Update on the Critical Care Management of Severe Burns

Journal of Intensive Care Medicine
26(4) 223-236
ª The Author(s) 2011
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DOI: 10.1177/0885066610390869
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Update on the Critical Care
Management of Severe Burns
Kevin R. Kasten, MD1, Amy T. Makley, MD1, and
Richard J. Kagan, MD, FACS1,2
Abstract
Care of the severely injured patient with burn requires correct diagnosis, appropriately tailored resuscitation, and definitive
surgical management to reduce morbidity and mortality. Currently, mortality rates related to severe burn injuries continue to
steadily decline due to the standardization of a multidisciplinary approach instituted at tertiary health care centers. Prompt
and accurate diagnoses of burn wounds utilizing Lund-Browder diagrams allow for appropriate operative and nonoperative
management. Coupled with diagnostic improvements, advances in resuscitation strategies involving rates, volumes, and fluid
types have yielded demonstrable benefits related to all aspects of burn care. More recently, identification of comorbid conditions such as inhalation injury and malnutrition have produced appropriate protocols that aid the healing process in severely
injured patients with burn. As more patients survive larger burn injuries, the early diagnosis and successful treatment of secondary and tertiary complications are becoming commonplace. While advances in this area are exciting, much work to elucidate immune pathways, diagnostic tests, and effective treatment regimens still remain. This review will provide an update on
the critical care management of severe burns, touching on accurate diagnosis, resuscitation, and acute management of this
difficult patient population.
Keywords
burn, ICU, resuscitation, inhalation, sepsis, nutrition
Received January 8, 2010, Received Revised February 19, 2010. Submitted March 25, 2010.
Introduction
Evaluation of the Burn Wound
Burn injuries account for 500 000 medical visits annually, of
which 40 000 require hospitalization.1 A total of 67% of
reported burns in the United States involve less than 10%
total body surface area (TBSA) with a mortality rate under
0.5%. Proper diagnosis and treatment by emergency room
physicians and general practitioners is vital for good long
term outcomes.1-4 In those patients requiring hospitalization,
appropriate resuscitation, nutritional support, and early surgical treatment can minimize morbidity and mortality rates,5
especially when treatment occurs in one of the 125 hospitals
with specialized burn centers.1 The evolution of burn
management in the context of specialized care in dedicated
treatment centers has led not only to an overall decrease in
burn-related mortality, but also to a marked increase in the
LA50 (mean extent of burn associated with 50% mortality)
for burn injuries from 40% to >90% TBSA (Figure 1).6-9
Whether treating a burned individual as inpatient or outpatient, appropriate knowledge of burn shock and resuscitation,
nutrition requirements, and wound care will aid the clinician
in the management of the patient.
The skin is composed of 2 distinct layers and provides protection against fluid loss, mechanical damage, and infection. The
epidermis consists of keratinocytes, melanocytes, and
Langerhan’s cells, while the dermis consists of structural proteins and cells responsible for tensile strength.10 Blood vessels,
hair follicles, and sweat glands are rooted in the dermis. Preservation of these dermal structures following superficial injury is
responsible for the regeneration of epidermal cells required for
primary healing.11
The depth and extent of injury depend on the mechanism of
burn and duration of exposure to the heat source. Scald burns
are associated with a robust pro-inflammatory response leading
1
2
Department of Surgery, University of Cincinnati, Cincinnati, OH, USA
Shriners Hospitals for Children-Cincinnati, OH, USA
Corresponding Author:
Richard J. Kagan, Shriners Hospitals for Children, University of Cincinnati
College of Medicine, 3229 Burnet Avenue, Cincinnati, OH 45229, USA
Email: [email protected]
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Journal of Intensive Care Medicine 26(4)
Figure 1. Schematic view of increased LA50 over time. A representation of the developments in burn care over the past 70 years that
have allowed for a steady increase in total body surface area (TBSA) burn size from which 50% of patients will survive.
to increased systemic complications,12 while flame burns are
often associated with an increased incidence of inhalation
injury, an independent risk factor for mortality.5,11 Chemical
burns involve prolonged tissue damage even after removal of the
inciting agent, and in the case of hydrofluoric acid, can produce
life-threatening electrolyte abnormalities. Electrical burns
require close evaluation for cardiac abnormalities and compartment syndrome due to muscle necrosis. Regardless of mechanism, outcomes are directly influenced by burn depth, % TBSA
involvement, patient age, and the ability of the treating clinician
to properly assess and manage all aspects of the burn injury.
