tracheal)
q 2 h
Bronchodilators
q 2 h
Aerosolized heparin/acetylcysteine
q 2 h alternating
Heparin 5000–10 000 units with 3 mL NS
q 4 h
Alternated with acetylcysteine 20% 3 mL
q 4 h

Total Burn Care
35
412
By using skin substitutes such as allograft, xenograft, and
Integra (Fig. 35.7), the burn wound can be covered and
protected until a donor site is available for grafting. Cultured
epidermal autograft (CEA) is available for massive burn inju­
ries (Fig. 35.8). Although it is an effective way to cover large
burns where donor sites are limited, it may not be the most
cost-effective approach. A group of patients treated with
CEA had greater hospital costs, a longer stay, and more
reconstructive admissions than conventional treatment with
meshed autograft skin.46
Traditionally, topical antimicrobials were the most com­
monly used treatment in partial-thickness burns. One of the
drawbacks of using topical antimicrobials in burn wounds
is pain. The current recommended treatment for partial-
thickness burns, primarily scalds <30% TBSA, is immediate
application of Biobrane. Biobrane can be safely used in
Commercially available tube feeding formulas are hyper­
osmolar and should be diluted to 0.5–0.75 strength because
of the high incidence of subsequent diarrhea if used full
strength.
Several formulas are available to estimate caloric require­
ments in burn patients. Since caloric demands are related to
burn size, caloric support should be given in amounts
calculated based on body surface area in children. A series
of different formulas based on body surface area have
been developed at Shriners Hospitals for Children, Galves­
ton, to meet the differing requirements of the various
age groups.38–40 The Curreri formula has likewise been
amended to reflect the differing demands of the pediatric
group (Table 35.6).
Growth
Hypermetabolism and catabolism persist long after the
wound is closed.41 Protein breakdown continues 6–9 months
after severe burn. There is almost a complete lack of bone
growth for 2 years after injury. This results in long-term
osteopenia, which may adversely affect peak bone mass
accumulation in children.42,43 Children with >40% TBSA
burn have a linear growth delay of height and weight despite
adequate nutritional support and maximal exercise during
post-burn year 1, which slowly resolves to near normal dis­
tribution by post-burn year 3.44
Management of burn wound
One of the most important advances in the care of burn
patients is the early surgical excision and grafting of the burn
wound. Improvements in the treatment of burn wounds
with the practice of early excision and grafting, along with
improvements in fluid resuscitation and the general care of
burn patients, have reduced the incidence of fatal sepsis in
burned patients.45 Prior to early excision and grafting, third-
degree burns were treated by removing small amounts of
eschar at a time, approximately 10–15%, followed by graft­
ing. Commonly, eschar was allowed to separate with lysis by
bacterial enzymes. This led to a high incidence of invasive
infection and wound sepsis and a prolonged hospital stay,
with increased mortality. Today massive excision can be
easily managed in children, leading to shorter hospital stays
and reduced mortality.46,47 Early excision of massive burns in
the first 24 hours is safe and effective.48
Figure 35.7  Dermal and skin substitutes can be used as temporary cover
for severe burns. Integra, a bilaminar skin substitute, can replace homografts
as temporary cover. The Silastic superficial layer can be removed after 3
weeks and a super-thin autograft then placed on top. The entire wound can
be covered with Integra, which is subsequently autografted when donor
sites are available. (Reprinted with permission from Barret J, Herndon DN, eds. Color atlas
of burn care. London: WB Saunders; 2001: 107, Plate 6.95.)
Figure 35.8  The cultured epidermal autografts are ready to use 18–21 days
later. Extreme care with handling is needed because of the fragility of the
cultured cells. (Reprinted with permission from Barret J, Herndon DN, eds. Color atlas of
burn care. London: WB Saunders; 2001: 106, Plate 6.89.)
Table 35.6  Nutritional requirements for children
Galveston
Modified Curreri
Infant burn
2100 kcal/m2 + 1000 kcal/m2
burn
BMR + 15 kcal/%
Toddler burn
BMR + 25 kcal/%
Child burn
1800 kcal/m2 + 1300 kcal/m2
burn
BMR + 40 kcal/%
Adolescent burn
1500 kcal/m2 + 1500 kcal/m2
burn

Special considerations of age: the pediatric burned patient
413
many months. Burn injury can cause intense pain. Pain can
also exist as a constant state throughout the hospitalization.
Morphine sulfate is one of the most commonly used anal­
gesia in pediatric burn patients.60 It should be given intrave­
nously, and not intramuscularly. Fentanyl can be also used.
Fentanyl Oralet has been used successfully in the tub room
for dressing change and wound care (10 µg/kg). Most out­
patients are treated with hydrocodone/acetaminophen, and
some require longer-acting narcotics such as methadone.
Rehabilitation
One of the integral parts of successful treatment of burn
injury is rehabilitation. During the acute phase of burn care,
splints and proper positioning are used to minimize joint
deformities and contractures. Splints are used continuously
except during a therapy session. They are fabricated to each
patient’s needs and used from the first day of hospitalization.
Bedside therapy, including passive and active range of
motion, is started early. Patients with leg graft are kept on
bed rest after the operation, but on postoperative day 4 they
are started on ambulation. Early therapy and ambulation are
the keys to success of long-term rehabilitation in burned
children. When patients are discharged from their acute care
hospitalization, they undergo rigorous therapies, including
stretching, range of motion and strengthening exercises.
Prevention
Prevention remains the single best way to reduce pediatric
burn injuries. National prevention and education efforts
have positively affected the number of pediatric burns each
year. Lowering the temperature set point on hot water heaters
and teaching families to check the bath water temperature
before placing a child in the bath has reduced scald injuries.
Prevention groups have worked with gas hot water heater
companies and the Consumer Product Safety Commission
children, even in infants under 2 years of age. When applied
within 48 hours of injury, there is no difference in infection
rates between Biobrane and topical antimicrobials. Further,
application of Biobrane versus topical antimicrobials leads
to less pain, shorter hospitalizations, and shorter healing
times.49–51 Other dressings such as Acticoat, Aquacel, and
Silverlon are available for partial-thickness burns that can be
left on for several days or longer, and reduce pain the associ­
ated with dressing changes.52,53
It may be difficult clinically to determine the depth of
scald burns during the early post-burn period as the wounds
may be indeterminate and contain a mixture of superficial
and deep partial-thickness burns and sometimes even full-
thickness burns. Indeterminate-depth scald burns in young
children are best managed with delayed surgery instead of
early excision. Unless the wound is clearly full thickness, the
scald burn should be conservatively managed for approxi­
mately 2 weeks to allow the wound to heal or demarcate
(Figs 35.9 and 35.10). This delayed surgery results in smaller
area of wound excised and less blood loss.54
Large scald burns can be treated with allograft or xenograft,
which significantly reduces the pain involved with dressing
change and wound care. Scald burns >20% TBSA and of
indeterminate depth were randomized to treatment with
allograft versus topical antimicrobial therapy. Treatment
with allograft led to a shorter time to healing and less pain.55
In another study, patients with >40% TBSA burn were rand­
omized to allograft skin or topical antimicrobial. Patients
who received treatment with allograft skin had a significantly
shorter hospital stay.56
Pain management
Pediatric patients do not always express their pain in the
same way as adults.57 Children may display pain through
fear, anxiety, agitation, anger, aggression, tantrums, depres­
sion, withdrawal, and regression.58,59 How the child’s experi­
ence of pain from the burn injury and the hospitalization is
managed clinically will have lasting psychological effects for
Figure 35.9  Superficial and small areas of deep second-degree scald burns
before topical treatment: 25% total body surface area. (Reprinted with permission
from Barret J, Herndon DN, eds. Color atlas of burn care. London: WB Saunders; 2001: 79,
Plate 5.39.)
Figure 35.10  Deep second-degree burns treated for 10 days with silver
sulfadiazine. Note that the edges are regenerating. Pseudo-eschar
challenges the evaluation of the wounds. Foul smell, discoloration,
surrounding cellulitis, and eschar separation are signs of infection. (Reprinted
with permission from Barret J, Herndon DN, eds. Color atlas of burn care. London: WB
Saunders; 2001: 77, Plate 5.31.)

