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http://jic.sagepub.com/Journal of Intensive Care Medicine

http://jic.sagepub.com/content/26/4/223Theonline version of this article can be found at:

DOI: 10.1177/0885066610390869

2011 26: 223J Intensive Care Med

Kevin R. Kasten, Amy T. Makley and Richard J. KaganUpdate on the Critical Care Management of Severe Burns

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Update on the Critical CareManagement of Severe Burns

Kevin R. Kasten, MD1

, Amy T. Makley, MD1

, andRichard J. Kagan, MD, FACS1,2

Abstract

Care of the severely injured patient with burn requires correct diagnosis, appropriately tailored resuscitation, and definitivesurgical 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. Promptand 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 fluidtypes have yielded demonstrable benefits related to all aspects of burn care. More recently, identification of comorbid con-

ditions such as inhalation injury and malnutrition have produced appropriate protocols that aid the healing process in severelyinjured patients with burn. As more patients survive larger burn injuries, the early diagnosis and successful treatment of sec-ondary and tertiary complications are becoming commonplace. While advances in this area are exciting, much work to elu-

cidate immune pathways, diagnostic tests, and effective treatment regimens still remain. This review will provide an update onthe 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

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 surgi-

cal treatment can minimize morbidity and mortality rates,5

especially when treatment occurs in one of the 125 hospitalswith 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 outpati-

ent, appropriate knowledge of burn shock and resuscitation,

nutrition requirements, and wound care will aid the clinician

in the management of the patient.

Evaluation of the Burn Wound

The skin is composed of 2 distinct layers and provides protec-

tion against fluid loss, mechanical damage, and infection. The

epidermis consists of keratinocytes, melanocytes, and

Langerhans cells, while the dermis consists of structural pro-

teins and cells responsible for tensile strength.10 Blood vessels,

hair follicles, and sweat glands are rooted in the dermis. Preser-

vation 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 ofburn and duration of exposure to the heat source. Scald burns

are associated with a robust pro-inflammatory response leading

1 Department of Surgery, University of Cincinnati, Cincinnati, OH, USA2 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]

Journal of Intensive Care Medicine

26(4) 223-236

The Author(s) 2011

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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 compart-

ment syndrome due to muscle necrosis. Regardless of mechan-

ism, 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 fol-

lowing 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, wet-appearing, 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 partial-

thickness burns merit distinction because deep partial-

thickness 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 typi-

cally insensate from superficial nerve injury.

The calculated% TBSA is an independent risk factor corre-

lating 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 patients hand

to estimate 1% of normal body surface area are methods for

burn size estimation.15 The rule of nines is a rough estima-

tion of adult body surface area which often overestimates burn

size in children, supporting the need for age-specific body surfacearea charts such as the Lund Browder diagram.16 (Figure 2).

Newer methods to calculateburn surfacearea using computerized

imaging, 2- and 3-dimensional graphics, and body contour repro-

ductions 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

Figure 1. Schematic view of increased LA50over time.A representation of the developments in burn care over the past 70 years thathave allowed for a steady increase in total body surface area (TBSA) burn size from which 50% of patients will survive.

224 Journal of Intensive Care Medicine 26(4)



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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 min-

imum 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 tai-

lored evaluation given the propensity for compartment syn-

drome, 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 com-

plicated 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

Figure 2. Shriners Hospitals for Children Burn Diagram (Lund-Browder). This adaptation of the Lund-Browder diagram is utilized in ourhospital for estimation of depth and extent of burn in the acute patient.