First-degree burns are characterized by erythematous
changes, lack of blistering, and significant pain. Wounds
blanch easily on examination and heal within 2 to 3 days following desquamation of dead cells. Scarring is rare and these
injuries should not be included in the estimate of burn size.11
Superficial partial-thickness burns involve the entire
epidermis, typically forming fluid-containing blisters at the
dermal-epidermal junction. Wounds are erythematous, wetappearing, painful, and blanch with pressure. As the deeper
dermis is left undamaged, wounds heal within 2 weeks without
the need for skin grafting.11 Superficial and deep partialthickness burns merit distinction because deep partialthickness burns behave clinically like third-degree burns. Deep
partial thickness burns blister, but the blister base will have a
mottled pink and white appearance due to partially damaged
blood vessels. These wounds do not easily blanch and are less
painful than superficial burns due to concomitant nerve injury.
Some burn surgeons advocate initial monitoring of these areas
for up to 14 days to allow wound demarcation, resulting in
fewer operations and less-extensive grafting. Rarely, wounds
heal without surgical intervention, but remain at risk for
developing hypertrophic burn scars and/or contractures.11
Full-thickness, or third-degree, burns are defined by complete
involvement of all skin layers and require definitive surgical
management. These wounds are white, cherry red, brown or
black in color, and do not blanch with pressure. They are typically insensate from superficial nerve injury.
The calculated % TBSA is an independent risk factor correlating with length of hospital stay and mortality5; however, the
extent of burn injury is overestimated by up to 75% of initial
care providers.13 Incorrect wound extent calculation leads to
over-resuscitation, inappropriate transfer to burn centers, and
poor use of limited resources.14 Burn diagrams, the ‘‘rule of
nines,’’ and using the palm and fingers of the patient’s hand
to estimate 1% of normal body surface area are methods for
burn size estimation.15 The ‘‘rule of nines’’ is a rough estimation of adult body surface area which often overestimates burn
size in children, supporting the need for age-specific body surface
area charts such as the Lund Browder diagram.16 (Figure 2).
Newer methods to calculate burn surface area using computerized
imaging, 2- and 3-dimensional graphics, and body contour reproductions are currently being researched to improve accuracy in
initial wound assessment.17
Early Management and Resuscitation
of Burn Injuries
Approximately 10% of burns present with additional traumatic
injuries, so all patients should be evaluated and managed using
Kasten et al
225
Figure 2. Shriners Hospitals for Children Burn Diagram (Lund-Browder). This adaptation of the Lund-Browder diagram is utilized in our
hospital for estimation of depth and extent of burn in the acute patient.
Advanced Burn Life Support protocols.11 Burn wounds are
initially washed with tepid water18 following removal of the
heat source. Chemical burns are copiously irrigated for a minimum of 15 minutes. Ice or iced water increases tissue damage
and is contraindicated due to the risk of hypothermia in patients
sustaining extensive burns.19,20 Electrical injuries mandate tailored evaluation given the propensity for compartment syndrome, cardiac dysrhythmias, muscle necrosis, and
multiorgan system involvement.21 Approximately 60% to
70% of burns seen in emergency departments involve less than
10% TBSA and are treated with minor debridement, oral
hydration, topical wound care, and outpatient follow-up.22
Patients who fail outpatient therapy or require supplemental
nutrition or hydration need continued care as inpatients. In such
cases, the optimal treatment and management of large or complicated burn injuries is in a high volume center.11,23 Current
American Burn Association (ABA) guidelines recommend the
transfer of patients meeting specific criteria, including patients
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Journal of Intensive Care Medicine 26(4)
Table 1. Estimated Fluid Resuscitation Requirements for a 12 Year Old Child with 25% Total Body Surface Area Scald Burns. Hourly fluid
administration is guided by the response to treatmenta
Shriners Hospital—Cincinnati
First 8 Hours
3550 cc/LR
443.8 cc/h
Parkland Formula
Modified Brooke Formula
Second 16 Hours
First 8 Hours
Second 16 Hours
First 8 hours
Second 16 Hours
3550 cc/LR
221.9 cc/hr
2500 cc/LR
312.5 cc/h
2500 cc/LR
156.3 cc/h
1250 cc/LR
156.3 cc/h
1250 cc/LR
78.1 cc/h
a
Initial vital signs in the ER include a weight of 50 kg, height of 145 cm, heart rate of 130 bpm, blood pressure of 90/45, and respiratory rate of 23 with an oxygen
saturation of 94% on room air. The following are indicated resuscitation regimens, all titrated based on the patient’s urine output.
at extremes of age, large burns, or burns involving critical
anatomy. Prior to transfer, wounds should be covered with
clean, dry material or nonadherent gauze.24 The use of wet
dressings should be avoided to prevent development of
hypothermia in patients with large burn wounds.23 Tetanus prophylaxis, appropriate pain control, and placement of a urinary
catheter in patients being actively resuscitated are all necessary
prior to transport.