Total Burn Care
35
414
Further reading
Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic
response to severe burn injury. Ann Surg. 2008 Sep;248(3):387-
401. (Overview of response to severe burn injury.)
Lee JO, Benjamin D, Herndon DN. Nutrition support strategies for
severely burned patients. Nutr Clin Pract. 2005 Jun;20(3):325-330.
(Overview of nutritional support of burn patients.)
Mlcak RP, Suman OE, Herndon DN. Respiratory management of
inhalation injury. Burns. 2007 Feb;33(1):2-13. (Excellent overview
of management of inhalation injury.)
Thompson P, Herndon DN, Abston S, et al. Effect of early excision on
patients with major thermal injury. J Trauma. 1987 Feb;27(2):205-
207. (Review of early excision of burn wounds.)
Williams FN, Jeschke MG, Chinkes DL, et al. Modulation of the
hypermetabolic response to trauma: temperature, nutrition, and
drugs. J Am Coll Surg. 2009 Apr;208(4):489-502. (Excellent
overview of hypermetabolic response to burn injury.)
(CPSC) to provide education to raise gas water heaters
12 inches off the ground, which significantly reduces the risk
of accidental explosions and fires.
Much work still needs to be done in the area of ‘child fire
play’. Three-quarters of ‘child fire play’ involves matches or
lighters. All matches and other ignition sources must be
placed out of reach of children. A positive step toward pre­
vention occurred in 1994 when the CPSC put into effect a
child-resistant lighter to protect children. The importance of
placing smoke detectors in multiple areas in a house has
received much public education. Current prevention educa­
tion focuses on children, and especially infants that are not
able to remove themselves from a fire. One way to protect
infants and children is to dress them in fire-resistant sleep­
wear and clothing to protect them from a burn injury if a
fire does occur.
Educating children as early as possible that fire is danger­
ous is imperative. Providing safe environments for children
and providing appropriate education is the responsibility of
healthcare providers, the adults that care for them, and the
community at large.
 
Access the complete reference list online at

Special considerations of age: the pediatric burned patient
414.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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reduces calories required to maintain weight in pediatric patients
with burns. J Burn Care Rehabil. 1990 Sep-Oct;11(5):405-409.
41. Hart DW, Wolf SE, Mlcak RP, et al. Persistence of muscle
catabolism after severe burn. Surgery. 2000 Aug;128(2):312-319.
42. Klein GL, Herndon DN, Langman CB, et al. Long-term reduction
in bone mass after severe burn injury in children. J Pediatr. 1995
Feb;126(2):252-256.
43. Klein GL, Wolf SE, Goodman WG, et al. The management of
acute bone loss in severe catabolism due to burn injury. Horm
Res. 1997;48(Suppl 5):83-87.
44. Rutan RL, Herndon DN. Growth delay in postburn pediatric
patients. Arch Surg. 1990 Mar;125(3):392-395.
45. Merrell SW, Saffle JR, Larson CM, et al. The declining incidence of
fatal sepsis following thermal injury. J Trauma. 1989 Oct;29(10):
1362-1366.
46. Herndon DN, Parks DH. Comparison of serial debridement and
autografting and early massive excision with cadaver skin overlay

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in the treatment of large burns in children. J Trauma. 1986
Feb;26(2):149-152.
47. Thompson P, Herndon DN, Abston S, et al. Effect of early
excision on patients with major thermal injury. J Trauma. 1987
Feb;27(2):205-207. (Review of early excision of burn wounds.)
48. Barret JP, Wolf SE, Desai M, et al. Total burn wound excision of
massive paediatric burns in the first 24 hours post-injury. Ann
Burns Fire Disasters. 1999;12(1):25-27.
49. Barret JP, Dziewulski P, Ramzy PI, et al. Biobrane versus 1% silver
sulfadiazine in second-degree pediatric burns. Plast Reconstr Surg.
2000 Jan;105(1):62-65.
50. Lal SO, Barrow RE, Wolf SE, et al. Biobrane improves wound
healing in burned children without increased risk of infection.
Shock. 2000 Sep;14(3):314-319.
51. Lang EM, Eiberg CA, Brandis M, et al. Biobrane in the treatment
of burn and scald injuries in children. Ann Plast Surg. 2005
Nov;55(5):485-489.
52. Varas RP, O’Keeffe T, Namias N, et al. A prospective, randomized
trial of Acticoat versus silver sulfadiazine in the treatment of
partial-thickness burns: which method is less painful? J Burn Care
Rehabil. 2005 Jul-Aug;26(4):344-347.
53. Caruso DM, Foster KN, Blome-Eberwein SA, et al. Randomized
clinical study of Hydrofiber dressing with silver or silver
sulfadiazine in the management of partial-thickness burns. J Burn
Care Res. 2006 May-Jun;27(3):298-309.
54. Desai MH, Rutan RL, Herndon DN. Conservative treatment of
scald burns is superior to early excision. J Burn Care Rehabil. 1991
Sep-Oct;12(5):482-484.
55. Rose JK, Desai MH, Mlakar JM, et al. Allograft is superior to
topical antimicrobial therapy in the treatment of partial-thickness
scald burns in children. J Burn Care Rehabil. 1997 Jul-Aug;18(4):
338-341.
56. Naoum JJ, Roehl KR, Wolf SE, et al. The use of homograft
compared to topical antimicrobial therapy in the treatment of
second-degree burns of more than 40% total body surface area.
Burns. 2004 Sep;30(6):548-551.
57. Schecter N, Allen DA, Hanson K. Status of pediatric pain control:
a comparison of hospital analgesic usage in children and adults.
Pediatrics. 1986 Jan;77(1):11-15.
58. Stevens B, Hunsberger M, Browne G. Pain in children: theoretical
research and practice dilemmas. J Pediatr Nurs. 1987 Jun;2(3):
154-166.
59. Staddard FJ. Coping with pain: a developmental approach to
treatment of burned children. Am J Psychiatry. 1982 Jun;139(6):
736-740.
60. Ratcliff S, Brown A, Rosenberg L, et al. The effectiveness of a pain
and anxiety protocol to treat the acute pediatric burn patient.
Burns. 2006 Aug;32(5):554-562.

