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CHAPTER 19  

Burns
Marc G. Jeschke, David N. Herndon

OUTLINE
Etiology of Burn Injury
Pathophysiology of Burn Injury
Basic Treatment of Burn Injury
Specific Treatment of Burns
Attenuation of the Hypermetabolic Response
Special Considerations: Electrical and Chemical Burns
Outcomes
Burn Units
Summary

More than 500,000 burn injuries occur annually in the United prevention strategies. Overall, no single group is immune to the
States.1 Although most of these burn injuries are minor, approxi- public health debt caused by burns.
mately 40,000 to 60,000 burn patients require admission to a Location plays a major role in the risk for and treatment of a
hospital or major burn center for appropriate treatment. The burn. The available resources in a given community greatly influ-
devastating consequences of burns have been recognized by the ence morbidity and mortality. A lack of adequate resources affects
medical community and significant amounts of resources and the education, rehabilitation, and survival rates for burn victims.
research have been dedicated, successfully improving these dismal An individual with a severe burn in a resource-rich environment
statistics.2 Specialized burn centers (Box 19-1) and advances in can receive care within minutes, whereas a burned person in an
therapy strategies, based on improved understanding of resuscita- austere environment may suffer for an extended time waiting for
tion, enhanced wound coverage, more appropriate infection care. Ideal treatment of burns requires the collaboration of sur-
control, improved treatment of inhalation injury, and better geons, anesthesiologists, occupational therapists and physiothera-
support of the hypermetabolic response to injury, have further pists, nurses, nutritionists, rehabilitation therapists, and social
improved the clinical outcome of this unique population of workers just to accommodate the very basic needs of a major burn
patients during the past years.3,4 However, severe burns remain a survivor.10 Any delay in reaching these resources compounds a
devastating injury affecting nearly every organ system and leading delay in resuscitation and thus adds to the mortality risk.11 For
to significant morbidity and mortality.5,6 those who have access to adequate burn care, survival from a
major burn is the rule, no longer the exception. In fact, the sur-
vival rate for all burns is 94.6%, but for at-risk populations, in
communities lacking medical, legal, and public health resources,
ETIOLOGY OF BURN INJURY survival can be nearly impossible.8
There is no greater trauma than major burn injury, which can be
classified according to different burn causes and different depths
(Box 19-2). Of all cases, nearly 4000 people die of complications PATHOPHYSIOLOGY OF BURN INJURY
related to thermal injury.7 As in all trauma-related deaths, burn
deaths generally occur either immediately after the injury or weeks Local Changes
later as a result of multisystem organ failure. Sixty-six percent of Locally, thermal injury causes coagulative necrosis of the epider-
all burns occur at home, and fatalities are predominant in the mis and underlying tissues; the depth of injury depends on the
extremes of age—the very young and the elderly. The most temperature to which the skin is exposed, the specific heat of the
common causes of burn are flame and scald burns.8 Scald burns causative agent, and the duration of exposure. Burns are classified
are most common in children up to 5 years of age.8 There is a into five different causal categories and depths of injury. The
significant percentage of burns in children that are due to child causes include injury from flame (fire), hot liquids (scald), contact
abuse. A number of risk factors have been linked to burn injury, with hot or cold objects, chemical exposure, and conduction of
specifically age, location, demographics, and low economic status.9 electricity (Box 19-2). The first three induce cellular damage
These risk factors underscore the fact that most burn injuries by the transfer of energy, which induces coagulation necrosis.
and fatalities are preventable and mandate intervention and Chemical burns and electrical burns cause direct injury to cellular

505
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506 SECTION III  Trauma and Critical Care

membranes in addition to the transfer of heat and can cause a area immediately surrounding the necrotic zone has a moderate
coagulation or colliquation necrosis. degree of insult with decreased tissue perfusion. This is termed
The skin, which is the largest organ of the human body, pro- the zone of stasis and, depending on the wound environment, can
vides a staunch barrier in the transfer of energy to deeper tissues, either survive or go on to coagulative necrosis. The zone of stasis
thus confining much of the injury to this layer. Once the inciting is associated with vascular damage and vessel leakage. Thrombox-
focus is removed, however, the response of local tissues can lead ane A2, a potent vasoconstrictor, is present in high concentrations
to injury in the deeper layers. The area of cutaneous or superficial in burn wounds, and local application of inhibitors improves
injury has been divided into three zones: zone of coagulation, zone blood flow and decreases the zone of stasis. Antioxidants, brady-
of stasis, and zone of hyperemia (Fig. 19-1). The necrotic area of kinin antagonists, and subatmospheric wound pressures also
burn where cells have been disrupted is termed the zone of coagula- improve blood flow and affect the depth of injury. Local endo-
tion. This tissue is irreversibly damaged at the time of injury. The thelial interactions with neutrophils mediate some of the local
inflammatory responses associated with the zone of stasis. Treat-
ment directed at the control of local inflammation immediately
BOX 19-1  Burn Unit Organization and after injury may spare the zone of stasis, indicated by studies
Personnel demonstrating the blockage of leukocyte adherence with anti-
CD18 or anti-intercellular adhesion molecules; monoclonal anti-
Experienced burn surgeons (burn unit director and qualified surgeons)
bodies improve tissue perfusion and tissue survival in animal
Dedicated nursing personnel
models. The last area is the zone of hyperemia, which is character-
Physical and occupational therapists
ized by vasodilation from inflammation surrounding the burn
Social workers
wound. This region contains the clearly viable tissue from which
Dietitians
the healing process begins and is generally not at risk for further
Pharmacists
necrosis.
Respiratory therapists
Psychiatrists and clinical psychologists Burn Depth
Prosthetists
The depth of burn varies by the degree of tissue damage. Burn
depth is classified into degree of injury in the epidermis, dermis,
subcutaneous fat, and underlying structures (Fig. 19-2).
BOX 19-2  Burn Classifications First-degree burns are, by definition, injuries confined to the
epidermis. First-degree burns are painful and erythematous and
Causes
blanch to the touch with an intact epidermal barrier. Examples
Flame: damage from superheated, oxidized air
include sunburn or a minor scald from a kitchen accident. These
Scald: damage from contact with hot liquids
burns do not result in scarring, and treatment is aimed at comfort
Contact: damage from contact with hot or cold solid materials
with the use of topical soothing salves with or without aloe and
Chemicals: contact with noxious chemicals
oral nonsteroidal anti-inflammatory agents.
Electricity: conduction of electrical current through tissues
Second-degree burns are divided into two types: superficial and
Depths deep. All second-degree burns have some degree of dermal damage,
First degree: injury localized to the epidermis by definition, and the division is based on the depth of injury into
Superficial second degree: injury to the epidermis and superficial dermis the dermis. Superficial dermal burns are erythematous and painful,
Deep second degree: injury through the epidermis and deep into the dermis blanch to touch, and often blister. Examples include scald injuries
Third degree: full-thickness injury through the epidermis and dermis into from overheated bathtub water and flash flame burns. These
subcutaneous fat wounds spontaneously re-epithelialize from retained epidermal
Fourth degree: injury through the skin and subcutaneous fat into underlying structures in the rete ridges, hair follicles, and sweat glands in 1
muscle or bone to 2 weeks. After healing, these burns may have some slight skin
discoloration in the long term. Deep dermal burns into the

Epidermis
Zone of
coagulation

Zone of
stasis

Dermis
Zone of
hyperemia

FIGURE 19-1  Zones of Injury after a Burn. The zone of coagulation is the portion irreversibly injured.
The zones of stasis and hyperemia are defined in response to the injury.

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CHAPTER 19  Burns 507

First degree 9%
Epidermis Adult body % of total
Superficial 1%
second degree Part BSA
Front
Arm 9% 18%
Dermis
Deep
second degree Head 9%
9% 9%
Back
Neck 1% 18%
Subcutaneous fat
Third degree
Leg 18%

18% 18%
Muscle Anterior trunk 18%
Fourth degree
Posterior trunk 18%
FIGURE 19-2  Depths of a Burn. First-degree burns are confined to
the epidermis. Second-degree burns extend into the dermis (dermal
burns). Third-degree burns are “full thickness” through the epidermis
and dermis. Fourth-degree burns involve injury to underlying tissue
structures, such as muscle, tendons, and bone.

reticular dermis appear more pale and mottled, do not blanch to


touch, but remain painful to pinprick. These burns heal in 2 to Child body % of total
5 weeks by re-epithelialization from hair follicles and sweat gland 18%
keratinocytes, often with severe scarring as a result of the loss of Part BSA
dermis. Front
Third-degree burns are full thickness through the epidermis 18%
9% 9% Arm 9%
and dermis and are characterized by a hard, leathery eschar Back
that is painless and black, white, or cherry red. No epidermal or 18% Head and neck 18%
dermal appendages remain; thus, these wounds must heal by
re-epithelialization from the wound edges. Deep dermal and full- Leg 14%
thickness burns require excision with skin grafting from the 14% 14%
patient to heal the wounds in a timely fashion. Anterior trunk 18%
Fourth-degree burns involve other organs beneath the skin,
such as muscle, bone, and brain. Posterior trunk 18%
Currently, burn depth is most accurately assessed by judgment
of experienced practitioners. Accurate depth determination is FIGURE 19-3  Estimation of burn size using the rule of nines. BSA,
critical to wound healing as wounds that will heal with local treat- body surface area. (From Advanced Burn Life Support Provider Manual,
ment are treated differently from those requiring operative inter- Chicago, IL, 2005, American Burn Association.)
vention. Examination of the entire wound by the physicians
ultimately responsible for their management then is the “gold the wound for a determination of its size. This method is crucial
standard” used to guide further treatment decisions. New tech- in evaluating burns of mixed distribution.
nologies, such as the multisensor laser Doppler flowmeter, hold Children have a relatively larger portion of the body surface
promise for quantitative determination of burn depth. Several area in the head and neck, which is compensated for by a relatively
reports claim superiority of this method over clinical judgment in smaller surface area in the lower extremities. Infants have 21% of
the determination of wounds requiring skin grafting for timely the TBSA in the head and neck and 13% in each leg, which
healing, which may lead to a change in the standard of care in the incrementally approaches the adult proportions with increasing
near future. age. The Berkow formula is used to accurately determine burn
size in children (Table 19-1).
Burn Size
Determination of burn size estimates the extent of injury. Burn size Systemic Changes
is generally assessed by the “rule of nines” (Fig. 19-3). In adults, Severe burns covering more than 20% TBSA in adults and 40%
each upper extremity and the head and neck are 9% of the total TBSA in pediatric patients are typically followed by a period of
body surface area (TBSA), the lower extremities and the anterior stress, inflammation, and hypermetabolism, characterized by a
and posterior trunk are 18% each, and the perineum and genitalia hyperdynamic circulatory response with increased body tempera-
are assumed to be 1% of the TBSA. Another method of estimating ture, glycolysis, proteolysis, lipolysis, and futile substrate cycling
smaller burns is to equate the area of the open hand (including the (Fig. 19-4). These responses are present in all trauma, surgical,
palm and the extended fingers) of the patient to be approximately and critically ill patients, but the severity, length, and magnitude
1% TBSA and then to transpose that measurement visually onto are unique for burn patients.5

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508 SECTION III  Trauma and Critical Care

TABLE 19-1  Berkow Formula to Estimate Burn Size (%) Based on Area of Burn in an Isolated
Body Part*
BODY PART 0-1 YEARS 1-4 YEARS 5-9 YEARS 10-14 YEARS 15-18 YEARS ADULT
Head 19 17 13 11 9 7
Neck 2 2 2 2 2 2
Anterior trunk 13 13 13 13 13 13
Posterior trunk 13 13 13 13 13 13
Right buttock 2.5 2.5 2.5 2.5 2.5 2.5
Left buttock 2.5 2.5 2.5 2.5 2.5 2.5
Genitalia 1 1 1 1 1 1
Right upper arm 4 4 4 4 4 4
Left upper arm 4 4 4 4 4 4
Right lower arm 3 3 3 3 3 3
Left lower arm 3 3 3 3 3 3
Right hand 2.5 2.5 2.5 2.5 2.5 2.5
Left hand 2.5 2.5 2.5 2.5 2.5 2.5
Right thigh 5.5 6.5 8 8.5 9 9.5
Left thigh 5.5 6.5 8 8.5 9 9.5
Right leg 5 5 5.5 6 6.5 7
Left leg 5 5 5.5 6 6.5 7
Right foot 3.5 3.5 3.5 3.5 3.5 3.5
Left foot 3.5 3.5 3.5 3.5 3.5 3.5
*Estimates are made, recorded, and then summed to gain an accurate estimate of the body surface area burned.

Vascular permeability
and edema Altered hemodynamics

Immunosuppression Severe burn Hypermetabolism

Decreased renal blood flow Increased gut mucosal


permeability

FIGURE 19-4  Systemic effects of a severe burn.