Burn Resuscitation
Delay in resuscitation increases mortality following severe
burn injury.5 Intravenous access can be obtained peripherally
with small burns but requires central placement for most burns
greater than 20% TBSA. Balanced crystalloid infusion should
begin after intravenous access is gained, customarily using the
Parkland or modified Brooke formulas as initial guidance. The
Parkland formula was developed in the 1970s by Baxter and
Shires who discovered that resuscitating with a higher volume
in the first 8 hours improved cardiac output.25 Pruitt et al
altered the original Brooke formula to demonstrate that a lower
volume of fluid achieves the same endpoints of resuscitation as
the Parkland formula.25 The modified Brooke formula calls for
2 mL/kg per %TBSA burn of balanced salt solution over the
first 24 hours following injury, while the Parkland formula
recommends 4 mL/kg per %TBSA burn. Although both
formulas call for the subsequent titration of fluid rates, in a
comparative analysis the Parkland formula more often resulted
in over-resuscitation and was an independent risk factor for
mortality.26 However, a separate comparative study found no
clinical differences in outcomes between patients resuscitated
using these 2 formulas.27
Consensus fluid resuscitation by standardized formula has
not been reached.25 At our institution, resuscitation includes
the administration of estimated basal fluid requirements in
addition to the replacement of extensive fluid losses secondary
to burn injury (Table 1). Regardless of the resuscitation formula used, all rely on accurate assessment of extent and depth
of burn and prompt tailoring of the infusion rate to the individual patient. Resuscitation should be titrated to clinical endpoints including urine output (30-50 mL per hour in adults
and 0.5-1 mL per kg per hour in children26) and hemodynamic
parameters.25 Evaluation of hemodynamic parameters customarily involves cardiac monitoring, continuous pulse oximetry, and invasive or noninvasive blood pressure measurement.
Swan-Ganz catheters have fallen out of favor in the
management of ICU patients but may be helpful in monitoring
the resuscitation of the acute burn patient. Newer products such
as the NICO (Philips Respironics) and Vigileo Monitor
(Edwards Lifesciences) allow measurement of cardiac output
and other systemic parameters in patients with burn via
end-tidal carbon dioxide and an arterial line, respectively.28,29
Noninvasive methods of cardiac output measurement include
esophageal Doppler and pulse contour cardiac output, both
demonstrating results comparable to invasive techniques.30
To help avoid the complications of inadequate or excessive
resuscitation, current research is examining the utility and efficacy of closed-loop autonomous resuscitation.31
Historically, initial resuscitation formulas called for the use
of albumin during the first 24 hours following injury as an
adjunct to crystalloid.25 This was advocated because serum
protein levels decrease rapidly after burn injury, sometimes
resulting in crystalloid resuscitation failure.32 In fact, patients
receiving colloid as part of their resuscitation require less crystalloid and total fluid compared to resuscitation with crystalloid
only.33 However, recent evidence demonstrates colloid resuscitation does not affect mortality and is more expensive than
crystalloid solutions.34 The theoretical reduction in complications and mortality from colloid use has not been proven in prospective human trials and is only used in patients unresponsive
to resuscitation with crystalloid.
Complications of Resuscitation
Delayed or inadequate resuscitation results in poor perfusion to
both vital organs and the evolving burn wound itself. This can
lead to necrosis of previously viable tissue, along with progression of superficial burns to deeper injuries requiring grafting.35
A recent review of the literature demonstrates that a significant
proportion of burn injuries are resuscitated with fluid volumes
in excess of that calculated by the Parkland formula, mostly
due to the use of bolus therapy (ie, ATLS, PALS).32,36 The
development of compartment syndromes in the extremities,
torso, or abdomen has been linked to the presence of deep,
full-thickness circumferential burns and the volume of fluid
infused.37 The systemic inflammatory response associated with
larger burns leads to microcirculatory leak, vasodilatation, and
decreased cardiac output and contractility.38 Clinical suspicion
is supported by findings of delayed capillary refill, cyanosis,
paresthesias, and diminished pulses. Compartment pressures
Kasten et al
can be measured by placement of an 18-g needle connected to
an arterial pressure transducer under the eschar into the subfascial tissue. Pressures above 30 mm Hg in any compartment are
considered diagnostic. Treatment necessitates decompression
via escharotomy and/or fasciotomy by experienced practitioners. Escharotomy includes incision along the full length
of eschar with extension into viable unburned tissue, typically
using electrocautery. Fasciotomies involve the surgical opening of the full length of fascial compartments. In both cases,
a tissue bulge is often noted indicating adequate release of compartment pressure. The success of these procedures can be
quantified by measuring both prerelease and postrelease pressures using a bedside manometric device. While escharotomies
are commonly performed at the bedside using mild sedation,
fasciotomies may need to be performed in an operating room
under general anesthesia. Due to increased morbidity from
withheld, delayed, or incorrectly executed procedures, these
procedures should only be performed by experienced practitioners at the time of diagnosis.39
Abdominal distention, oliguria, and difficulties with
mechanical ventilation may signal development of an abdominal compartment syndrome (ACS). Abdominal compartment
syndrome significantly decreases perfusion to vital organs
including the small and large bowel, liver, and kidneys, contributing to the development of multisystem organ failure.25 Early
recognition of abdominal hypertension through serial bladder
pressure evaluation40 can allow for timely decompressive
laparotomy and avoidance of the sequelae caused by prolonged
tissue ischemia. Percutaneous drainage with peritoneal dialysis
catheters may be an effective alternative to laparotomy, preventing the significantly increased morbidity and mortality
related to fluid loss through an open abdomen.