©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00036-9
Care of geriatric patients
Laura J. Porro, Robert H. Demling, Clifford T. Pereira, David N. Herndon
Introduction
The quality of life in developed countries has improved over
the past 50 years, increasing the average lifespan by nearly
30 years.1 Individuals aged 65 years and over account for
13% of the US population. This ‘elderly’ population is pro­
jected to double from 40.2 million in 2010 to 88.5 million
by 2050. Such population aging is unprecedented.2 By 2050,
the number of elderly persons in the world is expected to
exceed the number of young for the first time in history.3
This trend presents a special challenge, as the elderly will
constitute an ever-growing segment of the average surgeon’s
practice and will influence clinical decisions, ethical deci­
sions, and healthcare costs.
A multicenter study conducted in Tokyo found that 25%
of burned patients were over 65 years old.4 A systematic
review of over 186 500 patients in Europe showed that 10–
16% were in this age range.5 In the US, geriatric patients
constitute about 10% of the major burn population. The
anticipated rise in the geriatric population makes under­
standing age-related physiological and metabolic changes
even more important for the burn care professional.6–8 The
elderly and the very young are most likely to die from severe
burns.9–12 Nearly 12 deaths per day result from residential
fires, with infants, toddlers, and the elderly representing the
high-mortality population.10,11 Adults over 65 years old have
a mortality from burns that is six times the national average.9
Treatment of these patients remains a greater challenge than
treatment of middle-aged and younger patients, as lower
physiological reserves and higher underlying comorbidities
reduce the margin for error.
Epidemiology
Contact with flame is the main (50%) cause of burn injury.
One-third of injuries result from cooking accidents: scalds
in 20% of cases and contact with hot objects in about 9%
of cases.6–8,13,14 The latter cause is more prevalent in the
elderly, reflecting increased psychological and physical dis­
ability. This fact is also reflected in the rate of fire-related
deaths in individuals over 75 years old, which is four times
the national average. The male-to-female ratio decreases
progressively as age increases, with women exceeding the
number of men in the 75 years and older group (compared
to the 5 : 1 male-to-female ratio for young adult burn
victims).14 This ratio is explained by the fact that 95% of
burns in elderly people occur at home, compared to less than
half in younger adults. Therefore, prevention must be focused
on the home.15 Prevention should also focus on the fact that
30% of geriatric patients are the victims of self-neglect, and
at least 10% are the victims of elder abuse.13
Outcome
Mortality has diminished among all age groups in recent
decades.5,14,16 Technological progress as well as advances
in fluid resuscitation, early burn wound excision, skin
grafting, and pharmacotherapy have improved survival. As
expected, mortality and morbidity are higher in geriatric
burn patients.1,2,10–12,14,17 Mortality is 50% in young adults
with a burn covering 80% of the total body surface area
(TBSA) and in individuals aged 60 and older with burns
covering only 35% TBSA.6,12 Pereira et al.16 analyzed 1674
patients admitted to the Shriners Burn Hospital, Galveston,
Texas, between 1989 and 2005 as well as 179 autopsies con­
ducted during this period to study mortality trends and
primary causes of death in the entire age spectrum over time.
They found that mortality has indeed been reduced in all
age groups, including the elderly (>65), over the last decade.
Lung injury and sepsis were the commonest primary causes
of death noted at autopsy. An increase in the weights of
heart, lung, spleen, and liver was noted in all age groups post
mortem. Fogerty et al. reported an 83% reduction in the
odds of death and a 50% reduction in the odds of sepsis in
elderly patients treated with a statin before injury.18 Pomahac
et al. reported that increased levels of creatinine at the time
of admission were associated with increased mortality.19
Gender dimorphism exists in mortality rates of patients
over 65 years old. The National Burn Repository 2009
reported an overall greater mortality in women than in men,
but a lower disparity during recent years. Age, TBSA burned,
and inhalation injury are associated with increased mortal­
ity. The mortality rate is 9.7% for patients aged 60–69 years,
17% for patients aged 70–79 years, and 28.6% for patients
over 80 years of age. 14
Geriatric patients also experience greater long-term disa­
bility following burn injury. Only about 50% of elderly
patients with a major burn return home within the first
year,7,16,20 whereas 90% of young adults return home. The
increased risk factors present in this population explain
these statistics. The increased complications seen in elderly
burn patients may also result from more cautious and less
aggressive treatments. This is due to existing beliefs that
elderly burn patients cannot tolerate eschar excision as well
CHAPTER 36 
Access the complete reference list online at

IN THIS CHAPTER
PowerPoint Presentation Online

Total Burn Care
36
416
TBSA burned, and presence of inhalation injury.17 Pneumo­
nia contributes to increase mortality, especially in the elderly.
Decreased lean body mass
Aging leads to progressive decreases in lean body mass.31 The
lean mass or body protein compartment is responsible
for all the physiological and metabolic activity needed for
survival, and any significant decrease is detrimental. Any
pre-existing loss will result in increased morbidity, early
onset of immune deficiency, organ dysfunction, weakness,
and impaired wound healing.29,32,33 Losses are caused by
multiple factors, including impaired nutrition, reduced
mobility, and age-related decreases in endogenous anabolic
hormones, human growth hormone, and testosterone.25,29
Decreased anabolic activity prolongs recovery time and
greatly delays restoration of muscle. Importantly, elderly
people respond to exogenous anabolic stimuli such as tes­
tosterone analogs, human growth hormone, and resistance
exercise similarly to the younger population. Therefore, exer­
cise, high-protein nutrition, and anabolic agents are essential
for recovery.34–36
Aging skin and wound healing
Aging produces significant changes in the skin. Because of
these changes, more deep burns occur in the elderly than
in younger patients.24,37,38 After the age of 65 the turnover
rate of the epidermis decreases by 50%. A flattening of the
rete pegs and fewer epidermal-lined skin appendages are
present. These properties significantly delay healing of
partial-thickness burns.24,37,38
In addition to the above-mentioned changes, a progressive
thinning of the dermis occurs, along with a decrease in both
collagen content and matrix, especially glycosaminoglycan.
The latter is responsible for loss of skin turgor. There is also
a decrease in vascularity, macrophages, and fibroblasts. The
thinner dermis with less blood flow explains the greater
amount of deep burn, and the decreased cellularity explains
the decrease in all phases of healing (Box 36.2).37,38
Treatment
In general, elderly patients are treated identically to younger
patients, except that massive burns are more commonly
managed expectantly. Some differences exist in responses to
burn injury between children and adults; however, no evi­
dence supports changing the treatment protocol. Current
differences in burn management among patient groups are
related to comorbid conditions and adversities that may arise.
as their younger counterparts, resulting in a greater delay in
the excision of burned tissue.21 However, despite these risk
factors, elderly patients have repeatedly been shown to toler­
ate multiple, early surgical procedures, and early wound
closure corresponds to a better outcome in these patients.22–24
Risk factors
A number of well-recognized risk factors are present in
elderly people. Increased risk of infections, pulmonary dis­
eases, and sepsis as well as the variability of comorbidities
present in these patients will increase morbidity after a burn.
Some of the more prominent factors are shown in Box 36.1.
Decreased cardiopulmonary reserve
Aging reduces pulmonary reserve for both gas exchange and
lung mechanics.25 Elderly people are more prone to pulmo­
nary failure, the major cause of burn-related death. The pres­
ence of atherosclerosis, coronary artery disease, and previous
myocardial infarcts is also common.
Chronic illness including malnutrition
Numerous diseases are common in the elderly. Some of
these, such as swallowing disorders (presbyphagia), can
lead to malnutrition.26 Some degree of protein–energy mal­
nutrition is found in over 50% of elderly burn patients on
admission.27 This, in combination with burn-induced hyper­
metabolic responses and protein catabolism, can substan­
tially reduce lean body mass in just a few weeks. Daily
protein requirements are higher in the elderly than in the
younger population.28
Malnutrition increases morbidity and mortality after
a burn and may increase the risk of burn injury in the
elderly.27–29 Nutritional support is a critical in improving the
clinical outcome of these patients. Use of a screening tool at
admission to assess the nutritional status of elderly patients
is necessary.30
Infections
Pneumonia and urinary tract infections are the most preva­
lent complications in elderly burn patients.14 The develop­
ment of pneumonia seems to correlate with the male gender,
Box 36.1  Risk factors in elderly people
•
Chronic illness, e.g., adult diabetes
•
Effects of aging, e.g., presbyphagia
•
Cardiovascular disease, e.g., previous infarct
•
Pulmonary reserve decreased with age
•
Infections, e.g., pneumonia and UTI
•
Unintentional weight loss
•
Decrease in lean body mass
•
Impaired nutrition with presence of deficiency states in energy,
protein, and macronutrients
•
Decreased endogenous anabolic hormones
•
Skin aging (thin, decreased synthesis)
Box 36.2  Aging of skin
•
Decreased epidermal turnover
•
Decrease in skin appendages
•
Thinning of dermis
•
Decreased vascularity
•
Decreased collagen and matrix
•
Decreased fibroblasts and macrophages