Kasten et al 225



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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 pro-

phylaxis, 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 includesthe 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 for-

mula used, all rely on accurate assessment of extent and depth

of burn and prompt tailoring of the infusion rate to the individ-

ual patient. Resuscitation should be titrated to clinical end-

points 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 custo-

marily involves cardiac monitoring, continuous pulse oxime-

try, 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, bothdemonstrating results comparable to invasive techniques.30

To help avoid the complications of inadequate or excessive

resuscitation, current research is examining the utility and effi-

cacy 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 crys-

talloid and total fluid compared to resuscitation with crystalloid

only.33 However, recent evidence demonstrates colloid resusci-

tation does not affect mortality and is more expensive thancrystalloid solutions.34 The theoretical reduction in complica-

tions and mortality from colloid use has not been proven in pro-

spective 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 progres-

sion of superficial burns to deeper injuries requiring grafting.35

A recent review of the literature demonstrates that a significantproportion 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

Table 1. Estimated Fluid Resuscitation Requirements for a 12 Year Old Child with 25% Total Body Surface Area Scald Burns. Hourly fluidadministration is guided by the response to treatmenta

Shriners HospitalCincinnati Parkland Formula Modified Brooke Formula

First 8 Hours Second 16 Hours First 8 Hours Second 16 Hours First 8 hours Second 16 Hours

3550 cc/LR 3550 cc/LR 2500 cc/LR 2500 cc/LR 1250 cc/LR 1250 cc/LR

443.8 cc/h 221.9 cc/hr 312.5 cc/h 156.3 cc/h 156.3 cc/h 78.1 cc/ha 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 oxygensaturation of 94% on room air. The following are indicated resuscitation regimens, all titrated based on the patients urine output.




6/15

can be measured by placement of an 18-g needle connected to

an arterial pressure transducer under the eschar into the subfas-

cial tissue. Pressures above 30 mm Hg in any compartment are

considered diagnostic. Treatment necessitates decompression

via escharotomy and/or fasciotomy by experienced practi-

tioners. Escharotomy includes incision along the full length

of eschar with extension into viable unburned tissue, typicallyusing electrocautery. Fasciotomies involve the surgical open-

ing of the full length of fascial compartments. In both cases,

a tissue bulge is often noted indicating adequate release of com-

partment pressure. The success of these procedures can be

quantified by measuring both prerelease and postrelease pres-

sures 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 practi-

tioners at the time of diagnosis.39

Abdominal distention, oliguria, and difficulties withmechanical ventilation may signal development of an abdom-

inal compartment syndrome (ACS). Abdominal compartment

syndrome significantly decreases perfusion to vital organs

including the small and large bowel, liver, and kidneys, contri-

buting 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, pre-

venting the significantly increased morbidity and mortality

related to fluid loss through an open abdomen.

Inhalation Injury

The development of pulmonary complications has been attrib-

uted to both excessive fluid resuscitation.41 and systemic

inflammation resulting in third spacing, accumulation of inter-

stitial edema, and symptoms of ARDS.42 The presence of inha-

lation injury creates an increased fluid requirement, further

complicating the resuscitation and management of a disease

process predictive of respiratory failure and increased mortal-

ity.5,11,34,43-51

The lower airway, consisting of the tracheobronchial tree

and lung parenchyma, is rarely injured by heated dry air dueto reflexive vocal cord closure and the evaporative cooling

capacity of the upper airway.52,53 Inhaled toxins activate alveo-

lar macrophages, initiating direct cellular damage54 with air-

way hyperemia visible shortly after injury. Inhalants also

induce an inflammatory response in the pulmonary parench-

yma with disruption of surfactant synthesis and worsening lung

compliance.55 Reactive oxygen species (ROS) are molecules

synthesized by phagocytic cells such as macrophages and neu-

trophils that increase vascular permeability with subsequent

extrusion of fluid, increased tissue edema, formation of airway

casts, and ultimately airway obstruction.56 Loss of ciliary

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 air-way injury. Inhalation injury may be present without evidence

of cutaneous injury. The physical exam should include inspec-

tion for soot in the oropharynx, carbonaceous sputum, singed

nasal or facial hairs, and face or neck burns. Signs of respira-

tory distress including wheezing, stridor, tachypnea, or hoarse-

ness, along with altered mental status, agitation, anxiety, or

obtundation, are strongly suggestive of inhalation injury.