Inhalation Injury
The development of pulmonary complications has been attributed to both excessive fluid resuscitation.41 and systemic
inflammation resulting in third spacing, accumulation of interstitial edema, and symptoms of ARDS.42 The presence of inhalation injury creates an increased fluid requirement, further
complicating the resuscitation and management of a disease
process predictive of respiratory failure and increased mortality.5,11,34,43-51
The lower airway, consisting of the tracheobronchial tree
and lung parenchyma, is rarely injured by heated dry air due
to reflexive vocal cord closure and the evaporative cooling
capacity of the upper airway.52,53 Inhaled toxins activate alveolar macrophages, initiating direct cellular damage54 with airway hyperemia visible shortly after injury. Inhalants also
induce an inflammatory response in the pulmonary parenchyma with disruption of surfactant synthesis and worsening lung
compliance.55 Reactive oxygen species (ROS) are molecules
synthesized by phagocytic cells such as macrophages and neutrophils that increase vascular permeability with subsequent
extrusion of fluid, increased tissue edema, formation of airway
casts, and ultimately airway obstruction.56 Loss of ciliary
227
action in the respiratory mucosa can lead to an increased
incidence of pulmonary infections.48
Diagnosis of Inhalation Injury
Closed-space burns involving steam, combustibles, hot gases
or explosions should alert the treating physician to possible airway injury. Inhalation injury may be present without evidence
of cutaneous injury. The physical exam should include inspection for soot in the oropharynx, carbonaceous sputum, singed
nasal or facial hairs, and face or neck burns. Signs of respiratory distress including wheezing, stridor, tachypnea, or hoarseness, along with altered mental status, agitation, anxiety, or
obtundation, are strongly suggestive of inhalation injury.
Patients may develop progressive respiratory failure upon completion of resuscitation, so clinical suspicion should remain elevated to allow prompt diagnosis.
As noninvasive monitoring of pulse oximetry in patients
with burn having inhalation injuries can be misleading, laboratory and invasive studies are helpful diagnostic adjuncts.
Arterial blood gas (ABG) analysis may indicate a component of
inhalation injury with a PaO2:FiO2 ratio < 300 upon completion
of resuscitation.57 Albeit controversial, this ratio has been
proposed as an indicator of poor outcome in patients with
burn.58-61 The half-life of carbon monoxide (CO) is 240 to 320
minutes, decreasing to 40 to 80 minutes with 100% normobaric
oxygen,62 so interpretation of carboxyhemoglobin values should
be correlated with elapsed time from injury and oxygen therapy
provided. If concerned, blood cyanide levels should be drawn,
carefully interpreted, and treatment initiated using amyl nitrate
perles, 10% sodium nitrite, and 25% sodium thiosulfate.63,64
Chest x-ray and computed tomography scans are insensitive
for inhalation injury diagnosis due to a relatively normal lung
and airway appearance early in the clinical course.65,66 Fiberoptic bronchoscopy is the gold standard for diagnosis as direct
visualization of the supra- and infraglottic airway allows for
quantification of hyperemia, edema, and carbonaceous material. Fiberoptic bronchoscopy can be therapeutic via removal
of excess exudate, plugs or casts, and placement of an endotracheal tube (ETT) or nasotracheal tube (NTT).67
Management of Inhalation Injury
With suspected inhalation injury, 100% oxygen should be initiated immediately with the duration of treatment dictated by
the patient’s condition and the return of the carboxyhemoglobin to normal levels, or below 10%.68,69 Vascular carboxyhemoglobin decreases much more rapidly with oxygen therapy
than carboxymyoglobin, especially in the context of continued
treatment with 100% FiO2. This is postulated to promote tissue
washout which may actually increase tissue levels of carbon
monoxide.70 Additionally, as cardiac muscle contains myoglobin, tissue washout may possibly contribute to myocardial
hypoxia.70 Because of this, we do not advocate sustained high
inspiration oxygen concentration in the treatment of CO poisoning once carboxyhemoglobin levels have normalized.
228
Figure 3. Edema associated with inhalation injury and resuscitation.
This photograph depicts facial edema due to severe inhalation injury
and burn shock resuscitation in a pediatric burn patient. Nasotracheal
intubation was performed early to prevent accidental loss of airway.