Hypermetabolic Response to Burn Injury decreases in cardiac output, oxygen consumption, and metabolic
Marked and sustained increases in catecholamine, glucocorticoid, rate as well as impaired glucose tolerance associated with its hyper-
glucagon, and dopamine secretion are thought to initiate the glycemic state. These metabolic variables gradually increase within
cascade of events leading to the acute hypermetabolic response the first 5 days after injury to a plateau phase (called the flow
with its ensuing catabolic state.12 The cause of this complex phase), characteristically associated with hyperdynamic circula-
response is not well understood. However, interleukins 1 and tion and the hypermetabolic state.12,14 Insulin release during this
6, platelet-activating factor, tumor necrosis factor, endotoxin, time was found to be twice that of controls in response to glucose
neutrophil adherence complexes, reactive oxygen species, nitric load,15 and plasma glucose levels are markedly elevated, indicating
oxide, and coagulation as well as complement cascades have the development of an insulin resistance.15 Current understanding
also been implicated in regulating this response to burn injury.13 has been that these metabolic alterations resolve soon after com-
Once these cascades are initiated, their mediators and byproducts plete wound closure. However, studies found that the hypermeta-
appear to stimulate the persistent and increased metabolic rate bolic response to burn injury may last for more than 12 months
associated with altered glucose metabolism seen after severe burn after the initial event.16 We found that sustained hypermetabolic
injury.13 alterations after a burn, indicated by persistent elevations of total
The postburn metabolic phenomena occur in a timely manner, urine cortisol levels, serum cytokines, catecholamines, and basal
suggesting two distinct patterns of metabolic regulation after energy requirements, were accompanied by impaired glucose
injury. The first phase occurs within the first 48 hours of injury metabolism and insulin sensitivity that persisted for up to 3 years
and has classically been called the ebb phase, characterized by after the initial burn injury.16

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CHAPTER 19  Burns 509

A 10-fold to 50-fold elevation of plasma catecholamines and burn wound to support the relatively inefficient anaerobic metabo-
corticosteroid levels occurs in major burns that persists up to 3 lism of fibroblasts and endothelial and inflammatory cells. The end
years after injury.5,14,16 Cytokine levels peak immediately after product of anaerobic glucose oxidation—lactate—is recycled to the
burn injury, approaching normal levels only after 1 month. Con- liver to produce more glucose through gluconeogenic pathways.5
stitutive and acute-phase proteins are altered beginning 5 to 7 Serum glucose and serum insulin increase after burn injury and
days after burn injury and remain abnormal throughout the acute remain significantly increased through the acute hospital stay.
hospital stay. Serum insulin-like growth factor I (IGF-I), IGF- Insulin resistance appears during the first week after burn injury
binding protein 3 (IGFBP-3), parathyroid hormone, and osteo- and persists significantly after discharge up to 3 years.14,16
calcin drop immediately after the burn injury 10-fold and remain Septic patients have a profound increase in metabolic rates and
significantly decreased up to 6 months compared with normal protein catabolism up to 40% more compared with those with
levels.14 Sex hormones and endogenous growth hormone levels like-size burns who do not develop sepsis.18,19 A vicious circle
decrease around 3 weeks after a burn injury (Fig. 19-5).14 develops, as patients who are catabolic are more susceptible to
For severely burned patients, the resting metabolic rate at sepsis because of changes in immune function and immune
thermal neutral temperature (30° C) exceeds 140% of normal at response. The emergence of multidrug-resistant organisms has led
admission and is reduced to 130% once the wounds are fully to increases in sepsis, catabolism, and mortality (Fig. 19-8). Mod-
healed, then to 120% at 6 months and 110% at 12 months after ulation of the hypermetabolic, hypercatabolic response, thus pre-
burn injury.14 Increases in catabolism result in loss of total body venting secondary injury, is paramount in the restoration of
protein, decreased immune defenses, and decreased wound structure and function of severely burned patients.
healing.5,14
Immediately after a burn injury, patients have low cardiac Inflammation and Edema
output characteristic of early shock. However, 3 to 4 days after Significant burns are associated with massive release of inflamma-
the burn injury, cardiac output is more than 1.5 times that of tory mediators, both in the wound and in other tissues. These
nonburned, healthy volunteers.14 The heart rate of pediatric burn mediators produce vasoconstriction and vasodilation, increased
patients approaches 1.6 times that of nonburned, healthy volun- capillary permeability, and edema locally and in distant organs.
teers.12 After a burn injury, patients have increased cardiac work.5 The generalized edema is in response to changes in Starling forces
Myocardial oxygen consumption surpasses that of marathon in both burned and unburned skin. Initially, the interstitial hydro-
runners and is sustained well into the rehabilitative period. static pressures in the burned skin decrease, and there is an associ-
There is profound hepatomegaly after injury. The liver increases ated increase in nonburned skin interstitial pressures. As the
its size by 225% of normal by 2 weeks after burn injury and plasma oncotic pressures decrease and interstitial oncotic pressures
remains enlarged at discharge by 200% of normal.14 increase as a result of increased capillary permeability–induced
After burn injury, muscle protein is degraded much faster than protein loss, edema forms in the burned and nonburned tissues.
it is synthesized.17 Net protein loss leads to loss of lean body mass The edema is greater in the burned tissues because of lower inter-
and severe muscle wasting, leading to decreased strength and stitial pressures.
failure to fully rehabilitate. Significant decreases in lean body mass Many mediators have been proposed to account for the changes
related to chronic illness or hypermetabolism can have dire con- in permeability after burn injury, including histamine, bradyki-
sequences. A 10% loss of lean body mass is associated with nin, vasoactive amines, prostaglandins, leukotrienes, activated
immune dysfunction. A 20% loss of lean body mass positively complement, and catecholamines, among others. Mast cells in the
correlates with decreased wound healing. A loss of 30% of lean burned skin release histamine in large quantities immediately after
body mass leads to increased risk for pneumonia and pressure injury, which elicits a characteristic response in venules by increas-
sores. A 40% loss of lean body mass can lead to death. Uncom- ing intercellular junction space formation. The use of antihista-
plicated severely burned patients can lose up to 25% of total body mines in the treatment of burn edema, however, has had limited
mass after acute burn injury.14 Protein degradation persists up to success. In addition, aggregated platelets release serotonin to play
nearly 1 year after severe burn injury, resulting in significant nega- a major role in edema formation. This agent acts directly to
tive whole body and cross-leg nitrogen balance (Fig. 19-6).5 increase pulmonary vascular resistance, and it indirectly aggravates
Protein catabolism has a positive correlation with increases in the vasoconstrictive effects of various vasoactive amines. Serotonin
metabolic rates. Severely burned patients have a daily nitrogen blockade improves cardiac index, decreases pulmonary artery
loss of 20 to 25 g/m2 of burned skin.5 At this rate, a lethal cachexia pressure, and decreases oxygen consumption after burn injury.
can be reached in less than 1 month. The protein loss of burned When the antiserotonin methysergide was given to animals after
pediatric patients leads to significant growth retardation for up to scald injury, wound edema formation decreased as a result of local
24 months after injury.16 effects.
Elevated circulating levels of catecholamines, glucagon, and Another mediator likely to play a role in changes in permeabil-
cortisol after severe thermal injury stimulate free fatty acids and ity and fluid shifts is thromboxane A2. Thromboxane increases
glycerol from fat, glucose production by the liver, and amino acids dramatically in the plasma and wounds of burned patients. This
from muscle (Fig. 19-7).5,12 Specifically, glycolytic-gluconeogenetic potent vasoconstrictor leads to vasoconstriction and platelet
cycling is increased 250% during the postburn hypermetabolic aggregation in the wound, contributing to expansion of the zone
response coupled with an increase of 450% in triglyceride–fatty of stasis. It also caused prominent mesenteric vasoconstriction and
acid cycling.5 These changes lead to hyperglycemia and impaired decreased gut blood flow in animal models that compromised gut
insulin sensitivity related to postreceptor insulin resistance demon- mucosal integrity and decreased gut immune function.
strated by elevated levels of insulin and fasting glucose and signifi-
cant reductions in glucose clearance. Whereas glucose delivery to Effects on Cardiovascular System
peripheral tissues is increased up to threefold, glucose oxidation is Microvascular changes induce cardiopulmonary alterations char-
restricted. Increased glucose production is directed, in part, to the acterized by loss of plasma volume, increased peripheral vascular

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Predicted REE (%)
160 Resting energy expenditure

30 Urine epinephrine

µg/24 hr
µmol/min/100 cc leg Percent predicted

180 Cardiac output

150 Protein breakdown

250 IGF-1
ng/ml

25

Lean body mass


0
% change

–10

Cytokines (IL-6)
1200
ng/ml

Sex hormones (testosterone)


110
ng/ml

40
Burn Dis- 6 9 12 18 24
event charge months months months months months
Time postburn

FIGURE 19-5  Physiologic and metabolic changes after severe burn injury. Changes are demonstrated in
resting energy expenditure (REE), stress hormones (epinephrine), cardiac function (cardiac output), gender
hormones (testosterone), cytokines (interleukin-6), and body composition (lean body mass). Data were sum-
marized from published works from our institution. Averages for burn patients are represented by solid
curves. Values from nonburned, normal patients are represented by dashed lines. (From Williams FN,
Jeschke MG, Chinkes DL, et al: Modulation of the hypermetabolic response to trauma: Temperature, nutri-
tion, and drugs. J Am Coll Surg 208:489–502, 2009.)

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CHAPTER 19  Burns 511

20
autopsy study, implying the therapeutic need to improve cardiac
Lean body mass stress and function.21

Effects on the Renal System


% change

Diminished blood volume and cardiac output result in decreased


renal blood flow and glomerular filtration rate. Other stress-
induced hormones and mediators, such as angiotensin, aldoste-
rone, and vasopressin, further reduce renal blood flow immediately
–20 after the injury. These effects result in oliguria, which, if left
untreated, will cause acute tubular necrosis and renal failure.
0.1 Twenty years ago, acute renal failure in burn injuries was almost
Protein catabolism
always fatal. Today, newer techniques in dialysis became widely
µmol/min/100 cc leg

used to support the kidneys during recovery. The latest reports


indicate an 88% mortality rate for severely burned adults and a
56% mortality rate for severely burned children in whom renal
failure develops in the postburn period. Early resuscitation
decreases risks of renal failure and improves the associated mor-
–0.1 bidity and mortality.11

Effects on the Gastrointestinal System


160 Resting energy expenditure The gastrointestinal response to burn is highlighted by mucosal
atrophy, changes in digestive absorption, and increased intestinal
% predicted

permeability. Atrophy of the small bowel mucosa occurs within


12 hours of injury in proportion to the burn size and is related
to increased epithelial cell death by apoptosis. The cytoskeleton
of the mucosal brush border undergoes atrophic changes associ-
ated with vesiculation of microvilli and disruption of the terminal
web actin filaments. These findings were most pronounced 18
<40% ≥40%
hours after injury, which suggests that changes in the cytoskele-
Burn size TBSA ton, such as those associated with cell death by apoptosis, are
FIGURE 19-6  Effect of burn size on body mass, resting energy expen- processes involved in the changed gut mucosa. Burn also causes
diture, and protein degradation. Changes in net protein balance of reduced uptake of glucose and amino acids, decreased absorption
muscle protein synthesis and breakdown induced by burn injury were of fatty acids, and reduction in brush border lipase activity. These
measured by stable isotope studies using d5-phenylalanine infusion. changes peak in the first several hours after burn injury and return
Graphs are averages ± standard error of the mean. The yellow bars to normal at 48 to 72 hours, a timing that parallels mucosal
represent patients with burns <40% total body surface area (TBSA). atrophy.
The blue bars represent patients with burns ≥40% TBSA. Values from Intestinal permeability to macromolecules, which are normally
nonburned, normal patients are represented by dashed lines. (From repelled by an intact mucosal barrier, increases after burn injury.
Williams FN, Jeschke MG, Chinkes DL, et al: Modulation of the hyper-
Intestinal permeability to polyethylene glycol 3350, lactulose, and
metabolic response to trauma: Temperature, nutrition, and drugs. J Am
Coll Surg 208:489–502, 2009.)
mannitol increases after injury, correlating to the extent of the
burn. Gut permeability increases even further when burn wounds
become infected. A study using fluorescent dextrans showed that
larger molecules appeared to cross the mucosa between the cells,
resistance, and subsequent decreased cardiac output immediately whereas the smaller molecules traversed the mucosa through the
after injury. Cardiac output remains depressed from decreased epithelial cells, presumably by pinocytosis and vesiculation.
blood volume and increased blood viscosity as well as decreased Mucosal permeability also paralleled increases in gut epithelial
cardiac contractility. Ventricular dysfunction in this period is apoptosis.
attributed to a circulating myocardial depressant factor present in Changes in gut blood flow are related to changes in permeabil-
lymphatic fluid, although the specific factor has never been iso- ity. Intestinal blood flow was shown to decrease in animals, a
lated. Burn patients with burns over 40% of their TBSA demon- change that was associated with increased gut permeability at 5
strated an increased cardiac output that significantly decreased hours after burn injury. This effect was abolished at 24 hours.
over time. This was accompanied by an increase in heart rate. Systolic hypotension has been shown to occur in the hours imme-
Severely burned pediatric patients had a marked tachycardia of diately after burn injury in animals with a 40% TBSA full-
160% to 170% predicted, which remained high at discharge from thickness injury. These animals showed an inverse correlation
the intensive care unit (ICU) at around 150%. Cardiac output at between blood flow and permeability to intact Candida.
admission was 150% and remained high at discharge at around
130% predicted. There is some evidence that heart rate remains Effects on the Immune System
elevated up to 2 years after burn injury.14 Increased cardiac stress Burns cause a global depression in immune function, which is
after burn injury is associated with myocardial depression, which shown by prolonged allograft skin survival on burn wounds.
was shown in several studies.20 The hypothesis that one of the Burned patients are then at great risk for a number of infectious
main contributors to mortality in large burns may be cardiac stress complications, including bacterial wound infection, pneumonia,
and myocardial dysfunction was confirmed in a retrospective and fungal and viral infections. These susceptibilities and

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512 SECTION III  Trauma and Critical Care

Burn wound

↑↑ Oxygen consumption ↑↑ 20-fold


Catecholamines Intestine

Heart Serum Alanine Ammonia

↑↑ Glucagon
↑↑ Cardiac output ↑↑ Heart rate ↑↑ Cortisol ↑↑ Insulin Glutamine

Glutamine
Nitrogen
↑↑ Kidney
Wasting
Ammonia

Bone
↓↓ Calcium Liver
Alanine Glutamine
↓↓ Magnesium Urea Ammonia
Muscle
Glucose Glycogen
Fat stores Glucose
Glucose
Glycolysis Lactate
↑ Fractures Glycolysis Lactate
↓ Bone mineral content
↓ Bone mineral density Pyruvate
Pyruvate
Lipid complexes
↑↑ Fatty acids
↑↑ Glycerol ↑↑ Lactate
FIGURE 19-7  Effects of metabolic dysfunction after burn injury. (From Williams FN, Jeschke MG, Chinkes
DL, et al: Modulation of the hypermetabolic response to trauma: Temperature, nutrition, and drugs. J Am
Coll Surg 208:489–502, 2009.)

conditions are based on depressed cellular function in all parts of antibody responses to infection. As this polarization increases, so
the immune system, including activation and activity of neutro- does the mortality rate. Administration of interleukin-10 antibod-
phils, macrophages, T lymphocytes, and B lymphocytes. With ies and growth hormone has partially reversed this response and
burns of more than 20% TBSA, impairment of these immune improved mortality rate after burn injury in animals. Burn also
functions is proportional to burn size. impairs cytotoxic T-lymphocyte activity as a function of burn size,
Macrophage production after burn injury is diminished, which thus increasing the risk of infection, particularly from fungi and
is related to the spontaneous elaboration of negative regulators of viruses. Early burn wound excision improves cytotoxic T-cell
myeloid growth. This effect is enhanced by the presence of endo- activity.
toxin and can be partially reversed with granulocyte colony-
stimulating factor (G-CSF) treatment or inhibition of prostaglandin BASIC TREATMENT OF BURN INJURY
E2. Investigators have shown that G-CSF levels actually increase
after severe burn. However, bone marrow G-CSF receptor expres- Prehospital Management
sion is decreased, which may in part account for the immunode- Before undergoing any specific treatment, burned patients must
ficiency seen in burns. Total neutrophil counts are initially be removed from the source of injury and the burning process
increased after burn injury, a phenomenon that is related to a stopped. Inhalation injury should always be suspected, and 100%
decrease in cell death by apoptosis. However, neutrophils that are oxygen should be given by face mask. While the patient is being
present are dysfunctional in terms of diapedesis, chemotaxis, and removed from the source of injury, care must be taken so that the
phagocytosis. These effects are explained, in part, by a deficiency rescuer does not become another victim. All caregivers should be
in CD11b/CD18 expression after inflammatory stimuli, decreased aware that they might be injured by contact with the patient or
respiratory burst activity associated with a deficiency in p47phox the patient’s clothing. Universal precautions, including wearing of
activity, and impaired actin mechanics related to neutrophil gloves, gowns, mask, and protective eyewear, should be used
motile responses. After 48 to 72 hours, neutrophil counts decrease whenever there is likely to be contact with blood or body fluids.
somewhat, like macrophages, with similar causes. Burning clothing should be extinguished and removed as soon as
T-helper cell function is depressed after a severe burn that is possible to prevent further injury. All rings, watches, jewelry, and
associated with polarization from the interleukin-2 and interferon-γ belts should be removed because they retain heat and can produce
cytokine-based T-helper 1 (Th1) response toward the Th2 response. a tourniquet-like effect. Room temperature water can be poured
The Th2 response is characterized by the production of interleukin-4 on the wound within 15 minutes of injury to decrease the depth
and interleukin-10. The Th1 response is important in cell-mediated of the wound, but any subsequent measures to cool the wound
immune defense, whereas the Th2 response is important in should be avoided to prevent hypothermia during resuscitation.