Care of geriatric patients
417
both male and female burn victims. However, the synthetic
analog oxandrolone is preferable as it possesses only 5% of
the virilizing androgenic effects of testosterone and is avail­
able in a peroral formulation. Oxandrolone restores lean
body mass and improves wound healing in burned adults,50
especially in emaciated subjects whose treatment has been
delayed.45,51 The effects of oxandrolone are independent of
age.49 Treatment of acute pediatric burn patients with oral
oxandrolone (0.1 mg/kg twice daily) enhances the efficiency
of protein synthesis and increases anabolic gene expression
in muscle. It also significantly increases lean body mass at 6,
9, and 12 months after burn, and bone mineral content
at 12 months after injury.54 Recombinant human growth
hormone has been successfully used in pediatric patients;55,56
however, it has several adverse effects, particularly during the
acute care of burned patients. The most notable of these is
hyperglycemia.57 In Europe, this agent has been shown to
increase mortality in critically ill, non-burned adults.58
Therefore, we do not recommend its use in the elderly.
β-Adrenergic blockade with propranolol during the acute
phase and long term attenuates the effects of the burn-
induced hypermetabolic response. In severely burned sub­
jects, titration of propranolol to reduce baseline heart rate
by 15–20% increases muscle–protein balance and dimin­
ishes obligatory thermogenesis, tachycardia, cardiac work,
resting energy expenditure, and fatty infiltration of the
liver.42,59,60 However, no study has directly focused on the
geriatric patient.
Pain, sedation, and comfort care
Geriatric burn patients are undertreated for pain because of
the misconception that less pain occurs with age.61 Both pain
and anxiety further increase the levels of catecholamine,
which is deleterious. Reduced clearance of many therapeutic
agents occurs with aging, necessitating lower dosages (Table
36.1).62 For this reason, pain assessment using reliable tools
is essential to create an individualized treatment plan, which
should also account for any comorbid conditions that may
be present on admission. Untreated pain and incorrect
sedation may result in post-traumatic stress disorder, major
Initial resuscitation
Improved fluid resuscitation over time is one of the factors
associated with decreased mortality. Compared to younger
patients, more fluid is required to resuscitate elderly patients
with the same burn size to avoid hypovolemia.39 This is
likely attributable to decreased skin turgor, which reduces
resistance to fluid accumulation or edema production.
Another possible factor is impaired cardiac function. Burn
depth, inhalation injury, and delayed resuscitation can influ­
ence fluid requirements.40 Benicke et al. developed a multi­
factorial resuscitation formula with a compensating factor
for advanced age that promises to help in the initial assess­
ment of fluid resuscitation.41 Early ventilatory support is
more commonly required because of decreased lung reserve
and earlier fatigue.
Wound management
Early removal of the burn wound and rapid closure with skin
grafts are essential for survival.22–24 Because the elderly have
thin skin, thermal injuries often create full-thickness wounds,
and skin grafts cannot always be obtained. In fact, they
might create a new wound.24 Thinner skin grafts are neces­
sary because of the thinner dermis, and healing time is pro­
longed.37 Gore found that donor site healing time decreased
substantially in elderly patients undergoing AlloDerm skin
grafting, allowing more patients to undergo operative wound
closure.24 Because older patients do tolerate operative proce­
dures, a conservative approach is not warranted. Because
multiple residual problems persist for years after injury,
patient orientation is crucial to understand the long-term
outcome of wound healing.
Metabolic and nutritional support
Although elderly patients do not generate the degree of
hypermetabolism seen in younger patients, the catabolic
response is comparable, necessitating a 1.5 g/kg/day protein
intake.42,43 Many older patients already have malnutrition
and lean mass deficits, as evidenced by prior weight loss.16
Therefore, the goal of nutritional support must be not only
maintenance, but also replacement therapy, especially
replacement of protein and micronutrients.29,31 Nutrient
supplements are invariably required. Most supplements are
protein hydrolysates, as the gut is more capable of absorbing
the peptides and amino acids than whole proteins broken
down from food.20,44
Anabolic agents are valuable adjuncts to optimal nutri­
tion.36,45–48 The effects of insulin and oxandrolone on post-
burn hypercatabolism have been studied in the pediatric
population, and these anabolic agents could be used in the
elderly, given that endogenous anabolic hormones are
decreased in this group after injury.47,49–51 Fram et al. recom­
mend continuous insulin infusions, with tight euglycemic
control, to restore insulin sensitivity, improve mitochondrial
oxidative capacity, and reduce resting energy expenditure.46
Lower-dose infusions of 9–10 U/h promote substantial
muscle anabolism without the need for additional large
doses of carbohydrate.52 Intensive insulin therapy during
acute care reduces morbidity, mortality, and complications
due to infection.47,53 Testosterone restoration is effective in
Table 36.1  Commonly used drugs requiring decreased doses in
elderly patients*
Drug
Comments
Barbiturates
Should be avoided. Paradoxical pharmacological
response, often leading to restlessness, agitation,
or psychosis due to decreased rate of elimination.
Benzodiazepines
Increased sensitivity to pharmacological effect;
some benzodiazepines may be metabolized more
slowly
Narcotic analgesics
Increased sensitivity to analgesic effects: possibly
impaired clearance
Tricyclic
antidepressants
Increased incidence of cardiac and hemodynamic
adverse effects; urinary retention and other
anticholinergic effects; decreased drug clearance
*Decreased dose due, in part, to decreased renal function in the elderly.