Rapid displacement of carboxyhemoglobin through hyperbaric oxygen (HBO) therapy has also been advocated due to the
neurologic sequelae related to CO poisoning. Unfortunately,
there is a paucity of evidence-based literature for HBO use with
regard to triggers for the initiation of therapy, the duration and
intensity of therapy, and the clinical benefit of such treatment.71 Additionally, the risk of complication from barotrauma
in patients with burn having suspected inhalation injury, combined with the risk of monitoring patients with severe burns
inside the chamber, likely outweighs any perceived benefit
from this therapy. Further studies are needed to fully address
the role of HBO therapy in patients with severe burns and/or
inhalation injuries.
Continuous pulse oximetry may be accurately utilized once
carboxyhemoglobin levels normalize. Inhalation injuries can
quickly progress to obstruction, hypoxia, and death, with limited ability to intubate late in the disease course, so timely
establishment of a definitive airway is required (Figure 3).
Early tracheostomy should be considered in any patient with
a projected need for mechanical ventilation longer than 2
weeks. Percutaneous tracheostomy placement in burn patients
was associated with lower complication rates and cost compared to open tracheostomy in a small, historically controlled
study.72 The question of open versus percutaneous tracheostomy is an important one and requires further exploration
through randomized controlled trials.
Patients with inhalation injury may require nonstandard
methods of ventilation such as volumetric diffusive respiratory
(VDR) and airway pressure release ventilation (APRV) modes.
Volumetric diffusive respiratory involves progressive accumulation of subtidal breaths and passive exhalation once a set airway pressure is met.73 Increased PaO2, PaO2:FiO2 ratio, and
decreased mean airway pressure have been demonstrated using
this mode, all without adversely affecting hemodynamics.73,74
This modality may also decrease the incidence of pneumonia
Journal of Intensive Care Medicine 26(4)
and mortality compared to individuals treated with conventional modes of ventilation.75-77 Airway pressure release ventilation uses high and low PEEP to provide adequate
oxygenation and recruitment of closed alveoli. Benefits include
reduced barotrauma, improved oxygenation and ventilation due
to improved V:Q matching, and decreased sedation and paralysis requirement. In those patients refractory to conventional
ventilation strategies, the use of venovenous extracorporeal
oxygenation (ECMO) is an option where available. While nonsurvivors were shown to have greater peak and mean airway
pressures prior to onset of extracorporeal life support
(ECLS).78 scattered reports throughout the literature show minimal improvement in mortality.79-81
Adjunctive therapies such as aggressive pulmonary toilet,
nitric oxide, nebulized heparin, N-acetylcysteine, and/or
bronchodilators should be considered. Inhaled nitric oxide provides variable improvement in PaO2:FiO2 ratios and survival in
patients responding to treatment.82 Therapy should be discontinued due to futility and cost if a response is not demonstrated
between doses of 5 and 20 ppm of nitric oxide within
60 minutes.82 Nebulized heparin and tissue plasminogen activator (TPA) have demonstrated potential efficacy in animal
and human studies through breakdown of fibrin deposition
associated with inhalation injury, maintenance of alveolar
structure, and reduced obstruction.83 Although survival benefit
has not clearly been demonstrated with Mucomyst use following pulmonary injury, N-acetylcysteine was noted to decrease
leukocytes in bronchoalveolar lavage.84-86 Aerosolized delivery of b2-agonists preferentially causes bronchodilation,
attenuation of lung inflammation, and may potentially improve
fluid clearance without systemic cardiac activation.87 While
corticosteroids demonstrate benefit in most chronic pulmonary
diseases, improvement in acute pulmonary inflammation secondary to inhalation injury and ARDS has not been definitively
demonstrated.68,88-90 Steroids for inhalation injury should be
used with caution until larger prospective studies are
completed.