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CHAPTER 19  Burns 513

160
period until several liters of volume are given to maintain homeo-
Metabolic rate stasis, resulting in significant airway edema.
The chest should be exposed to assess breathing; airway patency
% predicted

alone does not ensure adequate ventilation. Chest expansion and


equal breath sounds with CO2 return from the endotracheal tube
ensure adequate air exchange.
Blood pressure may be difficult to obtain in burned patients
with edematous or charred extremities. Pulse rate can be used as
an indirect measure of circulation; however, most burned patients
remain tachycardic even with adequate resuscitation. For the
100 primary survey of burned patients, the presence of pulses or
Protein breakdown
Doppler signals in the distal extremities may be adequate to
determine adequate circulation of blood until better monitors,
% change

such as arterial pressure measurements and urine output, can be


established.
In those patients who have been in an explosion or deceleration
accident, a possibility exists for spinal cord injury. Appropriate
cervical spine stabilization must be accomplished by whatever
means necessary, including use of cervical collars to keep the head
Net protein balance immobilized until the condition can be evaluated.
0.05
µmol/min/100 cc leg

Initial Wound Care


Prehospital care of the burn wound is basic and simple because it
requires only protection from the environment with application
of a clean dry dressing or sheet to cover the involved part. Damp
dressings should not be used. The patient should be wrapped in
a blanket to minimize heat loss and for temperature control
Nonseptic Septic during transport. The first step in diminishing pain is to cover the
wounds to prevent contact to exposed nerve endings. Intramus-
FIGURE 19-8  Effect of sepsis on resting energy expenditure, muscle cular or subcutaneous narcotic injections for pain should never
protein breakdown, and fractional synthetic rate of muscle protein syn- be used because drug absorption is decreased as a result of the
thesis compared with like-sized burns. Changes in net protein balance
peripheral vasoconstriction. This might become a problem later
of muscle protein synthesis and breakdown induced by burn injury were
measured by stable isotope studies using d5-phenylalanine infusion.
when the patient is resuscitated, and vasodilation increases absorp-
Graphs are averages ± standard error of the mean. The yellow bars tion of the narcotic depot with resulting apnea. Small doses of
represent nonseptic patients with burns ≥40% total body surface area intravenous morphine may be given after complete assessment of
(TBSA). The blue bars represent septic patients with burns ≥40% TBSA. the patient and after it is determined to be safe by an experienced
Values from nonburned, normal patients are represented by dashed practitioner.
lines. (From Williams FN, Jeschke MG, Chinkes DL, et al: Modulation Although prehospital management is simple, it is often diffi-
of the hypermetabolic response to trauma: Temperature, nutrition, and cult to enact, particularly in at-risk populations. A study in New
drugs. J Am Coll Surg 208:489–502, 2009.) Zealand showed that initial burn first aid treatment was inade-
quate in 60% of patients interviewed. These authors also showed
that inadequate first aid care was clearly associated with poorer
outcomes. They suggested that defined education programs tar-
Initial Assessment geted on at-risk populations might improve these outcomes.22
As with any trauma patient, the initial assessment of a burned
patient is divided into a primary and secondary survey. In the Transport
primary survey, immediate life-threatening conditions are quickly Rapid, uncontrolled transport of the burn victim is not a priority,
identified and treated. In the secondary survey, a more thorough except when other life-threatening conditions coexist. In most
head-to-toe evaluation of the patient is undertaken. incidents involving major burns, ground transportation of victims
Exposure to heated gases and smoke results in damage to the to the receiving hospital is appropriate. Helicopter transport is of
upper respiratory tract. Direct injury to the upper airway results greatest use when the distance between the accident and the hos-
in edema, which, in combination with generalized whole body pital is 30 to 150 miles. For distances of more than 150 miles,
edema associated with severe burn, may obstruct the airway. transport by fixed-wing aircraft is most appropriate. Whatever the
Airway injury must be suspected with facial burns, singed nasal mode of transport, it should be of appropriate size and have
hairs, carbonaceous sputum, and tachypnea. Upper airway emergency equipment available, with trained personnel on board,
obstruction may develop rapidly, and respiratory status must be such as nurses, physicians, paramedics, or respiratory therapists
continually monitored to assess the need for airway control and who are familiar with multiply injured trauma patients.
ventilatory support. Progressive hoarseness is a sign of impending
airway obstruction, and endotracheal intubation should be insti- Resuscitation
tuted early before edema distorts the upper airway anatomy. This Adequate resuscitation of the burned patient depends on the
is especially important in patients with massive burns, who may establishment and maintenance of reliable intravenous access.
appear to breathe without problems early in the resuscitation Increased times to beginning resuscitation of burned patients

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514 SECTION III  Trauma and Critical Care

result in poorer outcomes, and delays should be minimized. burns who were randomized to either hypertonic saline or lactated
Venous access is best attained through short peripheral catheters Ringer solution, resuscitation did not have significant differences
in unburned skin; however, veins in burned skin can be used and in volume requirements or changes in percentage of weight gain.
are preferable to no intravenous access. Superficial veins are often Other investigators found an increase in renal failure with hyper-
thrombosed in full-thickness injuries and therefore are not suit- tonic solutions that has tempered further efforts in this area of
able for cannulation. Saphenous vein cutdowns are useful in cases investigation. Some burn units successfully use a modified hyper-
of difficult access and are used in preference to central vein can- tonic solution of 1 ampule of sodium bicarbonate (50 mEq) in
nulation because of lower complication rates. In children younger 1 L of lactated Ringer solution. Further research should be done
than 6 years, experienced practitioners can use intraosseous access to determine the optimal formula to reduce edema formation and
in the proximal tibia until intravenous access is accomplished. to maintain adequate cellular function.
Lactated Ringer solution without dextrose is the fluid of choice Most burn units use something akin to either the Parkland or
except in children younger than 2 years, who should receive 5% Brooke formula, which calls for administration of varying amounts
dextrose in lactated Ringer solution. The initial rate can be rapidly of crystalloid and colloid for the first 24 hours. The fluids are
estimated by multiplying the TBSA burned by the patient’s weight generally changed in the second 24 hours, with an increase in
in kilograms and then dividing by 8. Thus, the rate of infusion colloid use. These are guidelines to direct resuscitation of the
for an 80-kg man with a 40% TBSA burn would be amount of fluid necessary to maintain adequate perfusion. In fact,
recent studies have shown that the Parkland formula often under-
80 kg × 40% TBSA 8 = 400 mL hr
estimates the volume of crystalloid received in the first 24 hours
This rate should be continued until a formal calculation of resus- after severe burn; this phenomenon has been termed fluid creep.
citation needs is performed. No clear single cause has been identified. More liberal use of
Many formulas have been devised to determine the proper opioid analgesia and positive pressure ventilation has been sug-
amount of fluid to give a burned patient, all originating from gested.24 The increased fluid volumes are not without conse-
experimental studies on the pathophysiology of burn shock. These quence; increased compartment pressures in the extremities,
experimental studies established the basis for modern fluid resus- abdomen, and most recently the orbit25 have been suggested as
citation protocols. They showed that edema fluid in burn wounds requiring monitoring and possible release to prevent increased
is isotonic and contains the same amount of protein as plasma morbidity and mortality. The abdominal compartment is clini-
and that the greatest loss of fluid is into the interstitium.23 They cally monitored through the Foley catheter. When the pressure
used various volumes of intravascular fluid to determine the increases toward and above 30 mm Hg, assurance of complete
optimal amount in terms of cardiac output and extracellular abdominal escharotomy is made, and paralytics are considered. If
volume in a canine burn model, and this was applied to the clini- the increased abdominal pressure persists (>30 mm Hg), an
cal realm in the Parkland formula. Plasma volume changes were improved outcome rests in the performance of a decompressive
not related to the type of resuscitation fluid in the first 24 hours, laparotomy. However, the patients who require this procedure
but thereafter colloid solutions could increase plasma volume by have mortality rates of 60% to nearly 100%, depending on the
the amount infused. From these findings, it was concluded that series. Therefore, monitoring of the resuscitation is crucial to
colloid solutions should not be used in the first 24 hours until ensure acceptable outcome. This is easily monitored in burned
capillary permeability returned closer to normal. Others have patients with normal renal function by following the volume of
argued that normal capillary permeability is restored somewhat urine output, which should be at 0.5 mL/hr in adults and 1.0 mL/
earlier after burn injury (6 to 8 hours), and therefore colloids kg/hr in children. Changes in intravenous fluid infusion rates
could be used earlier. should be made on an hourly basis determined by the response
Concurrently, researchers showed the hemodynamic effects of of the patient to the particular fluid volume administered. The
fluid resuscitation in burns, which culminated in the Brooke exact formulas are shown in Table 19-2.
formula. They found that fluid resuscitation caused an obligatory For burned children, formulas are commonly used that are
20% decrease in both extracellular fluid and plasma volume that modified to account for changes in surface area to mass ratios.
concluded after 24 hours. In the second 24 hours, plasma volume These changes are necessary because a child with a comparable
returned to normal with the administration of colloid. Cardiac burn to that of an adult requires more resuscitation fluid per
output was low in the first day despite resuscitation, but it subse- kilogram. The Galveston formula uses 5000 mL/TBSA burned
quently increased to supernormal levels as the flow phase of hyper-
metabolism was established. Since these studies, it has been found
that much of the fluid needs are due to “leaky” capillaries that TABLE 19-2  Resuscitation Formulas
permit passage of large molecules into the interstitial space to
CRYSTALLOID COLLOID FREE
increase extravascular colloid osmotic pressure. Intravascular
FORMULA VOLUME VOLUME WATER
volume follows the gradient to tissues, into both the burn wound
and the nonburned tissues. Approximately 50% of fluid resuscita- Parkland 4 mL/kg per % TBSA burn None None
tion needs are sequestered in nonburned tissues in 50% TBSA Brooke 1.5 mL/kg per % TBSA 0.5 mL/kg per % 2.0 L
burns. burn TBSA burn
Hypertonic saline solutions have theoretical advantages in Galveston 5000 mL/m2 burned area None None
burn resuscitation. These solutions decrease net fluid intake, (pediatric) + 1500 mL/m2 total area
decrease edema, and increase lymph flow, probably by the transfer These guidelines are used for the initial fluid management after a
of volume from the intracellular space to the interstitium. When burn injury. The response to fluid resuscitation should be
these solutions are used, hypernatremia must be avoided, and it continuously monitored, and adjustments in the rate of fluid
is recommended that serum sodium concentrations not exceed administration should be made accordingly. TBSA, total body surface
160 mEq/dL. However, for patients with more than 20% TBSA area.

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CHAPTER 19  Burns 515

(in m2) + 1500 mL/m2 total for maintenance in the first 24 hours.