Total Burn Care
36
418
investigations are necessary to determine the most appropri­
ate therapeutic regimen for reducing perioperative ischemia,
cardiac morbidity, and post-burn hypermetabolic responses
in the elderly.
Pulmonary complications are more strongly linked to
coexisting comorbidities than to chronological age.75 Because
of the prevalence of chronic obstructive pulmonary disease
and asthma in the elderly, physicians should be alert for
these conditions during the perioperative evaluation. Peri­
operative chest X-rays should be ordered selectively. With the
appropriate diagnosis, aggressive pulmonary rehabilitation
including exercise training, patient education, nutritional
counseling, smoking cessation, and medication optimiza­
tion is effective in elderly patients.75 All these aspects must
be integrated into long-term patient management. Aggres­
sive use of antibiotics, judicious use of bronchodilators,
adequate hydration and postural drainage, and chest physio­
therapy should also reduce the incidence of pneumonia.
Rehabilitation
Burn rehabilitation is a long multidisciplinary process that
aims to preserve patients’ functional ability and restore
independence. Physical and occupational therapy should
begin immediately after injury. Important components of
rehabilitation include wound healing, scar prevention and
correction, splinting, casting, traction, pressure therapy,
pharmacological
therapy,
exercise,
and
psychological
support. The elderly should be aggressively managed during
rehabilitation to avoid any further loss of function or
strength, which are difficult to recover. The geriatric patient
is capable of recovering muscle strength with resistance exer­
cise and should not be managed conservatively.76 As with
children, providing support and guidance for caretakers is
essential, as these individuals will be responsible for the
patient’s wellbeing upon discharge.77,78
Intentional burns in the elderly
Identifying physical abuse by burning in the elderly is dif­
ficult, as no pathognomonic signs exist. Although such abuse
is relatively rare, professionals consistently underestimate
the prevalence of elder abuse. The growth in the elderly
population makes it necessary to raise awareness among
health professionals and re-evaluate the clinical approach
and assessment for burn injuries inflicted intentionally or
negligently.79 The elderly often live alone, interacting pre­
dominantly with the caregivers who enact their abuse. These
individuals may keep their abuse a secret because of shame,
guilt, or fear of reprisals.80,81 Most forms of intentionally
inflicted burns have a higher associated morbidity and mor­
tality than equivalent accidental burns, in part due to com­
orbidity from other physical abuse, substance abuse, or
psychological problems that contributed to or resulted from
the inflicted burn. Elder mistreatment can be associated with
confidentiality difficulties, as they may not want abuse
reported. The priority of the examining doctor is to treat
life-threatening conditions. They should then promptly
record symptoms and signs of abuse or neglect (including
photographs). Deliberately inflicted burn injuries are best
depression, and delirium.63 In addition, although the burn
injury primarily determines the extent of the metabolic
response, metabolic rates are also greatly increased by oblig­
atory activity, background pain, procedure-related pain, and
anxiety. Judicious maximal narcotic support, appropriate
sedation, and supportive psychotherapy are mandatory to
minimize these effects.64 Combination drug therapy is often
required to achieve adequate analgesia. Different approaches
ranging from patient-controlled analgesia to virtual reality
have been found to ameliorate pain in burned patients.
Intravenous drug administration is still preferable during the
acute phase. A proactive geriatrics consultation team may
also be beneficial in managing pain. Use of only comfort
care measures needs to be strongly considered for elderly
patients with burns likely to be fatal.65
Perioperative optimization
Aging produces many changes in the cardiovascular system
that makes hemodynamic stability more difficult to achieve,
increasing adverse outcomes. Coronary artery disease is prev­
alent, being estimated to exceed 80% in patients over 80
years old.66 Elderly patients are at higher risk for congestive
heart failure, and special considerations should be taken
during acute and long-term treatments.67 The revised cardiac
risk index stratifies patients into risk groups and helps
identify those likely to need additional cardiac evaluation.68
Patients with minor perfusion abnormalities undergoing
low-risk surgery may not require catheterization, but should
be considered for prophylactic β-blockers and aspirin before
operation. High-risk subgroups of patients identified based
on clinical risk factors and positive non-invasive tests should
undergo cardiac catheterization. Patients with significant
cardiac lesions should have definitive coronary revasculari­
zation via angioplasty before large body surface area burns
are excised. The potential benefits of using β-adrenergic
blocking agents during the perioperative period have been
studied,69,70 as perioperative ischemic events are related to an
exaggerated postoperative sympathetic response that leads to
an increased heart rate.69–72 β-Blockade has an added advan­
tage in the burn patient.73 Severe thermal injury induces
hypermetabolism that persists for up to 9–12 months,60 with
deleterious consequences occurring in both the acute and
the convalescent phases. The resting metabolic rate in burn
patients doubles for those injuries covering >40% TBSA.59
Catecholamines are key in the initiation of various cascades
that stimulate post-burn hypermetabolism.74 Preventing ini­
tiation of these cascades by blocking the action of catecho­
lamines at the receptor level attenuates this response and
reduces supraphysiological thermogenesis,59 tachycardia,
cardiac work, and resting energy expenditure.74
The drawback of β-blockade in the elderly is that the aging
cardiovascular system is less responsive to β-receptor stimu­
lation. This decrease, together with anesthetic agents, may
lead to deleterious intraoperative hypotension in the pres­
ence of prophylactic β-blockade. Despite being well toler­
ated,69 β-blockers are still withheld in the elderly for fear
of drug-related complications. Individualized dosing of
β-blockers to control myocardial ischemia postoperatively
may be more beneficial because of differences in coronary
anatomy and ischemic thresholds among patients. Further

Care of geriatric patients
419
communication between the burn team and patients or their
surrogates is critical for guiding therapy and achieving
acceptable outcomes.
Further reading
American Burn Association. National Burn Repository 2009: American
Burn Association; 2009.
Demling RH. ‘The incidence and impact of pre-existing protein energy
malnutrition on outcome in the elderly burn patient population.’
J Burn Care Rehabil. 2005;26(1):94-100.
Koupil J, Brychta P, Rihova H, et al. Special features of burn injuries
in elderly patients. Acta Chir Plast. 2001;43(2):57-60.
Manktelow A, Meyer AA, et al. Analysis of life expectancy and living
status of elderly patients surviving a burn injury. J Trauma.
1989;29(2):203-207.
McGill V, Kowal-Vern A, Gamelli RL. Outcome for older burn patients.
Arch Surg. Mar 2000;135(3):320-325.
Pereira CT, Barrow RE, Sterns AM, et al. Age-dependent differences in
survival after severe burns: a unicentric review of 1,674 patients
and 179 autopsies over 15 years. J Am Coll Surg. Mar 2006;202(3):
536-548.
managed by a multidisciplinary team of healthcare, social
service, and legal professionals.79
Conclusion
Despite the remarkable reduction in mortality in burned
children over recent decades, due mainly to the major
advances in patient management, we have not yet achieved
the same results in elderly patients. This age group still con­
stitutes a major challenge. Surgical decision making in these
patients must take into account physiological age, pre-burn
functional status, degree of impairment from comorbid
conditions, and clear treatment goals. No patient should be
denied an operation based on age alone, as age-related
declines in organ function are predictable for the population
but not necessarily for the individual. Currently, no ‘score’
can improve decisions based on a thorough evaluation
and discussion with the patient and family. Favorable out­
comes in elderly burn patient should pertain more to reliev­
ing suffering and maintaining independence and quality
of life, rather than expanding lifespan. Clear, repeated
 