Patients may develop progressive respiratory failure upon com-

pletion of resuscitation, so clinical suspicion should remain ele-

vated to allow prompt diagnosis.

As noninvasive monitoring of pulse oximetry in patients

with burn having inhalation injuries can be misleading, labora-

tory and invasive studies are helpful diagnostic adjuncts.Arterial blood gas (ABG) analysis may indicate a component of

inhalation injury with a PaO2:FiO2ratio < 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

Fiber-

optic bronchoscopy is the gold standard for diagnosis as direct

visualization of the supra- and infraglottic airway allows for

quantification of hyperemia, edema, and carbonaceous mate-

rial. Fiberoptic bronchoscopy can be therapeutic via removal

of excess exudate, plugs or casts, and placement of an endotra-

cheal tube (ETT) or nasotracheal tube (NTT).67

Management of Inhalation Injury

With suspected inhalation injury, 100% oxygen should be ini-

tiated immediately with the duration of treatment dictated bythe patients condition and the return of the carboxyhemoglo-

bin to normal levels, or below 10%.68,69 Vascular carboxyhe-

moglobin 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 myoglo-

bin, 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 poi-

soning once carboxyhemoglobin levels have normalized.

Kasten et al 227



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Rapid displacement of carboxyhemoglobin through hyper-

baric 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 treat-

ment.71 Additionally, the risk of complication from barotrauma

in patients with burn having suspected inhalation injury, com-

bined 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 lim-

ited 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 com-

pared to open tracheostomy in a small, historically controlled

study.72

The question of open versus percutaneous tracheost-omy 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 accumu-

lation of subtidal breaths and passive exhalation once a set air-

way 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

and mortality compared to individuals treated with conven-

tional modes of ventilation.75-77 Airway pressure release venti-

lation 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 paraly-

sis requirement. In those patients refractory to conventionalventilation strategies, the use of venovenous extracorporeal

oxygenation (ECMO) is an option where available. While non-

survivors 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 min-

imal 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 pro-

vides variable improvement in PaO2:FiO2ratios and survival in

patients responding to treatment.82 Therapy should be discon-

tinued due to futility and cost if a response is not demonstrated

between doses of 5 and 20 ppm of nitric oxide within60 minutes.82 Nebulized heparin and tissue plasminogen acti-

vator (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 follow-

ing pulmonary injury, N-acetylcysteine was noted to decrease

leukocytes in bronchoalveolar lavage.84-86 Aerosolized deliv-

ery 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 sec-

ondary 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 Respira-

tory quotient is unreliable in evaluating the nutrition status of

patients with burn.101 Overfeeding results from excess carbo-

hydrate or fat intake, both detrimental to the critically ill patient

with burn. Excess carbohydrate consumption increases CO2production, fat stores, hepatic dysfunction, hyperglycemia, and

Figure 3. Edema associated with inhalation injury and resuscitation.This photograph depicts facial edema due to severe inhalation injuryand burn shock resuscitation in a pediatric burn patient. Nasotrachealintubation was performed early to prevent accidental loss of airway.




8/15

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 hos-

pital 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 heal-

ing, mediation of inflammation, suppression of the hypermeta-bolic 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 concentra-

tions are known to rapidly fall after burn injury. Replacement

does not stimulate production of endogenous albumin nor has

replacement demonstrated clinical benefits related to pulmon-

ary function, wound healing, gastrointestinal function, or mor-

tality.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 nutri-

tional markers such as transferrin, carotene, iron, and calciumare 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 extrac-

tion.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 periph-

eral 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 sup-

port the conclusion that multiple factors play a role in the meta-

bolic 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 sup-

plementation in patients with burn. Maintenance of gut integ-

rity 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 contro-

versial as studies have demonstrated mixed results.118,119 If

oral caloric intake will be inadequate at 5 to 7 days following

injury, placement of a nasoduodenal feeding tube is recom-

mended. 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 tothe 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, rando-