Nutritional Support in Burns
Burns induce a hypermetabolic state that may persist for up to
12 months following injury.91,92 Many metabolic disturbances
following burn injuries are related to systemic inflammation
and altered hypothalamic function, with resultant increases in
temperature setpoint and production of catecholamines
(reviewed in93). This leads to increased protein catabolism and
lipolysis, culminating in decreased lean body mass, poor
wound healing, and weakened host defenses. Most equations
often overestimate the energy requirements of patients with
burn, with indirect calorimetry remaining the gold standard for
calculating resting energy expenditure (REE).94-100 Respiratory quotient is unreliable in evaluating the nutrition status of
patients with burn.101 Overfeeding results from excess carbohydrate or fat intake, both detrimental to the critically ill patient
with burn. Excess carbohydrate consumption increases CO2
production, fat stores, hepatic dysfunction, hyperglycemia, and
Kasten et al
wound-healing duration.57,93,102 Protein excess does not offset
hypercatabolism, and may actually increase it.102 While some
studies have demonstrated improved survival and reduced hospital stay with underfeeding of nonburned critically ill
patients,102 this strategy is harmful in patients with extensive
burn injuries. Appropriate nutrition is required for wound healing, mediation of inflammation, suppression of the hypermetabolic response, and reduction of sepsis-related morbidity and
mortality.103
Serum albumin levels are often used to monitor nutrition
status in critically ill patients. In the patient with burn, albumin
is a poor surrogate for nutritional status as serum concentrations are known to rapidly fall after burn injury. Replacement
does not stimulate production of endogenous albumin nor has
replacement demonstrated clinical benefits related to pulmonary function, wound healing, gastrointestinal function, or mortality.93 Serial measurement of prealbumin is advocated for
long-term monitoring of nutrition as it is a distinct marker for
protein synthesis, while the one-time measurement of nutritional markers such as transferrin, carotene, iron, and calcium
are unreliable indicators of nutrition status.104 Monitoring of
glucose levels remains a central part of nutritional management
in patients with burn. Hyperglycemia occurs in most patients
with burn regardless of injury severity due to an increased rate
of glucose production and impaired tissue glucose extraction.105,106 Modulation of the inflammatory response with tight
glucose control produces improved survival, sepsis control, and
wound healing.107-109 Interestingly, propranolol also aids in
restoration of glycemic control, in addition to reducing peripheral lipolysis and enhancing the immune response to sepsis via
mediation of catecholamine release during severe burn
injury.110 A retrospective review demonstrated a significant
decrease in mortality and healing time for burn patients on beta
blockade therapy prior to injury, an effect not seen when beta
blockade was initiated in the hospital following injury.111
However, in a prospective, randomized trial, decreased healing
time and hospital length of stay was demonstrated after beta
blockade initiation following injury.112 Additionally, beta
blockade in pediatric patients with burn has been associated
with decreased cardiac work, reversal of catabolism,
and attenuation of the inflammatory response without an
increased risk of infection or sepsis.113-115 These findings support the conclusion that multiple factors play a role in the metabolic response to severe burn trauma and further investigation
with randomized controlled trials is required.
Enteral and Parenteral Support
Enteral feeding is the ideal route for caloric and nutrient supplementation in patients with burn. Maintenance of gut integrity is hypothesized to reduce the risk of bacterial
translocation and subsequent sepsis.116,117 The role of specialty
amino acids, proteins, and fatty acids present in commercial
enteral formulations for pediatric patients with burn is controversial as studies have demonstrated mixed results.118,119 If
oral caloric intake will be inadequate at 5 to 7 days following
229
injury, placement of a nasoduodenal feeding tube is recommended. Initial timing of enteral nutrition after burn injury is
controversial, although most burn clinicians advocate starting
feeds within hours of injury unless contraindicated. Studies
demonstrating reversal of hypermetabolism, hypercatabolism,
and systemic inflammation in burn animals receiving early
nutrition have not been replicated in humans, possibly due to
the inability to realistically start ‘‘early’’ enteral feeding within
1 to 2 hours of burn.103 Improvement in clinical measures such
as decreased length of stay, infection, and mortality have also
not conclusively been shown when compared to later initiation
of enteral feeding (>72 hours).100 The risk of adverse events
including errors in tube placement, aspiration, and intestinal
necrosis underlies arguments to delay initiation of feeding until
burn resuscitation has been completed. In a prospective, randomized trial, Gottschlich et al found 4 out of 5 patients who
developed an abdominal catastrophe from intestinal necrosis
were in the early feeding arm of the study.103 Possible explanations include hypotensive episodes during early burn resuscitation and altered gut perfusion during burn shock, combined
with the increased intestinal blood flow demand with feeding.103 Despite some of these concerns, initiation of enteral
nutrition upon patient stabilization is considered standard of
care.
Parenteral nutrition (PN), while a mainstay of therapy for
many critically ill patients, is reserved for burn patients unable
to tolerate enteral feedings due to severe diarrhea or an organic
gastrointestinal problem. Increased complication rates in
patients with burn on PN are mostly due to central venous
catheter infections. Peripheral parenteral nutrition (PPN) is
generally not an option due to inadequate calorie delivery and
high risk of peripheral soft tissue damage from extravasation.
Vitamin and Steroid Supplementation
Vitamin A has been shown to aid wound healing following
burn injury and is replaced in patients with >20% TBSA
burns.120 Vitamin C plays a vital role in collagen synthesis and
wound healing, necessitating its supplementation. Wound exudates were found to be the primary site of loss for trace elements,121 suggesting patients with burn may require
additional supplementation compared to other critically ill
patients. The trace element zinc is necessary for wound healing, and decreased zinc levels in septic patients may be associated with subsequent adverse events.57 For these reasons, zinc
supplementation is oftentimes included in enteral nutrition formulas. More studies are needed to determine the role of trace
element supplementation in pediatric patients with burn.
Negative nitrogen balance is often seen during the first 1 to
2 weeks postburn due to hypercatabolism in burns and loss of
lean body mass.100 To combat this, the effectiveness of anabolic agents such as oxandrolone in restoration of lean body
mass, improved wound healing, improved nutritional status,
and liver function has been studied.57,122 The impact of anabolic steroids on the course of burn disease is controversial.