This formula accounts for both maintenance needs and the
increased fluid requirements of a child with a burn. All of the
formulas listed in Table 19-2 calculate the amount of volume
given in the first 24 hours, half of which is given in the first 8
hours.
The use of albumin during intravenous resuscitation has
recently come under criticism. The Cochrane group showed in a
meta-analysis of 31 trials that the risk of death was higher in
burned patients receiving albumin compared with those receiving
crystalloid, with a relative risk of death at 2.40 (95% confidence
interval, 1.11 to 5.19). Another meta-analysis of all critically ill
patients refuted this finding, showing no differences in relative
risk between albumin-treated and crystalloid-treated groups. In
fact, as quality of the trials improved, the relative risks were
reduced. Additional recent evidence suggests that albumin supple-
mentation even after resuscitation does not affect the distribution
of fluid among the intracellular and extracellular compartments.
What we can conclude from these trials and meta-analyses is that
albumin used during resuscitation is at best equal to crystalloid FIGURE 19-9  Recommended escharotomies. In limbs requiring
escharotomies, the incisions are made on the medial and lateral sides
and at worst detrimental to the outcome of burned patients. For
of the extremity through the eschar. In the case of the hand, incisions
these reasons, we cannot recommend the use of albumin during are made on the medial and lateral digits and on the dorsum of the
resuscitation. hand.
To combat any regurgitation with an intestinal ileus, a naso-
gastric tube should be inserted in all patients with major burns to
decompress the stomach. This is especially important for all tissues until formal excision. If vascular compromise has been
patients being transported in aircraft at high altitudes. In addition, prolonged, reperfusion after an escharotomy may cause reactive
all patients should be restricted from taking anything by mouth hyperemia and further edema formation in the muscle, making
until the transfer has been completed. Decompression of the continued surveillance of the distal extremities necessary. Increased
stomach is usually necessary because the apprehensive patient will muscle compartment pressures may necessitate fasciotomies. The
swallow considerable amounts of air and distend the stomach. In most common complications associated with these procedures are
addition, a Dobhoff tube should be placed into the first part of blood loss and the release of anaerobic metabolites, causing tran-
the duodenum to continuously feed the severely burned. sient hypotension. If distal perfusion does not improve with these
Recommendations for tetanus prophylaxis are based on the measures, central hypotension from hypovolemia should be sus-
condition of the wound and the patient’s immunization history. pected and treated.
All patients with burns of more than 10% TBSA should receive A constricting truncal eschar can cause a similar phenomenon,
0.5 mL of tetanus toxoid. If prior immunization is absent or except the effect is to decrease ventilation by limiting chest excur-
unclear or the last booster dose was more than 10 years ago, 250 sion. Any decrease in ventilation of a burned patient should
units of tetanus immune globulin are also given. produce inspection of the chest with appropriate escharotomies
to relieve the constriction and to allow adequate tidal volumes.
Escharotomies This need becomes evident in a patient on a volume-control
When deep second- and third-degree burn wounds encompass the ventilator whose peak airway pressures increase.
circumference of an extremity, peripheral circulation to the limb
can be compromised. Development of generalized edema beneath SPECIFIC TREATMENT OF BURNS
a nonyielding eschar impedes venous outflow and eventually
affects arterial inflow to the distal beds. This can be recognized by Inhalation Injury
numbness and tingling in the limb and increased pain in the Even though mortality from major burns has significantly
digits. Arterial flow can be assessed by determination of Doppler decreased during the past 20 years, inhalation injury still consti-
signals in the digital arteries and the palmar and plantar arches in tutes one of the most critical concomitant injuries following
affected extremities. Capillary refill can also be assessed. Extremi- thermal insult. Approximately 80% of fire-related deaths result
ties at risk are identified either on clinical examination or on not from burns but from inhalation of the toxic products of
measurement of tissue pressures higher than 40 mm Hg. These combustion, and inhalation injury has remained associated with
extremities require escharotomies, which are releases of the burn an overall mortality rate of 25% to 50% when patients require
eschar performed at the bedside by incision of the lateral and ventilator support for more than 1 week after injury.11,26 Early
medial aspects of the extremity with a scalpel or electrocautery diagnosis of bronchopulmonary injury is thus critical for survival
unit. The entire constricting eschar must be incised longitudinally and is conducted primarily clinically, based on a history of closed-
to completely relieve the impediment to blood flow (Fig. 19-9). space exposure, facial burns, and carbonaceous debris in mouth,
The incisions are carried down onto the thenar and hypothenar pharynx, or sputum. Evidence-based experience on diagnosis of
eminences and along the dorsolateral sides of the digits to com- inhalation injury, however, is rare. Chest radiographs are routinely
pletely open the hand, if it is involved. If it is clear that the wound normal until complications, such as infections, have developed.
will require excision and grafting because of its depth, escharoto- The standard diagnostic method should therefore be bronchos-
mies are safest to restore perfusion to the underlying nonburned copy of the upper airway of every burn patient. Gamelli and

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516 SECTION III  Trauma and Critical Care

others established a grading system of inhalation injury (0 to 4) methicillin-resistant Staphylococcus aureus and gram-negative
derived from findings at initial bronchoscopy and based on organisms such as Pseudomonas and Klebsiella.28
Abbreviated Injury Score criteria.27 Bronchoscopic criteria that are
consistent with inhalation injury included airway edema, inflam- Wound Care
mation, mucosal necrosis, presence of soot and charring in the After the airway is assessed and resuscitation is under way, atten-
airway, tissue sloughing, and carbonaceous material in the airway. tion must be turned to the burn wound. Treatment depends on
The treatment of inhalation injury should start immediately with the characteristics and size of the wound. All treatments are aimed
the administration of 100% oxygen by face mask or nasal cannula. at rapid and painless healing. Current therapy directed specifically
Maintenance of the airway is critical. As mentioned before, if early toward burn wounds can be divided into three stages: assessment,
evidence of upper airway edema is present, early intubation is management, and rehabilitation. Once the extent and depth of
required because the upper airway edema normally increases the wounds have been assessed and the wounds have been thor-
during 9 to 12 hours. Prophylactic intubation without good indi- oughly cleaned and débrided, the management phase begins. Each
cation, however, should not be performed. wound should be dressed with an appropriate covering that serves
Advances in ventilator technology and treatment of inhalation several functions. First, it should protect the damaged epithelium,
injury have resulted in some improvement in mortality. Mechani- minimize bacterial and fungal colonization, and provide splinting
cal ventilation with a lower tidal volume than traditionally used action to maintain the desired position of function. Second, the
resulted in decreased mortality and increased the number of days dressing should be occlusive to reduce evaporative heat loss and
without ventilator use. In addition, high-frequency ventilation to minimize cold stress. Third, the dressing should provide
decreased mortality to 29% from 41%. Management of inhala- comfort over the painful wound.
tion injury consists of ventilatory support, aggressive pulmonary The choice of dressing is based on the characteristics of the
toilet (Table 19-3), bronchoscopic removal of casts, and nebuliza- treated wound (Table 19-5). First-degree wounds are minor with
tion therapy. Nebulization therapy can consist of heparin, alpha minimal loss of barrier function. These wounds require no dress-
mimetics, or polymyxin B and is applied between two and six ing and are treated with topical salves to decrease pain and to keep
times a day. Pressure-control ventilation with permissive hyper- the skin moist. Systemic nonsteroidal anti-inflammatory agents
capnia is a useful strategy in the management of these patients, given by mouth assist in pain control. Second-degree wounds can
and PaCO2 levels of as much as 60 mm Hg can be well tolerated be treated with daily dressing changes with topical antibiotics,
if they are arrived at gradually. Prophylactic antibiotics are not cotton gauze, and elastic wraps. Alternatively, the wounds can be
indicated but are imperative with documented lung infections. treated with a temporary biologic or synthetic covering to close
Clinical diagnosis of pneumonia includes two of the following18: the wound. Deep second-degree and third-degree wounds require
chest radiograph revealing a new and persistent infiltrate, consoli- excision and grafting for sizable burns, and the choice of initial
dation, or cavitation; sepsis, as defined in Table 19-4; or a recent dressing should be aimed at holding bacterial proliferation in
change in sputum or purulence in the sputum as well as quantita- check and providing occlusion until the operation is performed.
tive culture. Clinical diagnosis can be modified after using micro-
biologic data of three categories according to the American Burn Antimicrobials
Association Consensus Conference to Define Sepsis and Infection The timely and effective use of antimicrobials has revolutionized
in Burns.18 Empirical choices for the treatment of pneumonia burn care by decreasing invasive wound infections. The untreated
before culture results are available should include coverage of burn wound rapidly becomes colonized with bacteria and fungi
because of the loss of normal skin barrier mechanisms. As the
organisms proliferate to high wound counts (>105 organisms
TABLE 19-3  Inhalation Treatments of per gram of tissue), they may penetrate into viable tissue. Organ-
isms then invade blood vessels, causing a systemic infection that
Smoke Inhalation Injury
often leads to the death of the patient. This scenario has become
TREATMENT TIME, DOSAGE, AND METHOD uncommon in most burn units because of the effective use of
Bronchodilators (Albuterol) q2h antibiotics and wound care techniques. The antimicrobials that
Nebulized heparin 5000-10,000 units with 3 mL normal are used can be divided into those given topically and those given
saline q4h systemically.
Nebulized acetylcysteine 20%, 3 mL q4h Available topical antibiotics can be divided into two classes:
Hypertonic saline Induces effective coughing salves and soaks. Salves are generally applied directly to the wound
Racemic epinephrine Reduces mucosal edema with cotton dressings placed over them, and soaks are generally
poured into cotton dressings on the wound. Each of these classes
of antimicrobials has advantages and disadvantages. Salves may be
applied once or twice a day but may lose their effectiveness
TABLE 19-4  Clinical Indications for between dressing changes. Frequent dressing changes can result in
shearing with loss of grafts or underlying healing cells. Soaks
Intubation
remain effective because antibiotic solution can be added without
CRITERIA VALUE removal of the dressing; however, the underlying skin can become
PaO2 <60 mm Hg macerated.
PaCO2 >50 mm Hg (acutely) Topical antibiotic salves include 11% mafenide acetate (Sulfa-
PaO2/FIO2 ratio <200 mylon), 1% silver sulfadiazine (Silvadene), polymyxin B, neomy-
Respiratory or ventilatory failure Impending cin, bacitracin, mupirocin, and the antifungal agent nystatin. No
Upper airway edema Severe single agent is completely effective, and each has advantages and
disadvantages. Silver sulfadiazine is the most commonly used. It

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CHAPTER 19  Burns 517

TABLE 19-5  Burn Wound Dressings


DRESSINGS ADVANTAGES AND DISADVANTAGES
Antimicrobial Salves
Silver sulfadiazine (Silvadene) Broad-spectrum antimicrobial; painless and easy to use; does not penetrate eschar; may leave black tattoos from silver
ion; mild inhibition of epithelialization
Mafenide acetate (Sulfamylon) Broad-spectrum antimicrobial; penetrates eschar; may cause pain in sensate skin; wide application may cause metabolic
acidosis; mild inhibition of epithelialization
Bacitracin Ease of application; painless; antimicrobial spectrum not as wide as above agents
Neomycin Ease of application; painless; antimicrobial spectrum not as wide
Polymyxin B Ease of application; painless; antimicrobial spectrum not as wide
Nystatin (Mycostatin) Effective in inhibiting most fungal growth; cannot be used in combination with mafenide acetate
Mupirocin (Bactroban) More effective staphylococcal coverage; does not inhibit epithelialization; expensive

Antimicrobial Soaks
0.5% Silver nitrate Effective against all microorganisms; stains contacted areas; leaches sodium from wounds; may cause methemoglobinemia
5% Mafenide acetate Wide antibacterial coverage; no fungal coverage; painful on application to sensate wound; wide application associated
with metabolic acidosis
0.025% Sodium hypochlorite (Dakin Effective against almost all microbes, particularly gram-positive organisms; mildly inhibits epithelialization
solution)
0.25% Acetic acid Effective against most organisms, particularly gram-negative ones; mildly inhibits epithelialization

Synthetic Coverings
OpSite Provides a moisture barrier; inexpensive; decreased wound pain; use complicated by transudate and exudate requiring
removal; no antimicrobial properties
Biobrane Provides a wound barrier; associated with decreased pain; use complicated by accumulation of exudate, risking invasive
wound infection; no antimicrobial properties
TransCyte Provides a wound barrier; decreased pain; accelerated wound healing; use complicated by accumulation of exudate; no
antimicrobial properties
Integra Provides complete wound closure and leaves a dermal equivalent; sporadic take rates; antimicrobial properties

Biologic Coverings
Xenograft (pig skin) Completely closes the wound; provides some immunologic benefits; must be removed or allowed to slough
Allograft (homograft, cadaver skin) Provides all the normal functions of skin; can leave a dermal equivalent; epithelium must be removed or allowed to slough

has a broad spectrum of activity because its silver and sulfa moi- and selected gram-negative bacteria. Nystatin, in either a salve or
eties cover gram-positive, most gram-negative, and some fungal powder form, can be applied to wounds to control fungal growth.
forms. Some Pseudomonas species possess plasmid-mediated resis- Nystatin-containing ointments can be combined with other
tance. Silver sulfadiazine is relatively painless on application, has topical agents to decrease colonization of both bacteria and
a high patient acceptance, and is easy to use. On occasion, patients fungus. The exception is the combination of nystatin and mafenide
complain of a burning sensation after it is applied, and, in a few acetate; each inactivates the other.
patients, a transient leukopenia develops 3 to 5 days after its Available agents for application as a soak include 0.5% silver
continued use. This leukopenia is generally harmless and resolves nitrate solution, 0.025% sodium hypochlorite (Dakin solution),
with or without treatment cessation. 0.25% acetic acid, and mafenide acetate as a 5% solution. Silver
Mafenide acetate is another topical agent with a broad spec- nitrate has the advantage of being painless on application and
trum of activity because of its sulfa moiety. It is particularly useful having complete antimicrobial effectiveness. The disadvantages
against resistant Pseudomonas and Enterococcus species. It also can include its staining of surfaces to a dull gray or black when the
penetrate eschar, which silver sulfadiazine cannot. Disadvantages solution dries. This can become a problem in deciphering wound
include painful application on skin, such as in second-degree depth during burn excisions and in keeping the patient and his
wounds. It also can cause an allergic rash, and it has carbonic or her surroundings clean of the black staining. The solution is
anhydrase inhibitory characteristics that can result in a metabolic hypotonic as well, and continuous use can cause electrolyte leach-
acidosis when it is applied over large surfaces. For these reasons, ing, with rare methemoglobinemia as another complication. A
mafenide sulfate is typically reserved for small full-thickness new commercial dressing containing biologically potent silver
injuries. ions (Acticoat) that are activated in the presence of moisture is
Petroleum-based antimicrobial ointments with polymyxin B, available. This dressing holds the promise of retaining the effec-
neomycin, and bacitracin are clear on application, are painless, tiveness of silver nitrate without the problems of silver nitrate
and allow easy wound observation. These agents are commonly soaks.
used for treatment of facial burns, graft sites, healing donor sites, Dakin solution (0.25% sodium hypochlorite) has effectiveness
and small partial-thickness burns. Mupirocin is a relatively new against most microbes; however, it also has cytotoxic effects on
petroleum-based ointment that has improved activity against the healing cells of patients’ wounds. Low concentrations of
gram-positive bacteria, particularly methicillin-resistant S. aureus sodium hypochlorite (0.025%) have fewer cytotoxic effects while