Access the complete reference list online at

Care of geriatric patients
419.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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20. Larson CM, Saffle JR, Sullivan J. Lifestyle adjustments in elderly
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21. Stern M. Comparison of methods of predicting burn mortality.
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24. Gore DC. Utility of acellular allograft dermis in the care of elderly
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25. Koupil J, Brychta P, Rihova H, et al. Special features of burn
injuries in elderly patients. Acta Chir Plast. 2001;43(2):57-60.
26. Schweizer V. [Swallowing disorders in the elderly]. Rev Med Suisse.
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27. Demling RH. The incidence and impact of pre-existing protein
energy malnutrition on outcome in the elderly burn patient
population. J Burn Care Rehabil. Jan-Feb 2005;26(1):94-100.
28. Ausman LRR. Nutrition and the elderly. In: Lindner MC, ed.
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29. Kagansky N, Berner Y, Koren-Morag N, et al. Poor nutritional
habits are predictors of poor outcome in very old hospitalized
patients. Am J Clin Nutr. Oct 2005;82(4):784-791; quiz 913-914.
30. Rasmussen HH, Holst M, Kondrup J. Measuring nutritional risk
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31. Forbes G. Body composition: influence of nutrition, disease
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diagnosis and treatment. Treat Endocrinol. 2005;4(5):293-309.
33. Kotler DP, Tierney AR, Wang J, et al. Magnitude of body-cell-mass
depletion and the timing of death from wasting in AIDS. Am J
Clin Nutr. Sep 1989;50(3):444-447.
34. Al-Mousawi AM, Williams FN, Mlcak RP, et al. Effects of exercise
training on resting energy expenditure and lean mass during
pediatric burn rehabilitation. J Burn Care Res. May-Jun
2010;31(3):400-408.
35. Demling R, DeSanti L. The beneficial effects of the anabolic
steroid oxandrolone in the geriatric burn population. Wounds. Feb
2003;15(2):54-58.
36. Jeschke MG, Barrow RE, Mlcak RP, et al. Endogenous anabolic
hormones and hypermetabolism – Effect of trauma and gender
differences. Ann Surg. May 2005;241(5):759-768.
37. Gosain A, DiPietro LA. Aging and wound healing. World J Surg.
Mar 2004;28(3):321-326.
38. Walter J, Maibach H. Age and skin structure and function, a
quantitative approach: blood flow pH, thickness and ultrasound
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39. Bowser-Wallace BH, Cone JB, Caldwell Jr FT. Hypertonic lactated
saline resuscitation of severely burned patients over 60 years of
age. J Trauma. Jan 1985;25(1):22-26.
40. Greenhalgh DG. Burn resuscitation. J Burn Care Res. Jul-Aug
2007;28(4):555-565.
41. Benicke M, Perbix W, Lefering R, et al. New multifactorial burn
resuscitation formula offers superior predictive reliability in
comparison to established algorithms. Burns. Feb 2009;35(1):
30-35.
42. Williams FN, Herndon DN, Jeschke MG. The hypermetabolic
response to burn injury and interventions to modify this
response. Clin Plast Surg. Oct 2009;36(4):583-596.
43. Wolfe RR. Herman Award lecture, 1996: Relation of
metabolic studies to clinical nutrition – The example of burn
injury. American Journal of Clinical Nutrition. Nov 1996;64(5):
800-808.
44. Lupschitz D. Approaches to the nutritional support of the older
patient. Clinic Geriatric Medicine. 1995;11:715-725.
45. Demling RH, DeSanti L. Oxandrolone, an anabolic steroid,
significantly increases the rate of weight gain in the recovery
phase after major burns. J Trauma. Jul 1997;43(1):47-51.
46. Fram RY, Cree MG, Wolfe RR, et al. Intensive insulin therapy
improves insulin sensitivity and mitochondrial function in
severely burned children. Crit Care Med. Jun 2010;38(6):
1475-1483.
47. Jeschke MG, Kulp GA, Kraft R, et al. Intensive insulin therapy in
severely burned pediatric patients: a prospective randomized trial.
Am J Respir Crit Care Med. Aug 1 2010;182(3):351-359.
48. Ziegler T. Growth hormone administration during nutritional
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49. Demling RH, DeSanti L. The rate of restoration of body weight
after burn injury, using the anabolic agent oxandrolone, is not
age dependent. Burns. Feb 2001;27(1):46-51.
50. Miller JT, Btaiche IF. Oxandrolone treatment in adults with severe
thermal injury. Pharmacotherapy. Feb 2009;29(2):213-226.
51. Wolf SE, Thomas SJ, Dasu MR, et al. Improved net protein
balance, lean mass, and gene expression changes with
oxandrolone treatment in the severely burned. Ann Surg. Jun
2003;237(6):801-810; discussion 810-811.
52. Ferrando AA, Chinkes DL, Wolf SE, et al. A submaximal dose of
insulin promotes net skeletal muscle protein synthesis in patients
with severe burns. Ann Surg. Jan 1999;229(1):11-18.
53. Hemmila MR, Taddonio MA, Arbabi S, et al. Intensive insulin
therapy is associated with reduced infectious complications in
burn patients. Surgery. Oct 2008;144(4):629-635; discussion
635-637.
54. Jeschke MG, Finnerty CC, Suman OE, et al. The effect of
oxandrolone on the endocrinologic, inflammatory, and
hypermetabolic responses during the acute phase postburn. Ann
Surg. Sep 2007;246(3):351-360; discussion 360-362.
55. Branski LK, Herndon DN, Barrow RE, et al. Randomized
Controlled Trial to Determine the Efficacy of Long-Term Growth
Hormone Treatment in Severely Burned Children. Ann Surg. Sep 2
2009.
56. Jeschke MG, Finnerty CC, Kulp GA, et al. Combination of
recombinant human growth hormone and propranolol decreases
hypermetabolism and inflammation in severely burned children.
Pediatr Crit Care Med. Mar 2008;9(2):209-216.
57. Singh KP, Prasad R, Chari PS, et al. Effect of growth hormone
therapy in burn patients on conservative treatment. Burns. Dec
1998;24(8):733-738.
58. Takala J, Ruokonen E, Webster NR, et al. Increased mortality
associated with growth hormone treatment in critically ill adults.
N Engl J Med. Sep 9 1999;341(11):785-792.
59. Herndon DN, Hart DW, Wolf SE, et al. Reversal of catabolism by
beta-blockade after severe burns. N Engl J Med. Oct 25
2001;345(17):1223-1229.
60. Pereira CT, Herndon DN. The pharmacologic modulation of the
hypermetabolic response to burns. Adv Surg. 2005;39:245-261.
61. Ferrell BA. Assessing pain in the elderly. Consult Pharm. May
2010;25(suppl A):5-10.
62. Tsujimoto G, Hashimoto K, Hoffman BB. Pharmacokinetic and
pharmacodynamic principles of drug therapy in old age. Part 2.
Int J Clin Pharmacol Ther Toxicol. Mar 1989;27(3):102-116.
63. Gregoretti C, Decaroli D, Piacevoli Q, et al. Analgo-sedation of
patients with burns outside the operating room. Drugs.
2008;68(17):2427-2443.
64. Murphy KD, Lee JO, Herndon DN. Current pharmacotherapy for
the treatment of severe burns. Expert Opin Pharmacother. Mar
2003;4(3):369-384.
65. Stassen NA, Lukan JK, Mizuguchi NN, et al. Thermal injury
in the elderly: when is comfort care the right choice? Am Surg.
Jul 2001;67(7):704-708.
66. Mangano DT. Perioperative cardiac morbidity. Anesthesiology.
Jan 1990;72(1):153-184.
67. Lenihan DJ, Uretsky BF. Nonpharmacologic treatment of
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477-488.
68. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and
prospective validation of a simple index for prediction of cardiac
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69. Mangano DT, Layug EL, Wallace A, et al. Effect of atenolol on
mortality and cardiovascular morbidity after noncardiac surgery.
Multicenter Study of Perioperative Ischemia Research Group.
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70. Wallace A, Layug B, Tateo I, et al. Prophylactic atenolol reduces
postoperative myocardial ischemia. McSPI Research Group.
Anesthesiology. Jan 1998;88(1):7-17.
71. Mangano DT, Hollenberg M, Fegert G, et al. Perioperative
myocardial ischemia in patients undergoing noncardiac surgery–I:
Incidence and severity during the 4 day perioperative period. The
Study of Perioperative Ischemia (SPI) Research Group. J Am Coll
Cardiol. Mar 15 1991;17(4):843-850.
72. Raby KE, Brull SJ, Timimi F, et al. The effect of heart rate control
on myocardial ischemia among high-risk patients after vascular
surgery. Anesth Analg. Mar 1999;88(3):477-482.
73. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol
on perioperative mortality and myocardial infarction in high-risk
patients undergoing vascular surgery. N Engl J Med 1999;24(341):
1789-1794.
74. Norbury WB, Herndon DN, Branski LK, et al. Urinary cortisol and
catecholamine excretion after burn injury in children. J Clin
Endocrinol Metab. Apr 2008;93(4):1270-1275.
75. Couser JI, Jr., Guthmann R, Hamadeh MA, et al. Pulmonary
rehabilitation improves exercise capacity in older elderly patients
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expectancy and living status of elderly patients surviving a burn
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planning and rehabilitation of the elderly surgical patient. Clin
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79. Greenbaum AR, Horton JB, Williams CJ, et al. Burn injuries
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80. Lowenstein A. Elder abuse and neglect—‘old phenomenon’: new
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Human Science Press; 1989.