A few small, single center studies have been unable to
230
demonstrate any clear benefits, in contrast to a multicenter trial
stopped prematurely because of significantly fewer hospital
days for patients with severe burn treated with oxandrolone.100,123,124 More studies are needed to clarify this contentious treatment question.
Wound Care
Improperly managed burn wounds may convert to deeper
wounds requiring definitive surgical management. Cleansing
and debridement of the wound is accomplished with mild soap
and water or with chlorhexadine/normal saline washes. Most
burn experts recommend debridement of all blisters larger than
0.5 cm to reduce the risk of bacterial colonization or infection.
Burn wounds become colonized in the first few hours with
gram-positive bacteria including Staphylococcus aureus and
epidermidis and are predominantly colonized with gut flora
such as Pseudomonas aeruginosa, Enterobacter cloacae, and
Escherichia coli by 5 days. Health care workers must be vigilant in hand washing and maintenance of a clean environment
around the wounds for prevention of cross-contamination in
these immunocompromised patients. Culture swabs of all
wound beds should be obtained upon admission and repeated
serially to monitor for changes in colonization. Quantitative
cultures of the burn to diagnose wound invasion are best
obtained by tissue biopsy, either in the operating room or at
bedside. Bacterial colonization of burn wounds does not
require systemic antibiotics but should be managed with early
debridement and/or excision, together with appropriate topical
and/or biologic dressings.
Cleansing and debridement is followed by application of a
topical antimicrobial agent intended to control colonization,
not sterilize the burn wound. Several layers of absorptive gauze
and Kerlix cover the wound to decrease evaporative water
losses.125 Minor burns can be managed with biologic dressings,
silver-coated dressings, or tribiotic ointment covered with nonadherent gauze. Commonly utilized topical agents include silver sulfadiazine (Silvadene), mafenide acetate (Sulfamylon),
and silver nitrate. Silvadene continues to demonstrate effective
control of burn wound colonization, while remaining inexpensive and easy to apply. However, eschar penetration is minimal
and complications related to leukopenia and hemolysis have
been reported.126 Mafenide acetate cream (Sulfamylon) is easy
to apply but is painful when applied to superficial partialthickness burns. Eschar penetration is greatest with Sulfamylon, making it the topical agent of choice in burns where the
eschar will not be excised immediately, or when control of
Pseudomonas aeruginosa is required. Metabolic acidosis may
occur with use as Sulfamylon is a carbonic anhydrase inhibitor.
Silver nitrate 0.5% solution has fallen out of favor due to electrolyte abnormalities and poor tissue penetration but may be
used as a reasonably effective agent for treatment of gramnegative or fungal colonization.
Aside from complications directly related to topical agents,
frequent dressing changes often result in traumatized epithelialization and delayed wound healing. Silvadene has been shown
Journal of Intensive Care Medicine 26(4)
to delay wound healing due to a direct toxic effect on keratinocytes127 (reviewed in ref 128). To combat this, silverimpregnated dressings such as Acticoat, Aquacel Ag, Mepitel,
and Mepilex have been developed to provide antimicrobial
coverage, adequate humidity, and decreased trauma, all with
less frequent dressing changes. Biosynthetic substitutes like
Biobrane are marketed as epidermal substitutes that allow for
faster re-epithelialization129; however, their use is limited due
to infectious complications.
In addition to topical therapies, deep burns are managed
with surgical excision and placement of xenograft, allograft,
autograft, or cultured skin substitutes (CSS; Figure 4). Skin
substitutes and replacements require adequate wound bed preparation to ensure minimal graft loss. Most experienced burn
surgeons advocate early wound excision within the first 1 to
7 days following thermal injury to attenuate the systemic
inflammatory effects of burns and reduce the risk of sepsis.131-135 In fact, no significant difference in infection or mortality rates was found when burn excision was performed at any
point between 2 and 7 days.136 Additionally, in a comparison of
adult patients over 30 years of age sustaining greater than 30%
TBSA injury, no difference in mortality was seen between
excision within the first 72 hours and conservative management with grafting after granulation of the wound bed.137 However, this same study found significantly decreased mortality
and length of hospital stay in pediatric patients and adults aged
17 to 30 years who underwent early excision compared to conservative management.137 The appropriate timing for burn
wound excision and grafting involves a number of important
factors including the age of the patient, extent and depth of
burn, comorbidities, hospital resources, and physician preference. It is therefore important that the surgeon always assess
the risks and/or benefits of delaying surgical treatment in
burn-injured patients. At our institution, a staged approach is
often taken for more extensive injuries. The burn wound is
excised and bleeding controlled on the first operative day.