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518 SECTION III  Trauma and Critical Care

maintaining most of the antimicrobial effects. Hypochlorite ion traction on the excised eschar as it passes through the knife or
is inactivated by contact with protein, so the solution must be dermatome. Adequate excision is signaled by a viable bleeding
continually changed. The same is true for acetic acid solutions, wound bed, which is usually fat.
which may be more effective against Pseudomonas. Mafenide Fascial excision.  This technique is reserved for burn extend-
acetate soaks have the same characteristics of the mafenide acetate ing down through the fat into muscle, when the patient presents
salve, except in liquid form. late with large infected wounds and life-threatening invasive
The use of perioperative systemic antimicrobials also has a role fungal infections. It involves surgical excision of the full thickness
in decreasing burn wound sepsis until the burn wound is closed. of the integument including the subcutaneous fat down to the
Common organisms that must be considered in choosing a peri- fascia using Goulian knives and No. 11 blades. Unfortunately,
operative regimen include S. aureus and Pseudomonas species, fascial excision is mutilating and leaves a permanent contour
which are prevalent in burn wounds. defect, which is nearly impossible to reconstruct. Lymphatic chan-
nels are excised in this technique, and peripheral lymphedema
Burn Wound Excision may develop.
Methods for handling burn wounds have changed in recent Most patients can be managed with layered excisions that
decades and are similar in adults and children. Increasingly aggres- optimize later appearance and function. Published estimates of
sive early tangential excision of the burn tissue and early wound the amount of bleeding associated with these operations range
closure primarily by skin grafts have led to significant improve- within 3.5% to 5% of the blood volume for every 1% of the body
ment of mortality rates and substantially lower costs in this par- surface excised. The control of blood loss is one of the main
ticular population of patients. Early wound closure has furthermore determinants for outcome.29 Therefore, several techniques should
been found to be associated with decreased severity of hypertro- be applied to control blood loss. Local application of fibrin or
phic scarring, joint contractures, and stiffness, and it promotes thrombin spray, topical application of epinephrine 1 : 10000 to
quicker rehabilitation. Techniques of burn wound excision have 1 : 20000, epinephrine-soaked laboratory pads (1 : 40000), and
evolved substantially during the past decade. In general, most immediate electrocautery of the blood vessel can control blood
areas are excised with a hand skin graft knife or powered derma- loss.30 The use of a sterilized tourniquet can also limit blood loss.
tome. Sharp excision with a knife or electrocautery is reserved for Last, pre-excisional tumescence with epinephrine saline can be
areas of functional cosmetic importance, such as the hand and used on the trunk, back, and extremities but not on the fingers.
face. In partial-thickness wounds, an attempt is being made to
preserve viable dermis, whereas in full-thickness injury, all necrotic Burn Wound Coverage
and infected tissue must be removed, leaving a viable wound After burn wound excision, it is vital to obtain wound closure.
bed of fascia, fat, or muscle. The following techniques are mainly Various biologic and synthetic substrates have been employed to
used. replace the injured skin after a burn. Autografts from uninjured
Tangential excision.  This technique, first described by Janze- skin remain the mainstay of treatment for many patients. Because
kovic in the 1970s, requires repeated shaving of deep dermal early wound closure using autograft may be difficult when full-
partial-thickness burns using a Braithwaite, Watson, or Goulian thickness burns exceed 40% TBSA, allografts (cadaver skin) fre-
knife or dermatome set at a depth 0.005 to 0.010 inch until a quently serve as skin substitute in severely burned patients (Fig.
viable dermal bed is reached, which is manifested clinically by 19-10). Although this approach is still commonly used in burn
punctate bleeding from the dermal wound bed. centers throughout the world, it bears considerable risks, includ-
Full-thickness excision.  A hand knife such as the Watson or ing antigenicity and cross-infection as well as limited availability.
powered dermatome is set at 0.015 to 0.030 inch, and serial passes Xenografts have been used for hundreds of years as temporary
are made excising the full-thickness wound. Excision is aided by replacement for skin loss. Even though these grafts provide a

Excised wound bed

4:1 meshed autograft

2:1 meshed allograft

FIGURE 19-10  Diagram of skin closure using widely meshed autografts. A widely meshed autograft is
placed on a freshly excised viable wound bed. The remaining open wound between the interstices of the
autograft is closed with an overlying layer of allograft, which can also be meshed to allow transudate,
exudate, and hematoma to escape.

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CHAPTER 19  Burns 519

biologically active dermal matrix, the immunologic disparities therefore not surprising that multiorgan failure is common in
prevent engraftment and predetermine rejection over time. burned patients.
However, both xenografts and allografts are a means of only tem-
porary burn wound cover. True closure can be achieved only with Etiology and Pathophysiology
living autografts or isografts. Autologous epithelial cells grown The progression from the systemic inflammatory response syn-
from a single full-thickness skin biopsy specimen have been avail- drome to multiorgan failure is not well explained, although some
able for nearly 2 decades. These cultured epithelial autografts have of the responsible mechanisms are recognized. Most of these are
been shown to decrease mortality in massively burned patients in found in patients with inflammation from infectious sources. In
a prospective, controlled trial. Our institution found cultured the burned patient, these infectious sources most likely emanate
epithelial autografts used in combination with wide mesh auto- from invasive wound infection or from lung infections (pneumo-
graft and allograft overlay in a population of pediatric patients nia). As organisms proliferate out of control, endotoxins are liber-
with burns of 90% or more TBSA to be associated with improved ated from gram-negative bacterial walls and exotoxins from
cosmetic results. However, widespread use of cultured autografts gram-positive and gram-negative bacteria. Their release causes the
has been primarily hampered by poor long-term clinical results, initiation of a cascade of inflammatory mediators that can result,
exorbitant costs, and fragility and difficult handling of these grafts; if unchecked, in organ damage and progression to organ failure.
these problems have been consistently reported by different burn On occasion, failure of the gut barrier with penetration of organ-
units treating deep burns, even when cells were applied on prop- isms into the systemic circulation may incite a similar reaction.
erly prepared wound beds. Alternatively, dermal analogues have However, this phenomenon has been demonstrated only in animal
been made available for clinical use in recent years. Integra was models, and it remains to be seen whether this is a cause of human
approved by the U.S. Food and Drug Administration for use in disease.
life-threatening burns and has been successfully used in immedi- Inflammation from the presence of necrotic tissue and open
ate and delayed closure of full-thickness burns, leading to reduc- wounds can incite an inflammatory mediator response similar to
tion in length of hospital stay, favorable cosmetics, and improved that seen with endotoxin. The mechanism by which this occurs,
functional outcome in a prospective and controlled clinical study. however, is not well understood. Regardless, it is known that a
Our group conducted a randomized clinical trial using Integra in cascade of systemic events is set in motion, either by invasive
the management of severe full-thickness burns of 50% TBSA or organisms or from open wounds, that initiates the systemic
more in a population of pediatric patients, comparing it with inflammatory syndrome, which may progress to multiorgan
standard autograft-allograft technique, and found Integra to be failure. Evidence from animal studies and clinical trials suggests
associated with attenuated hepatic dysfunction, improved resting that these events converge to a common pathway, which results
energy expenditure, and improved aesthetic outcome.31 Allo- in activation of several cascade systems. Those circulating media-
Derm, an acellular human dermal allograft, has been advocated tors can, if secreted in excessive amounts, damage organs distal
for the management of acute burns. Small clinical series and case from their site of origin. Among these mediators are endotoxin,
reports suggest that AlloDerm may be useful in the treatment of arachidonic acid metabolites, cytokines, neutrophils and their
acute burns. Tissue engineering technology is advancing rapidly. adherence molecules, nitric oxide, complement components, and
Fetal constructs have been successfully trialed by Hohlfeld and oxygen free radicals.
colleagues,32 and the bilaminar skin substitute of Boyce (cultured
skin substitute)33 is in clinical use and is very promising.30 Prevention
Advances in stem cell culture technology may represent another Because different cascade systems are involved in the pathogenesis
promising therapeutic approach to deliver cosmetic restoration for of burn-induced multiorgan failure, it is so far impossible to
burn patients. pinpoint a single mediator that initiates the event. Thus, because
the mechanisms of progression are not well known, prevention is
Multiorgan Failure currently the best solution. The current recommendations are to
Early, aggressive resuscitation regimens have improved survival prevent the development of organ dysfunction and to provide
rates dramatically. With the advent of vigorous fluid resuscitation, optimal support to avoid conditions that promote the onset.
irreversible burn shock has been replaced by sepsis and subsequent The great reduction of mortality from large burns was observed
multiorgan failure as the leading cause of death associated with with early excision and an aggressive surgical approach to deep
burns. In our pediatric burn population with burns of more than wounds. Early removal of devitalized tissue prevents wound infec-
80% TBSA, sepsis defined by bacteremia developed in 17.5% of tions and decreases inflammation associated with the wound. In
the children.11 The mortality rate in the whole group was 33%; addition, it eliminates small, colonized foci, which are a frequent
most of these deaths were attributable to multiorgan failure. Some source of transient bacteremia. Those transient bacteremias during
of the patients who died were bacteremic and “septic,” but most surgical manipulations may prime immune cells to react in an
were not. These findings highlight the observation that develop- exaggerated fashion to subsequent insults, leading to whole body
ment of multiorgan failure is often associated with infectious inflammation and remote organ damage. We recommend com-
sepsis, but infection is by no means required for development of plete early excision of clearly full-thickness wounds within 48
multiorgan failure. What is required is an inflammatory focus, hours of the injury or as early as possible.
which in severe burns is the massive skin injury that requires Oxidative damage from reperfusion after low-flow states makes
inflammation to heal. It has been postulated that the progression early, aggressive fluid resuscitation imperative. This is particularly
to multiorgan failure exists in a continuum with the systemic important during the initial phases of treatment and operative
inflammatory response syndrome. Nearly all burned patients meet excision with its attendant blood losses. Furthermore, the volume
the criteria for systemic inflammatory response syndrome as of fluid may not be as important as the timeliness with which it
defined by the consensus conference of the American College of is given. In the study of children with more than 80% TBSA
Chest Physicians and the Society of Critical Care Medicine. It is burns, it was found that one of the most important contributors

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520 SECTION III  Trauma and Critical Care

to survival was the time required to start intravenous resuscitation, Decreasing the volume of fluid being given can alleviate volume
regardless of the initial volume given. overload in burned patients. These patients have increased insen-
Topical and systemic antimicrobial therapy has significantly sible losses from the wounds, which can be roughly calculated at
diminished the incidence of invasive burn wound sepsis. Periop- 1500 mL/m2 TBSA + 3750 mL/m2 TBSA burned. Further losses
erative antibiotics clearly benefit patients with burn injuries of are accrued on air beds (1 L/day in an adult). Decreasing the
more than 30% TBSA. Vigilant and scheduled replacement of infused volume of intravenous fluids and enteral feedings to less
intravascular devices minimizes the incidence of catheter-related than the expected insensate losses alleviates fluid overload prob-
sepsis. We recommend changes of indwelling catheters every 5 lems. Electrolyte abnormalities can be minimized by decreasing
days. The first can be done over a wire using sterile Seldinger potassium administration in the enteral feedings and giving oral
technique, but the second change requires a new site. This proto- bicarbonate solutions. Almost invariably, severely burned patients
col should be kept as long as intravenous access is required. When require exogenous potassium because of the heightened aldoste-
possible, peripheral veins should be used for cannulation, even rone response that results in potassium wasting.
through burned tissue. The saphenous vein, however, should be If the problems listed earlier overwhelm the conservative mea-
avoided because of the high risk of thrombophlebitis. sures, some form of dialysis may be necessary. The indications for
Pneumonia, which contributes significantly to death in burned dialysis are volume overload and electrolyte abnormalities not
patients, should be vigilantly anticipated and aggressively treated. amenable to other treatments. Peritoneal dialysis is effective in
Every attempt should be made to wean patients as early as possible burned pediatric patients to remove volume and to correct elec-
from the ventilator to reduce the risk of ventilator-associated trolyte abnormalities. In adults, hemofiltration is an effective
nosocomial pneumonia. Furthermore, early ambulation is an approach. Continuous venous-venous hemodialysis is sometimes
effective means of preventing respiratory complications. With indicated because of the fluid shifts that occur. All hemodialysis
sufficient analgesics, even patients on continuous ventilatory techniques should be done in conjunction with experienced
support can be out of bed and in a chair. nephrologists who are well versed in these techniques.
The most common sources of sepsis are the wounds and the After dialysis is begun, renal function may return, especially in
tracheobronchial tree; efforts to identify causative agents should pediatric patients and adult patients who maintain some urine
be concentrated there. Another potential source, however, is the output. Therefore, patients requiring such treatment may not
gastrointestinal tract, which is a natural reservoir for bacteria. require lifelong dialysis. It is a clinical observation that whatever
Starvation and hypovolemia shunt blood from the splanchnic bed urine output was present will decrease once dialysis is begun, but
and promote mucosal atrophy and failure of the gut barrier. Early it may return in several days to weeks once the acute process of
enteral feeding reduces septic morbidity and prevents failure of closing the burn wound nears completion.
the gut barrier. At our institution, patients are fed immediately
through a nasogastric tube. Early enteral feedings are tolerated in Pulmonary Failure
burned patients, preserve the mucosal integrity, and may reduce Many burned patients require mechanical ventilation to protect
the magnitude of the hypermetabolic response to injury. Support the airway in the initial phases of their injury. We recommend
of the gut goes along with carefully monitored hemodynamics. that these patients be extubated as soon as possible after the risk
is diminished. A trial of extubation is often warranted in the first
Organ Failure few days after injury, and reintubation in this setting is not a
Even with the best efforts at prevention, the presence of the sys- failure. To perform this technique safely, however, requires the
temic inflammatory syndrome that is ubiquitous in burned involvement of experts in obtaining an airway. The goal is extuba-
patients may progress to organ failure. It was recently found that tion as soon as possible to allow the patients to clear their own
approximately 28% of patients with more than 30% TBSA burns airways because they can perform their own pulmonary toilet
will develop severe multiorgan dysfunction, of which 14% will better than through an endotracheal tube or tracheostomy. The
also develop severe sepsis and septic shock. The general develop- first sign of impending pulmonary failure is a decline in oxygen-
ment begins in either the renal or pulmonary system and can ation. This is best followed up with continuous oximetry, and a
progress through the liver, gut, hematologic system, and central decrease in saturation to less than 92% is indicative of failure.
nervous system. Whereas the development of multiorgan failure Increasing concentrations of inspired oxygen are necessary, and
does not predict mortality, a study found a greater than 50% when ventilation begins to fail, denoted by increasing respiratory
prevalence of multiorgan failure among nonsurvivors of burn rate and hypercapnia, intubation is needed.
injury.19 Some have stated that early tracheostomy (within the first
week) might be indicated in those with significant burn who are
Renal Failure likely to require long-term ventilation. In one study, it was found
With the advent of early aggressive resuscitation, the incidence of in severely burned children who underwent early tracheostomy
renal failure coincident with the initial phases of recovery has that the peak inspiratory pressures were lower after tracheostomy,
diminished significantly in severely burned patients. However, a with higher ventilatory volumes and pulmonary compliance and
second period of risk for the development of renal failure 2 to higher PaO2/FIO2 ratios. No instances of tracheostomy site infec-
14 days after resuscitation is still present. Renal failure is hall- tions or tracheal stenoses were identified in the 28 patients studied.
marked by decreasing urine output, fluid overload, electrolyte Another randomized study comparing those severely burned
abnormalities including metabolic acidosis and hyperkalemia, patients who underwent early tracheostomy with those who did
development of azotemia, and increased serum creatinine level. not found similar improvements in oxygenation; however, no
Treatment is aimed at averting complications associated with these significant differences could be found in outcome measures such
conditions. as ventilator days, length of stay, incidence of pneumonia, or
Urine output of more than 1 mL/kg is an adequate measure survival. In fact, 26% of those not undergoing tracheostomy were
of renal perfusion in the absence of underlying renal disease. successfully extubated within 2 weeks of admission, implying that