mized 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 explana-

tions include hypotensive episodes during early burn resuscita-

tion and altered gut perfusion during burn shock, combinedwith the increased intestinal blood flow demand with feed-

ing.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 exu-

dates were found to be the primary site of loss for trace ele-

ments,121 suggesting patients with burn may require

additional supplementation compared to other critically ill

patients. The trace element zinc is necessary for wound heal-

ing, and decreased zinc levels in septic patients may be associ-

ated with subsequent adverse events.57

For these reasons, zincsupplementation is oftentimes included in enteral nutrition for-

mulas. 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 ana-

bolic 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 ana-

bolic steroids on the course of burn disease is controversial.

A few small, single center studies have been unable to

Kasten et al 229



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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 oxandro-

lone.100,123,124 More studies are needed to clarify this conten-

tious 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 vigi-

lant in hand washing and maintenance of a clean environmentaround 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 non-

adherent gauze. Commonly utilized topical agents include sil-

ver sulfadiazine (Silvadene), mafenide acetate (Sulfamylon),

and silver nitrate. Silvadene continues to demonstrate effective

control of burn wound colonization, while remaining inexpen-

sive 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 partial-

thickness burns. Eschar penetration is greatest with Sulfamy-lon, making it the topical agent of choice in burns where the

eschar will not be excised immediately, or when control of

Pseudomonas aeruginosais 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 elec-

trolyte abnormalities and poor tissue penetration but may be

used as a reasonably effective agent for treatment of gram-

negative or fungal colonization.

Aside from complications directly related to topical agents,

frequent dressing changes often result in traumatized epithelia-

lization and delayed wound healing. Silvadene has been shown

to delay wound healing due to a direct toxic effect on keratino-

cytes127 (reviewed in ref 128). To combat this, silver-

impregnated 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 forfaster 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 pre-

paration 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 sep-

sis.131-135 In fact, no significant difference in infection or mor-

tality rates was found when burn excision was performed at any

point between 2 and 7 days.136 Additionally, in a comparison ofadult 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 manage-

ment with grafting after granulation of the wound bed.137 How-

ever, 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 con-

servative 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 prefer-

ence. 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 exci-

sions, 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. Unfortu-

nately, sepsis is an independent risk factor of mortality follow-

ing 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 uncer-

tainty due to altered physiology affecting clinical and labora-

tory parameters complicates therapeutic intervention. Signs




10/15

of sepsis, including elevated temperature, tachycardia, tachyp-

nea, 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 indi-

cators 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 sensitiv-

ity, specificity, and mortality correlation in patients with burn

having sepsis.140 However, procalcitonin was reported insuffi-

cient 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 toclarify 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 pro-

gression of superficial colonization to invasive sepsis. In addi-

tion, 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 tar-

geted to reduce catheter infection.149,150 Unfortunately, the

ability of antiseptic/antibiotic impregnated catheters to preventbloodstream infection was found to have no effect beyond that

of a comprehensive education strategy involving proper eva-

luation and maintenance of indwelling catheters.151 Timing

of central access exchange in the patient with burn is deter-

mined 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 appropri-

ately tailored antibiotic therapy.

Figure 4.Burn wounds healed with culture skin substitute (CSS). Shown is the back of a pediatric patient grafted with CSS (outlined by dashedlines) 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 inDermatology, Volume 23, Dorothy M. Supp, Steven T. Boyce, Engineered skin substitutes: practices and potentials, Pages 403-412, Copyright(2005), with permission from Elsevier.

Kasten et al 231



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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 effec-

tive management of the burn wound with topical and surgical

therapies, the severely injured burn patient can not only survivebut experience minimal short and long-term morbidities. Suc-

cess in these areas involves a multidisciplinary team trained

in current state-of-the-art interventions and therapies, with ulti-

mate 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.

FundingThe author(s) received no financial support for the research and/or

authorship of this article.

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