Donor site harvest and grafting then occurs on the following
operative day. This approach allows for more extensive excisions, shorter operating times, better temperature control, and
the ability to perform sheet grafting with improved hemostasis.
Definitive surgical management requires appropriate topical
antimicrobial therapy postoperatively for prevention of graft
loss and burn wound infection.
Sepsis in the Burn Patient
Improvements in resuscitation strategies and supportive care
have shifted the underlying cause of morbidity and mortality
in patients with burn from burn shock to infection. Unfortunately, sepsis is an independent risk factor of mortality following thermal injury, especially when multiorgan system failure
(MOSF) is present.138,139 Open wounds, injured lungs, central
venous catheters, and urinary catheters place the patient with
burn at constant risk of infection and sepsis. Diagnostic uncertainty due to altered physiology affecting clinical and laboratory parameters complicates therapeutic intervention. Signs
Kasten et al
231
Figure 4. Burn wounds healed with culture skin substitute (CSS). Shown is the back of a pediatric patient grafted with CSS (outlined by dashed
lines) and split-thickness skin autograft. A, At 2 weeks after grafting, the borders of the CSS were discernable but the wound was mostly closed.
B, At 10 weeks post-grafting, the healed CSS was pliable and hypopigmented observation of some pigmented foci. Reprinted from Clinics in
Dermatology, Volume 23, Dorothy M. Supp, Steven T. Boyce, Engineered skin substitutes: practices and potentials, Pages 403-412, Copyright
(2005), with permission from Elsevier.
of sepsis, including elevated temperature, tachycardia, tachypnea, and leukocytosis, may be present in the burned patient
without underlying infection. Laboratory markers including
peripheral white blood cell (WBC) levels, procalcitonin, C
reactive protein, and others have been proposed as early indicators of sepsis in the burn patient, all with mixed results.
Absolute values and trends in WBC, neutrophil percentage,
and body temperature are unable to predict bloodstream
infection in the burn patient.139 Although controversial, use
of procalcitonin level has been advocated due to its sensitivity, specificity, and mortality correlation in patients with burn
having sepsis.140 However, procalcitonin was reported insufficient as a single diagnostic marker for sepsis in patients with
burn141 and inferior to monitoring trends in CRP and platelet
count.142 As another marker, decreased Human Leukocyte
Antigen DR expression showed an inverse correlation between
and mortality in sepsis.143 Continued research is needed to
clarify the immune response to sepsis, ultimately aiding in
accurate diagnosis of infection.
Early markers of infection can alert physicians to initiate
treatment of unconfirmed but potentially fatal infections.
Breakdown of barrier function following burn injury provides
the largest entrance point for infection. Careful attention and
documentation by physicians and nursing staff of open wounds,
together with weekly or biweekly cultures, can prevent progression of superficial colonization to invasive sepsis. In addition, the topical and surgical therapies enumerated above are
first lines of care for the prevention of burn wound infections,
the most serious of which is invasive burn wound sepsis.
Pneumonia, while not as common as burn wound infection,
occurs in 4.5% of flame-injured patients and is associated with
increased days of mechanical ventilation, longer ICU stay,
and higher hospital cost.1,144 Aggressive bronchoscopy with
BAL confirms the infectious agent, provides antibiotic
sensitivity information for quick tailoring of antibiotics, and
subsequently decreases ventilator and ICU days.146 Following
recently released ABA guidelines for prevention, diagnosis
and treatment of pneumonia can reduce the complications
related to this disease process.146
Bloodstream and urinary tract infections are of constant
concern due to prolonged duration of catheter use.148 Newer
technologies have yielded silver-impregnated, chlorhexadine/
silver sulfadiazine coated, and antibiotic-coated catheters targeted to reduce catheter infection.149,150 Unfortunately, the
ability of antiseptic/antibiotic impregnated catheters to prevent
bloodstream infection was found to have no effect beyond that
of a comprehensive education strategy involving proper evaluation and maintenance of indwelling catheters.151 Timing
of central access exchange in the patient with burn is determined by the risk of colonization, need for placement through
burned versus unburned tissue, and physician preference.152
Prompt removal of all indwelling catheters when no longer
warranted provides the best prevention for infection in the
patient with burn. Blood and urinary tract infections are treated
with removal of the catheter whenever possible and appropriately tailored antibiotic therapy.
232
Conclusion
Dedication and research over the past 5 decades has produced
an enviable reduction in mortality for burn-injured patients
treated in the United States. With appropriate and tailored
resuscitation regimens, early enteral nutrition, quick and effective management of the burn wound with topical and surgical
therapies, the severely injured burn patient can not only survive
but experience minimal short and long-term morbidities. Success in these areas involves a multidisciplinary team trained
in current state-of-the-art interventions and therapies, with ultimate goal of restoring function and allowing psychosocial
reintegration.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interests with respect
to the authorship and/or publication of this article.
Funding
The author(s) received no financial support for the research and/or
authorship of this article.
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