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CHAPTER 19  Burns 521

they would not have required tracheostomy at all. It seems that ATTENUATION OF THE
although tracheostomy may be required in some severely burned HYPERMETABOLIC RESPONSE
patients on ventilatory support, the advantages of early tracheos-
tomy do not outweigh the disadvantages. Further data from other Nonpharmacologic Modalities
centers may change this conclusion in the future. Nutritional Support
The response to injury known as hypermetabolism occurs dra-
Hepatic Failure matically after severe burn. Increases in oxygen consumption,
The development of hepatic failure in burned patients is a chal- metabolic rate, urinary nitrogen excretion, lipolysis, and weight
lenging problem without many solutions. The liver synthesizes loss are directly proportional to the size of the burn. This response
circulating proteins, detoxifies the plasma, produces bile, and can be as high as 200% of the normal metabolic rate and returns
provides immunologic support. After severe burn injury, the liver to normal only with the complete closure of the wound. Because
increases in size to more than 200% of normal.14 When the liver the metabolic rate is so high, energy requirements are immense.
begins to fail, protein concentrations of the coagulation cascade These requirements are met by mobilization of carbohydrate, fat,
decrease to critical levels and the patient becomes coagulopathic. and protein stores. Because the demands are prolonged, these
Toxins are not cleared from the bloodstream, and concentrations energy stores are quickly depleted, leading to loss of active muscle
of bilirubin increase. Complete hepatic failure is not compatible tissue and malnutrition. This malnutrition is associated with func-
with life, but a gradation of liver failure with some decline of the tional impairment of many organs, delayed and abnormal wound
function is common. Efforts to prevent hepatic failure are the only healing, decreased immunocompetence, and altered cellular mem-
effective methods of treatment. brane active transport functions. Malnutrition in burns can be
With the development of coagulopathies, treatment should be subverted to some extent by delivery of adequate exogenous nutri-
directed at replacement of factors II, VII, IX, and X until the liver tional support. The goals of nutrition support are to maintain
recovers. Albumin replacement may also be required. Attention and to improve organ function and to prevent protein-calorie
to obstructive causes of hyperbilirubinemia, such as acalculous malnutrition.
cholecystitis, should be considered as well. Initial treatment of this Several formulas are used to calculate calorie requirements in
condition should be gallbladder drainage, which can be done burned patients. One formula multiplies the basal energy expen-
percutaneously. diture determined by the Harris-Benedict formula by 2 in burns
of 40% TBSA, assuming a 100% increase in total energy expen-
Hematologic Failure diture. When total energy expenditure was measured by the
Burned patients may become coagulopathic through two mecha- doubly labeled water method, actual expenditures were found to
nisms: (1) depletion and impaired synthesis of coagulation factors be 1.33 times the predicted basal energy expenditure for pediatric
and (2) thrombocytopenia. Factors associated with factor deple- patients with burns of more than 40% TBSA. To meet the
tion are through disseminated intravascular coagulation associated minimal needs of all the patients in this study, 1.55 times the
with sepsis. This process is also common with coincident head predicted basal energy expenditure would be required; however,
injury. With breakdown of the blood-brain barrier, brain lipids giving calorie loads in excess of this probably leads to fat accumu-
are exposed to the plasma, which activates the coagulation cascade. lation without affecting lean mass accretion. This correlated to 1.4
Varying penetrance of this problem results in differing degrees of times the measured resting energy expenditure by indirect calo-
coagulopathy. Treatment of disseminated intravascular coagula- rimetry. These studies indicate that the calculation of 2 times the
tion should include infusion of fresh-frozen plasma and cryopre- predicted basal energy expenditure might be too high.
cipitate to maintain plasma levels of coagulation factors. For Other commonly used calculations include the Curreri
disseminated intravascular coagulation induced by brain injury, formula, which calls for 25 kcal/kg/day plus 40 kcal per percent-
the concentration of fibrinogen and levels with cryoprecipitate are age of TBSA burned per day. This formula provides for mainte-
the most specific indicators. Impaired synthesis of factors from nance needs plus the additional calorie needs related to the burn
liver failure is treated as alluded to earlier. wounds. This formula was devised as a regression from nitrogen
Thrombocytopenia is common in severe burns from depletion balance data in severely burned adults. In children, formulas based
during burn wound excision. Platelet counts lower than 50,000 on body surface area are more appropriate because of the greater
are common and do not require treatment. Only when the bleed- body surface area per kilogram of weight. We recommend
ing is diffuse and is noted to occur from intravenous sites should the formulas depending on the child’s age (Table 19-6). These
administration of exogenous platelets of considered.
Paradoxically, it was found that severely burned patients are
also at risk for thrombotic and embolic complications likely TABLE 19-6  Formulas to Predict Calorie
related to immobilization. It was found that complications of deep
venous thrombosis were associated with increasing age, weight,
Needs in Severely Burned Children
and TBSA burned. These data intimate that deep venous throm- MAINTENANCE BURN WOUND
bosis prophylaxis would be prudent for adult patients in the AGE GROUP NEEDS NEEDS
absence of bleeding complications. Infants (0-12 months) 2100 kcal/% TBSA 1000 kcal/% TBSA
burned/24 hours burned/24 hours
Central Nervous System Failure
Children (1-12 years) 1800 kcal/% TBSA 1300 kcal/% TBSA
Obtundation is one of the hallmarks of sepsis, and burn burned/24 hours burned/24 hours
patients are no exception. A new onset of mental status changes Adolescents (12-18 years) 1500 kcal/% TBSA 1500 kcal/% TBSA
not attributed to sedative medications in a severely burned burned/24 hours burned/24 hours
patient should incite a search for a septic source. Treatment is
supportive. TBSA, total body surface area.

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522 SECTION III  Trauma and Critical Care

formulas were determined to maintain body weight in severely Exercise and Adjunctive Measures
burned children. The formulas change with age on the basis of A balanced physical therapy program is essential to restore meta-
the body surface area alterations that occur with growth. bolic variables and to prevent burn wound contracture. Progres-
The composition of the nutritional supplement is also impor- sive resistance exercises in convalescent burn patients can maintain
tant. The optimal dietary composition contains 1 to 2 g/kg/day and improve body mass, augment incorporation of amino acids
of protein, which provides a calorie to nitrogen ratio at around into muscle proteins, and increase muscle strength and the ability
100 : 1 with the earlier suggested calorie intakes. This amount of to walk distances by approximately 50%. It has been demon-
protein provides for the synthetic needs of the patient, thus strated that resistance exercising can be safely accomplished in
sparing to some extent the proteolysis occurring in the active pediatric burn patients without exercise-related hyperpyrexia as
muscle tissue. Nonprotein calories can be given either as carbo- the result of an inability to dissipate the generated heat. Although
hydrate or as fat. Carbohydrates have the advantage of stimulating the initial burn injury and sepsis-related complications principally
endogenous insulin production, which may have beneficial effects determine the extent of the metabolic response in burn victims,
on muscle and burn wounds as an anabolic hormone. In addition, obligatory activity, background and procedure-related pain, and
it was recently shown that almost all of the fat transported in anxiety also greatly increase metabolic rates. Judicious maximal
very-low-density lipoprotein after severe burn is derived from narcotic support, appropriate sedation, and supportive psycho-
peripheral lipolysis and not from de novo synthesis of fatty acids therapy are mandatory to minimize their effects.
in the liver from dietary carbohydrates. As fat transporters are
markedly decreased, we suggest use of a low-fat diet because Pharmacologic Modalities
additional fat to deliver noncarbohydrate calories has little Recombinant Human Growth Hormone
support. Daily intramuscular administration of recombinant human
The diet may be delivered in two forms: either enterally growth hormone (rhGH) at doses of 0.2 mg/kg as a daily injec-
through enteric tubes or parenterally through intravenous cathe- tion during acute burn care has favorably influenced the hepatic
ters. Parenteral nutrition may be given in isotonic solutions acute-phase response, increased serum concentrations of its sec-
through peripheral catheters or with hypertonic solutions in ondary mediator IGF-I, improved muscle protein kinetics, main-
central catheters. In general, the calorie demands of burned tained muscle growth, decreased donor site healing time by 1.5
patients prohibit the use of peripheral parenteral nutrition. Total days, improved resting energy expenditure, and decreased cardiac
parenteral nutrition delivered centrally in burned patients has output.34 These beneficial effects of rhGH are mediated by IGF-I,
been associated with increased complications and mortality rate and patients receiving treatment demonstrated 100% increases
compared with enteral feedings. Total parenteral nutrition is in serum IGF-I and IGFBP-3 relative to healthy individuals.
reserved only for those patients who cannot tolerate enteral feed- However, in a prospective, multicenter, double-blind, random-
ings. Enteral feeding has been associated with some complica- ized, placebo-controlled trial involving 247 patients and 285 criti-
tions, which include mechanical complications, enteral feeding cally ill nonburned patients, Branski and coworkers34 found that
intolerance, and diarrhea. high doses of rhGH (0.10 ± 0.02 mg/kg body weight) were
Interest in nutritional adjunctive treatment with anabolic associated with increased morbidity and mortality. Others
agents has recently received attention as a means to decrease lean demonstrated growth hormone treatment to be associated with
mass losses after severe injury. Agents used include growth hyperglycemia and insulin resistance. However, neither short-
hormone, insulin-like growth factor, insulin, oxandrolone, testos- term nor long-term administration of rhGH was associated with
terone, and propranolol. Each of these agents has different an increase in mortality in severely burned children.
actions to stimulate protein synthesis through an increase in
protein synthetic efficiency. Put simply, the free amino acids Insulin-like Growth Factor
available in the cytoplasm from stimulated protein breakdown Because IGF-I mediates the effects of growth hormone, the infu-
with severe injury or illness are preferentially shunted toward sion of equimolar doses of recombinant human IGF-I and
protein synthesis rather than export out of the cell. Some of these IGFBP-3 to burned patients has been demonstrated to effectively
agents, such as insulin and oxandrolone, have shown efficacy not improve protein metabolism in catabolic pediatric subjects and
only in improving protein kinetics but also in improving lean adults with significantly less hypoglycemia than with rhGH itself.
mass after severe burn. Further research will reveal whether these It attenuates muscle catabolism and improves gut mucosal integ-
biochemical and physiologic measures translate to improved rity in children with serious burns. Immune function is effectively
function. improved by attenuation of the type 1 and type 2 hepatic acute-
phase responses, increased serum concentrations of constitutive
Environmental Support proteins, and vulnerary modulation of the hypercatabolic use of
Burn patients can lose as much as 4000 mL/m2 burned skin per body protein.12 However, studies by Langouche and Van den
day of body water through evaporative loss from extensive burn Berghe35 indicate that the use of IGF-I alone is not effective in
wounds that have not definitively healed. The altered physiologic critically ill patients without burns.
state resulting from the hypermetabolic response attempts to at
least partly generate sufficient energy to offset heat losses associ- Oxandrolone
ated with this inevitable water loss. The body attempts to raise Treatment with anabolic agents such as oxandrolone, a testoster-
skin and core temperatures to 2° C above normal. Raising the one analogue that possesses only 5% of its virilizing androgenic
ambient temperature from 25° C to 33° C can diminish the effects, improves muscle protein catabolism through enhanced
magnitude of this obligatory response from 2.0 to 1.4 resting protein synthesis efficiency, reduces weight loss, and increases
energy expenditure in patients exceeding 40% TBSA (Fig. donor site wound healing. In a prospective randomized study,
19-11).12 This simple environmental modulation is an important Wolf and colleagues36 demonstrated that administration of 10 mg
primary treatment goal that frequently is not realized. of oxandrolone every 12 hours decreased hospital stay. In a large

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CHAPTER 19  Burns 523

0.05 0.05
Time to excision Effect of diet on net protein balance
during acute hospitalization
µmol/min/100 cc leg

µmol/min/100 cc leg
–0.05 –0.05
Early Late High fat High
carbohydrate

160 100
Ambient temperature Effect of exercise on LBM, strength,
and power over time
% basal metabolic rate

Peak torque (NM)


Exercise

No exercise

40

20 22 24 26 28 30 32 Admit Dis- 6 9 12 18 24
charge mon mon mon mon mon
Temperature (°C)
Time postburn

FIGURE 19-11  Nonpharmacologic modulations of the hypermetabolic response after burn injury. The effect
is demonstrated of early excision and grafting, environmental thermoregulation, high-carbohydrate diet, and
exercise on physiologic derangements after burn injury. Graphs are averages ± standard error of the mean.
The yellow bars represent patients with burns ≥40% total body surface area (TBSA) who had early excision.
The blue bars represent patients with burns ≥40% TBSA who had late excision of burn eschar. Averages
for burn patients are represented by solid curves. Values from nonburned, normal patients are represented
by dashed lines. LBM, lean body mass. (From Williams FN, Jeschke MG, Chinkes DL, et al: Modulation of
the hypermetabolic response to trauma: Temperature, nutrition, and drugs. J Am Coll Surg 208:489–502,
2009.)