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Introduction
Various surgical complications can occur in burn patients,
resulting from pathologic progression of the burn injury
itself to iatrogenic etiologies. Multiple organ system injuries
can exist that require both a thorough assessment and expe­
ditious management according to advanced trauma life
support (ATLS) guidelines. Patients with large total body
surface area (TBSA) burns generally require a prolonged hos­
pital stay with numerous debridement and skin grafting pro­
cedures that can be complicated by wound infection and
subsequent graft failure.
Burn patients are at risk for potential surgical complica­
tions involving multiple organ systems, particularly the gas­
trointestinal (GI) tract. Such complications include stress
gastritis and ulceration, acalculous cholecystitis, superior
mesenteric artery (SMA) syndrome, and pancreatitis. In this
patient population, the cause for occult systemic sepsis is
frequently attributed to GI sources, as evidenced by the
development of acute cholecystitis, ischemic bowel, hollow
viscus perforation, and intra-abdominal abscess. Necrotizing
enterocolotitis is a serious GI tract complication in burn
patients, representing a phenomenon of transient ischemia–
reperfusion injury to the gut. It can progress to full-thickness
necrosis of involved segments, perforation and rapid clinical
decline.
Abdominal compartment syndrome can occur during the
acute phase of massive fluid resuscitation in large TBSA
burned patients. Based on determination of increased intra-
abdominal pressures, a decompressive laparotomy may be
necessary to prevent further end-organ damage (cardio­
vascular collapse, oliguria, elevated peak pressures, and
intestinal ischemia). A major burn significantly affects
hemodynamics, and invasive monitoring may be necessary.
As a consequence, catheter-related vascular complications,
such as distal limb ischemia and catheter-associated sepsis,
can be seen with both arterial and venous vascular access.
Prolonged intravascular manipulation secondary to the need
for access predisposes to septic thrombophlebitis and is
associated with poor outcomes.
Because of delays in diagnosis and treatment, there is a
substantial increase in morbidity and mortality associated
with non-thermal complications in burn patients. As such,
these secondary and sometimes fatal complications demand
immediate recognition and treatment. Patients who suffer
major burn injury need diligent care and attention through­
out their hospital course to avoid complications arising
from various organ systems. This chapter reviews the fre­
quently encountered general surgical, non-thermal compli­
cations in burn patients with respect to diagnosis and
management.
Burns and trauma
Although the overall incidence of combined burn and trau­
matic injury is low, the mortality is nearly twice that of burns
without associated trauma.1 A retrospective study examined
upwards of 24 000 patients with burn, trauma, or combined
injuries and found the overall incidence of combined burn
and trauma rate to be low (3.8%),2 consistent with the
National Trauma Data Bank and National Burn Repository
data. Although there was no difference in length of stay,
injury severity scores, or mortality among burn or trauma
patients alone, there were significant increases in inhala­
tional injury, length of stay, and mortality in patients suffer­
ing from combined injuries (Table 37.1). This increase in
mortality was seen despite similar TBSA burns, demonstrat­
ing the additive effects of trauma and burns in these patients.2
In particular, approximately 24% of military burn injuries are
associated with concurrent traumatic injuries, compared to
the 2–7% of burn/trauma injuries found in civilians in the
same study.3 The most common civilian cause of burn/
trauma injury remains motor vehicle collisions (MVC). Of
the 500 000 individuals in the United States treated for
burn injuries, an estimated 7.2% are secondary to street or
highway accidents (American Burn Association, National
Burn Repository 2009). MVA victims that require extrication
and those that are ejected typically have the most severe
multitraumatic injuries. In order of frequency, injured organ
systems include musculoskeletal, head and neck, abdominal,
thoracic, and genitourinary. Industrial accidents, attempts
to escape house fires, explosions, and electrical burns with
falls account for the majority of other victims. High-voltage
electrical burns rarely occur at ground level and are often
accompanied by falls resulting in spinal cord injuries, solid
organ injury, intracerebral hemorrhage, and multiple frac­
tures, including vertebral, rib, pelvic, and long bones.
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00037-0
Surgical management of
complications of burn injury
Nadja C. Colon, Cameron Schlegel, Dai H. Chung
CHAPTER 37 
Access the complete reference list online at

IN THIS CHAPTER
PowerPoint Presentation Online

Total Burn Care
37
422
circulation should be assessed. Pericardial tamponade result­
ing from a heavy impact to the anterior chest wall can be
detected by focused assessment with sonography for trauma
(FAST) examination and managed with pericardiocentesis
or a pericardial window. Myocardial dysfunction may
be encountered, especially with electrical injuries, and dys­
rhythmias should be managed accordingly. If central venous
access is necessary, it should similarly be placed away from
burned tissue.
Associated injuries
Burns may also be associated with other traumatic injuries.
The cervical spine should be considered unstable until a
complete evaluation has been performed. Unstable cervical
spine fractures may be managed appropriately with traction
via halo or tongs. When necessary, intracranial pressure
monitoring via a bolt placed through unburned scalp is
preferred over a ventriculostomy. If a neurosurgical proce­
dure is required, debridement of the scalp and non-viable
tissue is completed at the same time as the craniotomy.
Orthopedic injuries – primarily fractures – comprise the
most commonly associated traumatic injury in thermally
injured patients. The burn surgeon and the orthopedist must
coordinate the optimal management of these patients. Ther­
apeutic decisions are based upon the following considera­
tions: stability of the fracture, the need for excision and
grafting of the burn, access required for adequate burn
wound care, and early aggressive physical therapy after the
injury. Although fractures away from the burns may be
managed with reduction and casting, in cases where fractures
are associated with severe soft tissue damage, internal fixa­
tion should be performed within 24–48 hours, prior to bac­
terial colonization of the wound. All open fractures must
have incision and drainage performed in the operating room
within 24 hours of the injury, and when open reduction
occurs through a burn, the wound should only be closed to
the level of fascia without drain placement. Using this
approach, early aggressive fracture treatment has been shown
to reduce orthopedic compli­cations without further risks of
infection, poor healing, or amputation. Antibiotic coverage
should be provided as deemed appropriate for the ortho­
pedic injury.
The diagnosis of intra-abdominal injury may prove diffi­
cult, as the abdominal examination is rather unreliable in
the face of a severe burn. In addition, hemodynamic changes
that occur with an intra-abdominal injury can be masked by
the physiologic response seen with intravascular volume
shifts and the exaggerated inflammatory response. Nonethe­
less, imaging modalities that are currently used to evaluate
trauma patients with blunt or penetrating mechanisms
should also be considered when evaluating a burned patient
with a suspected intra-abdominal injury. Diagnostic laparos­
copy can be a helpful adjunct in the evaluation of various
intra-abdominal injuries, such as bowel perforation and
ischemia, that are difficult to diagnose with computed
tomography (CT) alone. However, adequate abdominal CO2
insufflation is often difficult to achieve in patients with
significant eschar of the trunk. If laparotomy is warranted,
dehiscence of abdominal wounds is a frequent complica­
tion, independent of whether or not the burn wound was
traversed. If abdominal wall closure demonstrates significant
Primary assessment
In trauma patients with multiple organ system injuries, the
shocking appearance of the burn injury may unduly shift
attention away from the other seemingly underwhelming
injuries, resulting in delays in diagnosis. The initial assess­
ment of patients with combined thermal and other
traumatic injuries should center on airway, breathing, and
circulation according to the ATLS guidelines. With the excep­
tion of respiratory compromise secondary to circumferential
chest burns, the burn injury itself is usually not immediately
life-threatening. Inhalational injuries are common in burn
patients. Some of the common signs of inhalational injury
include cough, stridor, singed nasal hair, carbonaceous
sputum, and a hyperemic oropharynx. Asphyxia can be seen
with carbon monoxide and cyanide poisoning, for which
pulse oximetry is an unreliable measure of oxygenation. If
the respiratory distress is significant, intubation or a surgical
airway may be required, and although hypoxemia is usually
evident, the inhalational injury can evolve over hours such
that an initial chest radiograph and arterial blood gas
may be normal. Smoke inhalation induces a multitude of
physiologic changes which result in increased vascular
permeability and pulmonary edema, infiltration by leuko­
cytes, and bronchorrhea. Therefore, it is not unusual for
patients to escalate to unconventional modes of ventilation,
such as volumetric diffusive ventilation.
Once the airway has been secured, attention should focus
on the rest of the primary assessment. Third-degree circum­
ferential chest burns can impair respiratory mechanics and
require escharotomy to release the constrictive eschar. This
should be performed in a sterile manner with incisions
extending from the clavicle to the costal margin in the ante­
rior axillary line bilaterally, and may be joined by transverse
incisions. The more common thoracic injuries, such as rib
fractures, pneumothorax, and hemothorax, should be
managed as they would be in any other blunt or penetrating
thoracic injury. However, because burns carry such a high
risk of infection, thoracostomy tubes should be placed away
from burned skin whenever possible to reduce the risk of
infectious complications such as empyema. Finally, adequate
Table 37.1  Increased morbidity and mortality with combined
burn and trauma1
Trauma
(n = 22,284)
Burn
(n = 1717)
B/T (n = 92)
Age
35.1 (±27.5)
31.0 (±23.2)
40.1 (±25.4)*
TBSA
N/A
17.5% (±19.7)
20.8% (±24.4)
ISS
5.5 (±10.3)
12 (±14)
23 (±16)*
LOS (days)
5.3* (±12.2)
13.7 (±16.5)
18 (±20.8)
INH
N/A
11.0%
44.5%*
Mortality
4.3%
9.8%
28.3%*
*p < 0.05 (Age, B/T vs. Burn; ISS, B/T vs. Burn and Trauma; LOS, B/T vs. Trauma;
Mortality, B/T vs. Burn and Trauma)
B/T: burn/trauma; TBSA: total body surface area; ISS: injury severity score; LOS:
length of stay; INH: inhalation injury.