prospective, double-blinded, randomized single-center study, infiltration of the liver, which typically occurs in these patients as
oxandrolone given at a dose of 0.1 mg/kg every 12 hours short- the result of enhanced peripheral lipolysis and altered substrate
ened length of acute hospital stay, maintained lean body mass, handling. Reduction of hepatic fat results from decreased periph-
and improved body composition and hepatic protein synthesis eral lipolysis and reduced palmitate delivery and uptake by the
(Fig. 19-12).37 The effects were independent of age. Long-term liver, producing smaller livers that adversely affect diaphragmatic
treatment with this oral anabolic during rehabilitation in the function less frequently. Stable isotope and serial body composi-
outpatient setting is more favorably regarded than parenteral ana- tion studies showed that administration of propranolol reduces
bolic agents by pediatric subjects. Oxandrolone successfully abates skeletal muscle wasting and increases lean body mass after burn
the effects of burn-associated hypermetabolism on body tissues injury.12 The underlying mechanism of action of propranolol is
and significantly increases body mass over time, lean body mass still unclear; however, its effect appears to be due to an increased
(at 6, 9, and 12 months after burn injury), and bone mineral protein synthesis in the face of a persistent protein breakdown and
content by 12 months after injury versus unburned controls.38 reduced peripheral lipolysis.39 Data suggest that administration of
Patients treated with oxandrolone show few complications relative propranolol given at 4 mg/kg body weight every 24 hours also
to those treated with rhGH. However, although anabolic agents markedly decreases the amount of insulin necessary to decrease
can increase lean body mass, exercise is essential to development elevated glucose level after burn injury (unpublished data). Pro-
of strength. pranolol may thus constitute a promising approach to overcome
postburn insulin resistance.
Propranolol
β-Adrenergic blockade with propranolol represents probably the Attenuation of Hyperglycemia after Burn Injury
most efficacious anticatabolic therapy in the treatment of burns. Insulin
Long-term use of propranolol during acute care in burn patients, Insulin represents probably one of the most extensively studied
at a dose titrated to reduce heart rate by 15% to 20%, was noted therapeutic agents, and novel therapeutic applications are con-
to diminish cardiac work (Fig. 19-13). It also reduced fatty stantly being found. Besides its ability to decrease blood glucose

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524 SECTION III  Trauma and Critical Care

8 0.05
Protein fractional synthetic rate Net protein balance

µmol/min/100 cc leg
% day–1

–0.05

5 Lean body mass 10


Lean body mass
% change

% change
–5 –10
Placebo Propranolol
Strength compared to
5 nonburned children 6 × 105

Cardiac work (mmHg × mls


peak torque (nm)

per beat × beat per min)


Placebo
% change in

Propranolol
Normal

Placebo Oxandrolone
Admit Week 2 Week 3 D/C
FIGURE 19-12  Effect of oxandrolone treatment on the fractional syn- FIGURE 19-13  Effect of propranolol treatment on the fractional syn-
thetic rate of muscle protein synthesis, lean body mass, and strength.
thetic rate of muscle protein synthesis, lean body mass, and cardiac
Changes in net protein balance of muscle protein synthesis and break-
work. Changes in net protein balance of muscle protein synthesis and
down induced by burn injury were measured by stable isotope studies
breakdown induced by burn injury were measured by stable isotope
using d5-phenylalanine infusion. Graphs are averages ± standard error
studies using d5-phenyalanine infusion. Graphs are averages ± standard
of the mean. The yellow bars represent patients with burns ≥40% total
error of the mean. The yellow bars represent patients with burns ≥40%
body surface area (TBSA) who received no anabolic agents. The blue
total body surface area (TBSA) who received no anabolic agents. The
bars represent patients with burns ≥40% TBSA who were randomized
blue bars represent patients with burns ≥40% TBSA who were random-
to receive oxandrolone. (From Williams FN, Jeschke MG, Chinkes DL,
ized to receive propranolol. Values from nonburned, normal patients are
et al: Modulation of the hypermetabolic response to trauma: Tempera-
represented by dashed lines. (From Williams FN, Jeschke MG, Chinkes
ture, nutrition, and drugs. J Am Coll Surg 208:489–502, 2009.)
DL, et al: Modulation of the hypermetabolic response to trauma: Tem-
perature, nutrition, and drugs. J Am Coll Surg 208:489–502, 2009.)

concentration by mediating peripheral glucose uptake into skel-


etal muscle and adipose tissue and suppressing hepatic gluconeo-
genesis, insulin is known to increase DNA replication and protein was also found to significantly reduce newly acquired kidney
synthesis through control of amino acid uptake, to increase fatty injury, to accelerate weaning from mechanical ventilation, and to
acid synthesis, and to decrease proteinolysis.13 The last makes accelerate discharge from the ICU and the hospital.43 When given
insulin particularly attractive for the treatment of hyperglycemia during the acute phase, it not only improved acute hospital out-
in severely burned patients because insulin given during acute comes but also improved long-term rehabilitation and social
hospitalization has been shown to improve muscle protein syn- reintegration of critically ill patients during a period of 1 year,
thesis, to accelerate donor site healing time, and to attenuate lean indicating the advantage of insulin therapy.44,45 However, because
body mass loss and the acute-phase response (Fig. 19-14).13 In strict blood glucose control to maintain normoglycemia was
addition to its anabolic actions, insulin was shown to exert totally required to obtain the most clinical benefit, a dialogue has emerged
unexpected anti-inflammatory effects potentially neutralizing the between those who believe that tight glucose control is beneficial
proinflammatory actions of glucose.40,41 These results suggest a for patient outcome and others who fear that high doses of insulin
dual benefit of insulin administration: reduction of proinflamma- may lead to increased risk for hypoglycemic events and its associ-
tory effects of glucose by restoration of euglycemia and a proposed ated consequences in these patients. In fact, a multicenter trial in
additional insulin-mediated anti-inflammatory effect.42 Insulin Europe, Efficacy of Volume Substitution and Insulin Therapy in
administered to maintain glucose at levels below 110 mg/dL Severe Sepsis (VISEP), investigated the effects of insulin admin-
decreased mortality, incidence of infections, sepsis, and sepsis- istration on morbidity and mortality in patients with severe infec-
associated multiorgan failure in surgically critically ill patients. It tions and sepsis.46 The authors found that insulin administration

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CHAPTER 19  Burns 525

Metformin
8
Protein fractional synthetic rate Metformin (Glucophage), a biguanide, can be used as an alterna-
tive means to correct hyperglycemia in severely injured patients.
By inhibiting gluconeogenesis and augmenting peripheral insulin
% day–1

sensitivity, metformin directly counters the two main metabolic


processes that underlie injury-induced hyperglycemia. In addi-
tion, metformin has been rarely associated with hypoglycemic
events, thus possibly eliminating this concern associated with the
use of exogenous insulin. In a small randomized study reported
by Gore and colleagues,49 metformin reduced plasma glucose
5 Lean body mass concentration, decreased endogenous glucose production, and
accelerated glucose clearance in severely burned patients. A
follow-up study looking at the effects of metformin on muscle
% change

protein synthesis confirmed these observations and demonstrated


an increased fractional synthetic rate of muscle protein and
improvement in net muscle protein balance in metformin-treated
patients.49 Thus, analogous to insulin, metformin may have effi-
cacy in critically injured patients as both an antihyperglycemic
–5
and a muscle protein anabolic agent. Despite the advantages and
potential therapeutic uses, treatment with metformin or other
200 Blood glucose biguanides has been associated with lactic acidosis. To avoid
metformin-associated lactic acidosis, the use of this medication is
contraindicated in certain diseases or illnesses in which there is a
potential for impaired lactate elimination (hepatic or renal failure)
mg/dL

or tissue hypoxia, and it should be used with caution in subacute


burn patients.

Novel Therapeutic Options


Placebo Insulin
Other ongoing trials to decrease postburn hyperglycemia include
the use of glucagon-like peptide 1 and peroxisome proliferator-
FIGURE 19-14  Effect of insulin therapy on the fractional synthetic rate activated receptor gamma (PPAR-γ) agonists (e.g., pioglitazone,
of muscle protein synthesis, lean body mass, and average blood thioglitazones) or the combination of various antidiabetic drugs.
glucose levels. Changes in net protein balance of muscle protein syn- PPAR-γ agonists, such as fenofibrate, have been shown to improve
thesis and breakdown induced by burn injury were measured by stable insulin sensitivity in patients with diabetes. Cree and colleagues50
isotope studies using d5-phenylalanine infusion. Graphs are averages ±
found in a double-blind, prospective, placebo-controlled random-
standard error of the mean. The yellow bars represent patients with
burns ≥40% total body surface area (TBSA) who received no anabolic
ized trial that fenofibrate treatment significantly decreased plasma
agents or insulin. The blue bars represent patients with burns ≥40% glucose concentrations by improving insulin sensitivity and mito-
TBSA who were randomized to receive insulin. (From Williams FN, chondrial glucose oxidation. Fenofibrate also led to significantly
Jeschke MG, Chinkes DL, et al: Modulation of the hypermetabolic increased tyrosine phosphorylation of the insulin receptor and
response to trauma: Temperature, nutrition, and drugs. J Am Coll Surg insulin receptor-substrate 1 in muscle tissue after hyperinsulinemic-
208:489–502, 2009.) euglycemic clamp compared with placebo-treated patients, indi-
cating improved insulin receptor signaling.50

did not affect mortality, but the rate of severe hypoglycemia was
fourfold higher in patients receiving intensive insulin therapy SPECIAL CONSIDERATIONS: ELECTRICAL
compared with the conventional therapy group.46 Another large AND CHEMICAL BURNS
multicenter study examined the use of a continuous hyperinsu-
linemic, euglycemic clamp throughout ICU stay and found a Electrical Burns
dramatic increase in serious hypoglycemic episodes.47 The ideal Initial Treatment
target glucose range therefore has not been found, and several Three percent to 5% of all admitted burned patients are injured
groups are currently undertaking clinical trials to define ideal from electrical contact. Electrical injury is unlike other burn inju-
glucose levels for the treatment of ICU and burned patients. Cur- ries in that the visible areas of tissue necrosis represent only a small
rently, the Surviving Sepsis Campaign recommendation is to portion of the destroyed tissue. Electrical current enters a part of
maintain glucose levels below 150 mg/dL.48 However, maintain- the body, such as the fingers or hand, and proceeds through tissues
ing a continuous hyperinsulinemic, euglycemic clamp in burn with the lowest resistance to current, generally the nerves, blood
patients is particularly difficult because these patients are being vessels, and muscles. The skin has a relatively high resistance to
continuously fed large calorie loads through enteral feeding tubes electrical current and is therefore mostly spared. The current then
in an attempt to maintain euglycemia. Because burn patients leaves the body at a “grounded” area, typically the foot. Heat
require weekly operations and daily dressing changes, enteral generated by the transfer of electrical current and passage of the
nutrition needs occasionally to be stopped, which may lead to current itself then injures the tissues. During this exchange, the
disruption of gastrointestinal motility and increased risk of muscle is the major tissue through which the current flows, and
hypoglycemia.5 thus it sustains the most damage. Most muscle is close to bones.

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526 SECTION III  Trauma and Critical Care

Blood vessels transmitting much of the electricity initially remain solubilize the hemochromogens and to maintain urine output if
patent, but they may proceed to progressive thrombosis as the significant amounts are found in the serum. These patients also
cells either die or repair themselves, thus resulting in further tissue require additional intravenous volumes above predicted amounts
loss from ischemia. based on the wound area because most of the wound is deep and
Injuries are divided into high- and low-voltage injuries. Low- cannot be assessed by standard physical examination. In this situ-
voltage injury is similar to thermal burns without transmission to ation, urine output should be maintained at 2 mL/kg/hr.
the deeper tissues; zones of injury from the surface extend into
the tissue. Most household currents (110 to 220 V) produce this Delayed Effects
type of injury, which causes only local damage. The worst of these Neurologic deficits may occur. Serial neurologic evaluations
injuries are those involving the edge of the mouth (oral commis- should be performed as part of routine examination to detect any
sure) sustained when children gnaw on household electrical cords. early or late neuropathologic changes. Central nervous system
The syndrome of high-voltage injury consists of varying degrees effects, such as cortical encephalopathy, hemiplegia, aphasia, and
of cutaneous burn at the entry and exit sites combined with brainstem dysfunction injury, have been reported up to 9 months
hidden destruction of deep tissue. Often, these patients also have after injury; others report delayed peripheral nerve lesions char-
cutaneous burns associated with ignition of clothing from the acterized by demyelination with vacuolization and reactive gliosis.
discharge of electrical current. Initial evaluation consists of car- Another devastating long-term effect is the development of cata-
diopulmonary resuscitation if ventricular fibrillation is induced. racts, which can be delayed for several years. These complications
Thereafter, if the initial electrocardiogram findings are abnormal may occur in up to 30% of patients with significant high-voltage
or there is a history of cardiac arrest associated with the injury, injury, and patients should be made aware of their possibility even
continued cardiac monitoring is necessary along with pharmaco- with the best treatment.
logic treatment for any dysrhythmias. The most serious derange-
ments occur in the first 24 hours after injury. If patients with Chemical Burns
electrical injuries have no cardiac dysrhythmias on initial electro- Most chemical burns are accidental from mishandling of house-
cardiogram or recent history of cardiac arrest, no further monitor- hold cleaners, although some of the most dramatic presentations
ing is necessary. involve industrial exposures. Thermal burns are, in general, short-
Patients with electrical injuries are at risk for other injuries, term exposures to heat, but chemical injuries may be of longer
such as being thrown from the electrical jolt or falling from duration, even for hours in the absence of appropriate treatment.
heights after disengaging from the electrical current. In addition, The degree of tissue damage as well as the level of toxicity is
the violent tetanic muscle contractions that result from alternating determined by the chemical nature of the agent, the concentration
current sources may cause a variety of fractures and dislocations. of the agent, and the duration of skin contact. Chemicals cause
These patients should be assessed in the same manner as any other their injury by protein destruction, with denaturation, oxidation,
patient with blunt traumatic injuries. formation of protein esters, or desiccation of the tissue. In the
The key to managing patients with an electrical injury lies in United States, the composition of most household and industrial
the treatment of the wound. The most significant injury is within chemicals can be obtained from the Poison Control Center in the
the deep tissue, and subsequent edema formation can cause vas- area, which can give suggestions for treatment.
cular compromise to any area distal to the injury. Assessment Speed is essential in the management of chemical burns. For
should include circulation to distal vascular beds because immedi- all chemicals, lavage with copious quantities of clean water should
ate escharotomy and fasciotomy may be required. If the muscle be done immediately after removal of all clothing. Dry powders
compartment is extensively injured and necrotic, such that the should be brushed from the affected areas before irrigation. Early
prospects for eventual function are dismal, early amputation may irrigation dilutes the chemical, which is already in contact with
be necessary. We advocate early exploration of affected muscle the skin, and timeliness increases effectiveness. Several liters of
beds and débridement of devitalized tissues, with attention given irrigant may be required. For example, 10 mL of 98% sulfuric
to the deeper periosteal planes because this is the area with the acid dissolved in 12 L of water decreases the pH to 5.0, a range
most muscle tissue. Fasciotomies should be complete and may that can still cause injury. If the chemical composition is known
require nerve decompressions, such as carpal tunnel and Guyon (acid or base), monitoring of the spent lavage solution pH gives
canal releases. Tissue that has questionable viability should be left a good indication of lavage effectiveness and completion. A good
in place, with planned reexploration in 48 hours. Many such rule of thumb is to lavage with 15 to 20 L of tap water or more
reexplorations may be required until the wound is completely for significant chemical injuries. The lavage site should be kept
débrided. Electrical damage to vessels may be delayed, and the drained to remove the earlier, more concentrated effluent. Care
extent of necrosis may extend after the initial débridements. After should be taken to drain away from uninjured areas to avoid
the devitalized tissues are removed, closure of the wound becomes further exposure.
paramount. Although skin grafts suffice as closure for most All patients must be monitored according to the severity of
wounds, flaps may offer a better alternative, particularly with their injuries. They may have metabolic disturbances, usually from
exposed bones and tendons. Even exposed and superficially pH abnormalities, because of exposure to strong acids or caustics.
infected bones and tendons can be salvaged with coverage by If respiratory difficulty is apparent, oxygen therapy and mechani-
vascularized tissue. Early involvement by reconstructive surgeons cal ventilation must be instituted. Resuscitation should be guided
versed in the various methods of wound closure is optimal. by the body surface area involved (burn formulas); however, the
Muscle damage results in release of hemochromogens (myo- total fluid needs may be dramatically different from the calculated
globin), which are filtered in the glomeruli and may result in volumes. Some of these injuries may be more superficial than they
obstructive nephropathy. Therefore, vigorous hydration and infu- appear, particularly in the case of acids, and therefore require less
sion of intravenous sodium bicarbonate (5% continuous infusion) resuscitation volume. Injuries from bases, however, may penetrate
and mannitol (25 g every 6 hours for adults) are indicated to beyond that which is apparent on examination and therefore

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CHAPTER 19  Burns 527

Incident with chemical agent

Irrigate copiously with water (several liters)

Acid burns Alkali burns

Check surface pH Check surface pH

If <7, continue irrigating until pH If >7.5, continue irrigating


reaches the physiologic range until pH reaches the
(7–7.5). Take care to direct the physiologic range (7–7.5).
irrigant away from noninjured skin. pH should be checked again
Once wound pH reaches a after débridement because alkali
physiologic range, the injury agents can penetrate through
process has finished the surface. Thereafter, treat the
wound with standard techniques

FIGURE 19-15  Treatment of acid and alkali burns.

require more volume. For this reason, patients with chemical such as underneath the boots of a cement worker who seeks treat-
injuries should be observed closely for signs of adequate perfusion, ment hours after the exposure or after the cement penetrates
such as urine output. All patients with significant chemical inju- clothing and, when combined with perspiration, induces an exo-
ries should be monitored with indwelling bladder catheters to thermic reaction. Treatment consists of removal of all clothing and
accurately measure outputs. irrigation of the affected area with water and soap until all the
Operative débridement, if indicated, should take place as soon cement is removed and the effluent has a pH of less than 8. Inju-
as a patient is stable and resuscitated (Fig. 19-15). After adequate ries tend to be deep because of exposure times, and surgical exci-
lavage and débridement, burn wounds are covered with antimi- sion and grafting of the resultant eschar may be required.
crobial agents or skin substitutes. Once the wounds have stabilized
with the indicated treatment, they are taken care of as with any Acids
loss of soft tissue. Skin grafting or flap coverage is performed as Acid injuries are treated initially like any other chemical injury,
needed. with removal of all chemicals by disrobing the affected area and
copious irrigation. Acids induce protein breakdown by hydrolysis,
Alkali which results in a hard eschar that does not penetrate as deeply
Alkalis, such as lime, potassium hydroxide, bleach, and sodium as that caused by the alkalis. These agents also induce thermal
hydroxide, are among the most common agents involved in chem- injury by heat generation with contact of the skin, further causing
ical injury. Accidental injury frequently occurs in infants and soft tissue damage. Some acids have added effects, which are
toddlers exploring cleaning cabinets. There are three factors discussed here.
involved in the mechanism of alkali burns: (1) saponification of Formic acid injuries are relatively rare, usually involving an
fat causes the loss of insulation of heat formed in the chemical organic acid used for industrial descaling and as a hay preservative.
reaction with tissue; (2) massive extraction of water from cells Electrolyte abnormalities are of great concern for patients who
causes damage because of the hygroscopic nature of alkali; and have sustained extensive formic acid injuries, with metabolic aci-
(3) alkalis dissolve and unite with the proteins of the tissues to dosis, renal failure, intravascular hemolysis, and pulmonary com-
form alkaline proteinates, which are soluble and contain hydrox- plications (acute respiratory distress syndrome) being common.
ide ions. These ions induce further chemical reactions, penetrating Acidemia detected by a metabolic acidosis on arterial blood gas
deeper into the tissue. Treatment involves immediate removal of analysis should be corrected with intravenous sodium bicarbon-
the causative agent with lavage of large volumes of fluid, usually ate. Hemodialysis may be required when extensive absorption of
water. Attempts to neutralize alkali agents with weak acids are not formic acid has occurred. Mannitol diuresis is required if severe
recommended because the heat released by neutralization reac- hemolysis occurs after deep injury. A formic acid wound typically
tions induces further injury. Particularly strong bases should be has a greenish appearance and is deeper than what it initially
treated with lavage and consideration for the addition of wound appears to be; it is best treated by surgical excision.
débridement in the operating room. Tangential removal of affected Hydrofluoric acid is a toxic substance used widely in both
areas is performed until the tissues removed are at a normal pH. industrial and domestic settings and is the strongest inorganic acid
Cement (calcium oxide) burns are alkali in nature, occur com- known. Management of these burns differs from that of other acid
monly, and are usually work-related injuries. The critical sub- burns in general. Hydrofluoric acid produces dehydration and
stance responsible for the skin damage is the hydroxyl ion. Often, corrosion of tissue with free hydrogen ions. In addition, the fluo-
the agent has been in contact with the skin for prolonged periods, ride ion complexes with bivalent cations such as calcium and

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528 SECTION III  Trauma and Critical Care

magnesium to form insoluble salts. Systemic absorption of the from these devastating injuries. Because of these specialized
fluoride ion then can induce intravascular calcium chelation and resources, burned patients are best treated in such places. Patients
hypocalcemia, which causes life-threatening arrhythmias. Beyond with the following criteria should be referred to a designated burn
initial copious irrigation with clean water, the burned area should center:
be treated immediately with copious 2.5% calcium gluconate gel. • Partial-thickness burns of more than 10% TBSA
These wounds in general are extremely painful because of the • Burns involving the face, hands, feet, genitalia, perineum, or
calcium chelation and associated potassium release. This finding major joints
can be used to determine the effectiveness of treatment. The gel • Any full-thickness burn
should be changed at 15-minute intervals until the pain subsides, • Electrical burns, including lightning injury
an indication of removal of the active fluoride ion. If pain relief • Chemical burns
is incomplete after several applications or if symptoms recur, • Inhalation injury
intradermal injections of 10% calcium gluconate (0.5 mL/cm2 • Burns in patients with preexisting medical disorders that could
affected), intra-arterial calcium gluconate into the affected extrem- complicate management, prolong recovery, or affect outcome
ity, or both may be required to alleviate symptoms. If the burn is • Any patient with burns and concomitant trauma (such as
not treated in such a fashion, decalcification of the bone underly- fractures) in which the burn injury poses the greater immediate
ing the injury and extension of the soft tissue injury may occur. risk of morbidity and mortality. In such cases, if the trauma
All patients with hydrofluoric acid burns should be admitted poses the greater immediate risk, the patient may be initially
for cardiac monitoring, with particular attention paid to prolon- stabilized in a trauma center before being transferred to a burn
gation of the QT interval. A total of 20 mL of 10% calcium unit. The physician’s judgment is necessary in such situations
gluconate solution should be added to the first liter of resuscita- and should be in concert with the regional medical control
tion fluid, and serum electrolytes must be closely monitored. Any plan and triage protocols.
electrocardiographic changes require a rapid response by the treat- • Burned children in hospitals without qualified personnel or
ment team with intravenous calcium chloride to maintain heart equipment to care for children
function. Several grams of calcium may be required in the end • Burns in patients who will require special social, emotional, or
until the chemical response has run its course. Serum magnesium long-term rehabilitative intervention
and potassium also should be closely monitored and replaced. Specialized care for severely burned patients in burn centers
Speed is the key to effective treatment. has contributed to the significant improvements in morbidity and
mortality. Today, the overall LD50 for all burns is a 70% TBSA,
Hydrocarbons meaning that today, a 70% TBSA burn has a 50% mortality for
The organic solvent properties of hydrocarbons promote cell all ages.8 Twenty years ago, the LD50 was a 50% TBSA.
membrane dissolution and skin necrosis. Symptoms include ery-
thema and blistering, and the burns are typically superficial and
heal spontaneously. If they are absorbed systemically, toxicity can SUMMARY
produce respiratory depression and eventual hepatic injury
thought to be associated with benzenes. Ignition of the hydrocar- The treatment of burns is complex. Minor injuries can be treated
bons on the skin induces a deep full-thickness injury. in the community by knowledgeable physicians. Moderate and
severe injuries, however, require treatment in dedicated facilities
with resources to maximize the outcomes from these often devas-
tating events.
OUTCOMES Novel concepts and techniques have been proposed and sig-
Many of the treatments for burn are directed at improving func- nificantly improved during the past 30 years, resulting in a con-
tional, psychological, and work outcomes, which are only now siderable decline in burn-related deaths and hospital admissions
being systematically studied. Authors are now reporting new in the United States. The single greatest advancement in treating
methods to evaluate outcomes through burn-specific health scales patients with severe thermal injuries during the last 20 years has
and measures of adjustment. Authors found that severely burned probably been early excision and closure of the burn wound,
adult patients adjust relatively well, although some develop clini- leading to substantially reduced resting energy requirements and
cally significant psychological disturbances, such as somatization subsequent improvement of mortality rates in this particular
and phobic anxiety. Children with severe burns were found to population of patients. The adequate and rapid institution of fluid
have similar somatization problems as well as sleep disturbances resuscitation maintains tissue perfusion and prevents organ system
but in general were well adjusted. Time off work in adult patients failure. Sepsis is successfully controlled by early excision of burn
was found to be associated with increasing percentage TBSA wounds and topical antimicrobial agents. Patients suffering from
burned, psychiatric history, and extremity burns with considerable sustained inhalation injury require additional fluid resuscitation,
job disruption. In general, major burns can lead to significant humidified oxygen, and, occasionally, ventilatory support. Enteral
disturbances in psychiatric health and outcomes, but they can be tube feeding is commenced early to control stress ulceration, to
overcome. maintain intestinal mucosal integrity, and to provide fuel for the
resulting hypermetabolic state. Therapeutic approaches to over-
come this persistent hypermetabolism and associated hyperglyce-
BURN UNITS mia have remained challenging. At present, β-adrenergic blockade
with propranolol represents probably the most efficacious anti-
Improvements in burn care originated in specialized units specifi- catabolic therapy in the treatment of burns. Other pharmacologic
cally dedicated to the care of burned patients. These units consist strategies that have been successfully used to attenuate the hyper-
of experienced personnel with resources to maximize outcome metabolic response to burn injury include growth hormone,

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For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
CHAPTER 19  Burns 529

This landmark clinical trial showed that propranolol, a nonse-


rhGH * lective beta receptor antagonist, attenuates the profound
IGF-1 hypermetabolic response and the muscle-protein catabolism
High insulin * after severe burn injury.
Low insulin *
Oxandrolone Herndon DN, Tompkins RG: Support of the metabolic response
*
to burn injury. Lancet 363:1895–1902, 2004.
Propranolol *
rhGH and prop * This review was one of the premier articles to highlight the
many methods to attenuate the hypermetabolic response
and to thoroughly describe the physiologic and metabolic
0

25

0
75

50
0

00

02

05

07

10
.1

.0
.0

.0

0. derangements postburn.
0.

0.

0.

0.
–0

–0

–0

–0

*p <0.05 µmol/min/100 cc leg


Jeschke MG, Chinkes DL, Finnerty CC, et al: Pathophysiologic
FIGURE 19-16  Relative efficacy of the different anabolic agents to response to severe burn injury. Ann Surg 248:387–401, 2008.
improve muscle protein synthesis compared with standard of care
alone. Changes in net protein balance of muscle protein synthesis and This landmark clinical trial delineated the complexity of the
breakdown induced by burn injury were measured by stable isotope
hypermetabolic, hypercatabolic response to severe burn
studies using d5-phenylalanine infusion. *P < .05. Graphs are averages
± standard error of the mean. The yellow bars represent patients with
injury.
burns ≥40% total body surface area (TBSA) who received no anabolic
agents. The blue bars represent patients with burns ≥40% TBSA who Williams FN, Jeschke MG, Chinkes DL, et al: Modulation of the
were randomized to receive drug. (From Williams FN, Jeschke MG, hypermetabolic response to trauma: Temperature, nutrition, and
Chinkes DL, et al: Modulation of the hypermetabolic response to drugs. J Am Coll Surg 208:489–502, 2009.
trauma: Temperature, nutrition, and drugs. J Am Coll Surg 208:489–
502, 2009.) This review highlights the significant pharmacologic and non-
pharmacologic modulators of the postburn hypermetabolic
response that have been shown to improve morbidity and
mortality.
insulin-like growth factor, and oxandrolone (Fig. 19-16). Main-
taining blood glucose at levels below 110 mg/dL with intensive
Wolf SE, Rose JK, Desai MH, et al: Mortality determinants in
insulin therapy has been shown to reduce mortality and morbidity
massive pediatric burns. An analysis of 103 children with > or =
in critically ill patients; however, associated hypoglycemic events
80% TBSA burns (> or = 70% full-thickness). Ann Surg 225:554–
have led to the investigation of alternative strategies, including the
565, 1997.
use of metformin and the PPAR-γ agonist fenofibrate.
Further studies are needed to address the primary determinants
The treatment of severely burned pediatric patients and the
of death, inhalation injury complications, and pneumonia as well
major determinants of mortality are described in this article.
as to ameliorate pain and scar formation, which are the persistent
A formula was also devised to predict those who will survive
sequelae of this thermal injury. Better understanding of the basic
or succumb to their injuries.
mechanisms underlying the metabolic alterations after burn injury
may lead to the development of novel therapeutic options. Cen-
tralized care in burn units and multidisciplinary team approaches REFERENCES
will advance and extend current therapeutic strategies, thus further
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CHAPTER 19  Burns 531

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