Surgical management of complications of burn injury
423
burns, leading to surgical complications and worsened
outcomes.
The hypermetabolic response to burn injury plays a key
role in non-thermal complications and is characterized by
catabolic metabolism, hyperdynamic circulation, insulin
resistance, delayed wound healing, while increased risk of
infection.9 Poor fibroblast function contributes to impaired
wound healing, while leukocyte dysfunction and reduced
cellular immunity cause immunological compromise. Alter­
ations in stress hormone responses, cardiac output, lean
body mass, and sex hormones may persist for several years
post burn. Previous studies have demonstrated typical stress
responses to a variety of traumatic injuries, with a so-called
‘ebb’ phase resulting in a decrease in metabolism and tissue
perfusion, followed by a ‘flow’ phase 3–5 days following
injury.10 Early enteral feeding has been shown to blunt the
hypermetabolic response.11
Of all the potential mechanisms of injury, severe burns
result in the most dramatic metabolic response. The hyper­
metabolic phase results in the activation of the hypotha­
lamopituitary axis, sympathetic outflow, the acute-phase
response that promotes fat and protein breakdown, and glu­
coneogenesis.12 Excessive catabolism following a burn injury
encourages hyperglycemia and insulin resistance within the
first week after injury, both of which are associated with an
increase in morbidity and mortality in severely burned
patients. Recent trials have demonstrated that intensive
insulin therapy aimed at maintaining a daily average glucose
of 140 mg/dL improves immune function and reduces
sepsis, along with an attenuation of the inflammatory and
acute-phase response.13,14 As such, tight glucose control is
thought to be critical in improving the overall recovery of
burn patients.
As mentioned, a combination of hypoperfusion and
hypermetabolic response can lead to breakdown of the gut
mucosal barrier, resulting in bacterial translocation from
the gut, systemic inflammation, and ultimately, sepsis (Fig.
37.1). Numerous studies have demonstrated the association
between massive cutaneous burn injury and bacterial trans­
location.8,15 Following massive burn injury, the GI tract
mucosa sustains immediate atrophy, resulting in significant
gut barrier dysfunction. The increase in intestinal apoptosis
does not appear to be from mesenteric hypoperfusion
alone, but is speculated to be related to proinflammatory
mediators produced by the burn wound.15 An in vivo study
using a 30% TBSA burn model in rats confirmed that there
was increased bacterial translocation and permeability
to macromolecules that peaked at 18 hours post injury,
lending credence to the idea that disruption of intestinal
barrier integrity in severe burns can lead to sepsis from
bacterial translocation.16 Thus, interventions aimed at pre­
venting splanchnic hypoperfusion and hypermetabolism
may circumvent complications associated with severe burns.
Recent studies targeting the inflammatory response itself
provide insights into potential novel therapeutic targets,
such as p38 MAPK, which is involved in the production of
the proinflammatory mediators interleukin (IL)-1β, nitric
oxide, and cyclooxygenase (COX)-2. Additionally, p38 MAPK
is clinically associated with delayed intestinal transit, a
common burn complication. Studies inhibiting key steps
of the p38 MAPK pathway have demonstrated attenuation
of impaired intestinal transit in rodent models, and may
tension, the use of retention sutures should be considered.
Occasionally, a temporary abdominal closure may be
required to prevent abdominal compartment syndrome. In
cases where the bowel becomes massively edematous, a
vacuum-pack for the open abdomen will act as a temporiz­
ing measure for a delayed abdominal wall closure.
Vascular injuries may be difficult to diagnose in the pres­
ence of burned skin, significant soft tissue edema, compart­
ment syndrome, or hypotension. The principles in their
diagnosis remain the same, with an assessment of capillary
refill, neurologic deficits, and palpable pulses. A Doppler
ultrasound is a non-invasive bedside study that can easily be
performed to assess adequacy of arterial blood flow and can
be supplemented with an ankle–brachial index (ABI).
However, the data, especially the ABI, can be difficult to
interpret when extremities are burned full thickness or cir­
cumferentially. Although conventional angiography contin­
ues to be the gold standard in the diagnosis of major vascular
injuries, its benefits do not seem to outweigh its invasive
risks in the era of CT angiography. One study found that CT
angiography had a >95% sensitivity and specificity in the
diagnosis of traumatic arterial injuries of the extremity, with
poor arterial opacification being a disadvantage.4 Thus, CT
angiography is a reasonable tool in the diagnosis of major
vascular injuries. Should a vascular insult require repair, sub­
stantial consideration should be given to the choice of graft
(autologous versus synthetic), as contamination is not infre­
quent and only complicates the care of these critical patients.
The liberal use of prophylactic muscle flaps for graft coverage
has proved helpful.
Gastrointestinal tract complications
Although the superficial effects of burn injuries are often
striking, the systemic physiological response to these injuries
may result in significant end-organ dysfunction and cannot
be overemphasized. Burn injuries >30% TBSA produce a
physiological response leading to systemic shock, hyperme­
tabolism, and widespread immunosuppression.5 The com­
bination of intravascular fluid loss, vasoactive hormone
release, catabolism, and immune dysfunction results in the
non-thermal complications of burn injuries and has conse­
quently become the focus of preventative treatment and
molecular models in the design of future therapies.
Physiological changes in blood flow have a dramatic effect
on organ response to injury, healing, and permanent dys­
function. This has been particularly well demonstrated in the
GI tract, where a combination of diffuse capillary leak, hypo­
volemia, and the release of vasoconstrictive agents can cause
a selective decrease in splanchnic blood flow.6 Splanchnic
hypoperfusion occurs early in the post-burn period despite
adequate cardiac output and fluid resuscitation, as demon­
strated in 40% TBSA pig models that had an early reduction
in superior mesenteric blood flow associated with intestinal
mucosal hypoxia, acidosis, and increased bacterial transloca­
tion.7,8 The GI tract ischemia has multiple effects, including
ulcer formation (Curling’s ulcer), enterocolitis, and acalcu­
lous cholecystitis secondary to gallbladder ischemia and bile
stasis. Other abdominal organs, such as the kidneys and
liver, may endure end-organ damage when exposed to the
‘low-flow’ state associated with hypoperfusion following